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Muhammad, Aliyu, Oyeronke A. Odunola, Michael A. Gbadegesin, Abdullahi B. Sallau, Uche S. Ndidi, and Mohammed A. Ibrahim. "Inhibitory Effects of Sodium Arsenite and Acacia Honey on Acetylcholinesterase in Rats." International Journal of Alzheimer's Disease 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/903603.
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This study was conducted to investigate the effect of sodium arsenite and Acacia honey on acetylcholinesterase (AChE) activity and electrolytes in the brain and serum of Wistar rats. Male Wistar albino rats in four groups of five rats each were treated with distilled water, sodium arsenite (5 mg/kg body weight), Acacia honey (20% v/v), and sodium arsenite and Acacia honey, daily for one week. The sodium arsenite and Acacia honey significantlyP<0.05decreased AChE activity in the brain with the combined treatment being more potent. Furthermore, sodium arsenite and Acacia honey significantlyP<0.05decreased AChE activity in the serum. Strong correlation was observed between the sodium and calcium ion levels with acetylcholinesterase activity in the brain and serum. The gas chromatography mass spectrometry analysis of Acacia honey revealed the presence of a number of bioactive compounds such as phenolics, sugar derivatives, and fatty acids. These findings suggest that sodium arsenite and/or Acacia honey modulates acetylcholinesterase activities which may be explored in the management of Alzheimer’s diseases but this might be counteracted by the hepatotoxicity induced by arsenics.
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Shakya, Sangita, and B. Pradhan. "Isolation and Characterization of Arsenic Resistant Pseudomonas Stutzeri ASP3 for its Potential in Arsenic Resistance and Removal." Kathmandu University Journal of Science, Engineering and Technology 9, no. 1 (July 31, 2013): 48–59. http://dx.doi.org/10.3126/kuset.v9i1.63842.
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Inorganic arsenic both arsenite As (III) and arsenate As (V) constitute the highest toxicological risk associated with arsenic in drinking water. Novel methods are in demand for its removal from water, especially in rural areas. For this purpose, the potential of different microbes in arsenic resistance and removal from water has gained interests worldwide. This study investigates the arsenic resistance and removal capacity of a bacterial strain isolated from arsenic enriched water of Rautahat district in Nepal. The concentration of arsenic was by hydride generation atomic absorption spectrophotometer. The isolated bacterium showed high resistance to sodium arsenate up to 4,680.15 mg/l and sodium arsenite up to 649.55 mg/l. The bacterium also conferred multiple heavy metal resistance to zinc chloride (136.28 mg/l), copper sulphate (249.68 mg/l), mercuric chloride (5.43 mg/l) and silver nitrate (3.39 mg/l). The growth rate calculated in the presence of 129.01 mg/l of sodium arsenite was 0.35 h-1 with doubling time of 1.96 h. The strain showed growth in the range of 25–45 °C (optimum 30-35 °C), pH 6 – 9 (optimum 7.5-8.5) and tolerated up to 10% of NaCl. The PCR-based 16S rDNA sequence analysis revealed that the isolated As resistant bacterium is a close relative to P. stutzeri (99%) with 30 hits. The bacterium removed 82.97 % of As (V) and 49.4% of As (III) from culture medium amended with 200 mg/l sodium arsenate and 74.92 mg/l of sodium arsenite respectively.
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Divine Obichukwu Anakor and Kelechi Light Ekeke. "Effects of combined leaf extracts of Vernonia amygdalina and Ocimum gratissimum on biochemical parameters of sodium arsenite induced toxicity in albino Wister rat." World Journal of Advanced Research and Reviews 19, no. 2 (August 30, 2023): 669–74. http://dx.doi.org/10.30574/wjarr.2023.19.2.1624.
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This study was carried out to examine the effect of different leaf extract treatment on Sodium Arsenite toxicity in albino Wister rat model. Twenty-five (25) rats weighing between 120-270 g were used in this experiment and randomly divided into five (5) groups containing five rats each. Group 1 animals served as control and was administered placebo, while group 2 was induced with only sodium arsenite, 3 and 4 were both induced with sodium arsenite sand treated with Ocimum gratissimum ethanoic extract and Vernonia amygalina ethanoic extract respectively. Group 5 received concomitant administration of both extract after induction for 14 days. All drugs and extract administration were dose dependent on kilogram body weight using a cannula attached to a syringe. The result showed a significant elevation of sodium arsenite in group 2 serving as a biochemical marker defining sodium arsenide toxicity to living rat model tissue when compared to group 1. Group 5 showed no significant (p<0.05) difference when compared to group 1. Thus, showing an overall improvement in the effect of combined administration of the extract in the management of sodium arsenite level in sodium asenite induced toxicity when compared to groups 3 and 4 which may be associated with the phytochemicals present in both herbs.
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Bhatti, Zulfiqar Ali. "Removal of Arsenite and Arsenate by Indigenous Iron Ores of Pakistan." Pakistan Journal of Analytical & Environmental Chemistry 21, no. 2 (December 24, 2020): 293–302. http://dx.doi.org/10.21743/pjaec/2020.12.31.
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This study is focusing on the comparative study of arsenite and arsenate adsorption from the water via indigenous iron ores. The Sindh and Punjab provinces of Pakistan are badly affected by Arsenic (As) toxicity as the people are consuming arsenic contaminated groundwater. The aim of this study is to investigate the effect of anions on adsorption of arsenite As(III) and arsenate As(V). Impact of pH, contact time, adsorbent dose and shaking speed on adsorption of arsenite and arsenate is studied with the two selected iron ores from Hoshi and Shikarap from Balochistan. Hoshi and Shikarap ores exhibited higher As(III) and As (V) adsorption, respectively thus selected for further removal studies. Hoshi iron ore without sodium carbonate yields higher adsorption as compared to the samples with 100 mg/L and 1000 mg/L sodium carbonate in both As(III) and As(V). Hoshi ore exhibited the highest adsorption of 85% for As (V) without sodium phosphate dibasic and 83% for As(III). Shikarap ore for As(V) adsorbs 75% without sodium phosphate dibasic and 67% adsorption for As(III) without sodium phosphate dibasic. Shikarap ore with sodium silicate at 100 mg/L adsorbs 62% As(III) and at 1000 mg/L adsorb 52% As(III). Shikarap ore As(V) adsorption decreases from 75% without sodium silicate to 70% at 100 mg/L and even lower adsorption of 65% at a higher concentration of 1000 mg/L.
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Poudel, Pramod, Ashish Nepal, Rashmi Roka Magar, Pratibha Rauniyar, and Lil Buda Magar. "Screening of Potent Arsenic Resistant and Plant Growth Promoting Bacillus species from the Soil of Terai Region of Nepal." Tribhuvan University Journal of Microbiology 6 (December 6, 2019): 1–9. http://dx.doi.org/10.3126/tujm.v6i0.26572.
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Objectives: To isolate arsenic resistant Bacillus spp. and to determine plant growth promoting activities.
Methods: Eighteen soil samples were collected from the agricultural soil of Terai region of Nepal. Selective isolation of Bacillus species was done by heating the soil at 80 ºC for 15 minutes before the isolation. Nutrient agar was used as an isolation medium. Screening of arsenic resistant Bacillus species was done using nutrient agar supplemented with 100 ppm sodium arsenate and sodium arsenite. For plant growth promoting activity; IAA production was detected taking 0.1% tryptophane and measuring absorbance at 540 nm, NH3 production was tested by Nessler’s reagent and phosphate solubilization activity was detected by growing colonies on Pikovskaya’s agar. Sugar assimilation test was performed to identify the isolates. Most potent arsenic resistant isolate was identified by 16S rRNA gene sequencing.
Results: Among 54 randomly selected isolates, 42 were found to be Gram-positive rod-shaped, spore-forming while 12 isolates were Gram-negative bacteria. The isolates IN12a, M12a and BG34a showed growth on 100 ppm sodium arsenite containing NA. Only isolate M12a tolerated up to 1000 ppm and 15000 ppm of sodium arsenite and sodium arsenate respectively, while other isolates could not grow above 400 ppm sodium arsenite. The isolates IN12a and M12a were able to produce IAA and solubilize phosphate while BG34a could not. Both the isolates IN12a and M12a were able to utilize the sugars glucose, fructose, lactose, sucrose, galactose, mannose, mannitol, maltose and xylose. Based on the 16S rRNA gene sequencing, isolate M12a was identified to be Bacillus flexus with highest similarity of 99.2%.
Conclusion: Arsenic resistant and plant growth promoting Bacillus spp. was isolated from the agricultural soil of Terai region of Nepal
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Chanda, Dipanjan, Sung-Jin Kim, In-Kyu Lee, Minho Shong, and Hueng-Sik Choi. "Sodium arsenite induces orphan nuclear receptor SHP gene expression via AMP-activated protein kinase to inhibit gluconeogenic enzyme gene expression." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (August 2008): E368—E379. http://dx.doi.org/10.1152/ajpendo.00800.2007.
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Sodium arsenite has been demonstrated to alter the expression of genes associated with glucose homeostasis in tissues involved in the pathogenesis of type 2 diabetes; however, the underlying molecular mechanism has not been fully elucidated yet. In this study, we report that the sodium arsenite-induced gene expression of the small heterodimer partner (SHP; NR0B2), an atypical orphan nuclear receptor, regulates the expression of hepatic gluconeogenic genes. Sodium arsenite augments hepatic SHP mRNA levels in an AMP-activated protein kinase (AMPK)-dependent manner. Sodium arsenite activated AMPK and was shown to perturb cellular ATP levels. The arsenite-induced SHP mRNA level was blocked by adenoviral overexpression of dominant negative AMPK (Ad-dnAMPKα) or by the AMPK inhibitor compound C in hepatic cell lines. We demonstrated the dose-dependent induction of SHP mRNA levels by sodium arsenite and repressed the forskolin/dexamethasone-induced gene expression of the key hepatic gluconeogenic genes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase). Ad-dnAMPKα blocked the repressive effects of arsenite-induced SHP on PEPCK and G6Pase. Sodium arsenite inhibited the promoter activity of PEPCK and G6Pase, and this repression was abolished by small interfering (si)RNA SHP treatments. The knockdown of SHP expression by oligonucleotide siRNA SHP or adenoviral siRNA SHP released the sodium arsenite-mediated repression of forskolin/dexamethasone-stimulated PEPCK and G6Pase gene expression in a variety of hepatic cell lines. Results from our study suggest that sodium arsenite induces SHP via AMPK to inhibit the expression of hepatic gluconeogenic genes and also provide us with a novel molecular mechanism of arsenite-mediated regulation of hepatic glucose homeostasis.
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Ajit Kumar, Keshav Singh, Anand Pratap Singh, Sonal Singh, Prem Sagar, Shalini Yadav, Shekhar Biswas, and Sandeep Kumar. "A Critical Review on Hepatotoxicity in Albino Rats after Assessment of Sodium Arsenite." Journal of Science Innovations and Nature of Earth 4, no. 4 (December 30, 2024): 85–91. https://doi.org/10.59436/jsiane.306.2583-2093.
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In toxicological research, hepatotoxicity is a major worry, especially when looking at environmental contaminants like sodium arsenite. The health of people and animals is seriously endangered by sodium arsenite, a very poisonous substance that results from both natural and industrial processes and is found in air, water, and the soil. The hepatotoxic effects of sodium arsenite in Albino rats, a commonly utilized model organism for liver toxicity research, are extensively examined in this paper. With a focus on the consequences for the environment and public health, the paper summarizes previous research findings to clarify the impact of sodium arsenite on hepatic tissue in terms of biochemical, histological, and antioxidant indices. A detailed review of research indicates that sodium arsenite causes notable changes in indicators of liver function. Furthermore, exposure to sodium arsenite has been demonstrated to alter the liver histological architecture, resulting in inflammatory cell infiltration, sinusoidal dilatation, and hepatocyte destruction. The significance of dosage, exposure time, and delivery method in assessing the degree of hepatotoxic effects is also emphasized in this review. The administration methods, oral, intraperitoneal, or inhaled, have a major impact on sodium arsenite distribution and bioavailability, which in turn affects how hazardous it is. In conclusion, a great deal of research in albino rat models has shown that sodium arsenite is a serious hazard to liver health. We can more effectively handle the problems caused by this environmental toxin and protect the health of people and animals by improving our knowledge of sodium arsenite-induced hepatotoxicity.
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Alaniz-Andrade, Azucena Lucero, Consuelo Letechipía de León, Rosa María Ramírez-Santoyo, Jesús Guzmán-Moreno, and Luz Elena Vidales-Rodríguez. "Arsenic tolerance in bacterial cultures isolated from metal contaminated soil." Acta Universitaria 27, no. 3 (August 2, 2017): 9–18. http://dx.doi.org/10.15174/au.2017.1189.
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Several centuries of uninterrupted mining activities in Zacatecas, Mexico becomes a problem of soil pollution with toxic metals and metalloids as the arsenic. In this study, the arsenic-tolerance of ten bacterial isolates from a metal contaminated site were analyzed and high tolerance was observed in both solid (40 - 300 mM of sodium arseniate and 4 - 25 mM of sodium arsenite) and liquid media (7.2 and 11.3 mM arsenite). The arsenic tolerant isolates were identified by biochemical and 16S rRNA-encoding gene amplification analysis as members of the Bacillus, Micrococcus and Acinetobacter genus. A study of resistance to antibiotics revealed a high prevalence of resistance to beta-lactams and moderate prevalence to nitrofurantoin, vancomycin and ceftriaxone suggesting that antibiotic multiresistance of this isolates is probably related to arsenic tolerance throughout a plasmid or chromosomally encoded resistance mechanism.
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Parajuli, Pravin, Kuppan Gokulan, and Sangeeta Khare. "Preclinical In Vitro Model to Assess the Changes in Permeability and Cytotoxicity of Polarized Intestinal Epithelial Cells during Exposure Mimicking Oral or Intravenous Routes: An Example of Arsenite Exposure." International Journal of Molecular Sciences 23, no. 9 (April 27, 2022): 4851. http://dx.doi.org/10.3390/ijms23094851.
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The gastrointestinal tract (GIT) is exposed to xenobiotics, including drugs, through both: local (oral) and systemic routes. Despite the advances in drug discovery and in vitro pre-clinical models, there is a lack of appropriate translational models to distinguish the impact of these routes of exposure. Changes in intestinal permeability has been observed in different gastrointestinal and systemic diseases. This study utilized one such xenobiotic, arsenic, to which more than 200 million people around the globe are exposed via their food, drinking water, work environment, soil, and air. The purpose of this study was to establish an in vitro model to mimic gastrointestinal tract exposure to xenobiotics via oral or intravenous routes. To achieve this, we compared the route (mimicking oral and intravenous exposure to GIT and the dose response (using threshold approach) of trivalent and pentavalent inorganic arsenic species on the permeability of in vitro cultured polarized T84 cells, an example of intestinal epithelial cells. Arsenic treatment to polarized T84 cells via the apical and basolateral compartment of the trans-well system reflected oral or intravenous routes of exposure in vivo, respectively. Sodium arsenite, sodium arsenate, dimethyl arsenic acid sodium salt (DMAV), and disodium methyl arsonate hydrate (MMAV) were assessed for their effects on intestinal permeability by measuring the change in trans-epithelial electrical resistance (TEER) of T-84 cells. Polarized T-84 cells exposed to 12.8 µM of sodium arsenite from the basolateral side showed a marked reduction in TEER. Cytotoxicity of sodium arsenite, as measured by release of lactate dehydrogenase (LDH), was increased when cells were exposed via the basolateral side. The mRNA expression of genes related to cell junctions in T-84 cells was analyzed after exposure with sodium arsenite for 72 h. Changes in TEER correlated with mRNA expression of focal-adhesion-, tight-junction- and gap-junction-related genes (upregulation of Jam2, Itgb3 and Notch4 genes and downregulation of Cldn2, Cldn3, Gjb1, and Gjb2). Overall, exposure to sodium arsenite from the basolateral side was found to have a differential effect on monolayer permeability and on cell-junction-related genes as compared to apical exposure. Most importantly, this study established a preclinical human-relevant in vitro translational model to assess the changes in permeability and cytotoxicity during exposure, mimicking oral or intravenous routes.
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Bruez, Emilie, Philippe Larignon, Christophe Bertsch, Guillaume Robert-Siegwald, Marc-Henri Lebrun, Patrice Rey, and Florence Fontaine. "Impacts of Sodium Arsenite on Wood Microbiota of Esca-Diseased Grapevines." Journal of Fungi 7, no. 7 (June 22, 2021): 498. http://dx.doi.org/10.3390/jof7070498.
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Although sodium arsenite was widely used in Europe until its ban in 2003, its effects on microorganisms is not clearly understood. To improve our understanding of sodium arsenite curative effect on GTDs, grapevines displaying esca-foliar symptoms from different French regions (Alsace, Champagne, Languedoc) were treated or not with sodium arsenite, and analyzed for their wood microbiota. Using metabarcoding, we identified the fungal and bacterial taxa composition of microbiota colonizing woody trunk tissues. Large differences in fungal microbiota composition between treated and untreated grapevines were observed while no major impacts were observed on bacteria microbiota. The main fungal species detected in untreated necrotic woody tissues was Fomitiporia mediterranea (63–94%), a fungal pathogen associated with esca. The relative abundance of this fungal species significantly decreased after sodium arsenite treatment in the three vineyards, in particular in white-rot necrotic tissues and their borders (−90%). F. mediterranea was the most sensitive to sodium arsenite among fungi from grapevine woody tissues. These results strongly suggest that the effect of sodium arsenite on GTDs is due to its ability to efficiently and almost specifically eliminate F. mediterranea from white-rot necrotic tissues, allowing saprobic fungi to colonize the tissues previously occupied by this pathogenic fungus.
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Heikkila, J. J., S. P. Darasch, D. D. Mosser, and N. C. Bols. "Heat and sodium arsenite act synergistically on the induction of heat shock gene expression in Xenopus laevis A6 cells." Biochemistry and Cell Biology 65, no. 4 (April 1, 1987): 310–16. http://dx.doi.org/10.1139/o87-040.
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Heat shock protein (HSP) synthesis was studied in the Xenopus epithelial cell line A6 in response to heat and sodium arsenite, either singly or together. Temperatures of 33–35 °C consistently brought about the synthesis of HSPs at 87,73,70,54,31, and 30 kilodaltons (kDa), whereas sodium arsenite at 25–100 μM induced the synthesis of HSPs at 73 and 70 kDa. In cultures exposed to 10 μM sodium arsenite at 30 °C, HSP synthesis in the 68- to 73-kDa and 29- to 31-kDa regions was much greater than the HSP synthesis in response to each treatment individually. RNA dot blot analysis using homologous genomic subclones revealed that heat shock induced the accumulation of HSP 70 and 30 mRN As. The sizes of the HSP 70 and 30 mRN As determined by Northern hybridization were 2.7 and 1.5 kilobases, respectively. Sodium arsenite (10–100 μM) also induced the accumulation of both HSP 70 and 30 mRNAs. Finally, a mild heat shock (30 °C) plus a low concentration of sodium arsenite (10 μM) acted synergistically on HSP 70 and 30 mRN A accumulation in A6 cells. Thus sodium arsenite and heat act synergistically at the level of both HSP synthesis and HSP mRNA accumulation.
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Oladokun, Olayemi. "Tocopherol Enhances the Antioxidant Defense System and Histomorphometric Parameters in The Gastrointestinal Tract of Rats Treated with Sodium Arsenite." Nigerian Journal of Physiological Sciences 37, no. 1 (June 30, 2022): 83–92. http://dx.doi.org/10.54548/njps.v37i1.11.
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Arsenic compromises the gastrointestinal integrity and function via the body's anti-oxidative system breakdown. Hence, this study aimed to investigate the effects of tocopherol on redox imbalance and histoarchitectural alterations in rats' gastrointestinal tract exposed to sodium arsenite. Sodium arsenite and graded doses of tocopherol were administered orally into experimental rats assigned to different groups for four weeks concurrently. Redox status assay was done in homogenized samples by spectrophotometry. Parietal cell mass and mucous cell density (stomach), villus height and crypt depth (ileum), goblet cells count, and crypt depth (colon) were evaluated by histomorphometry. Inflammatory cells infiltration was also assessed using a semi-quantitative procedure. Sodium arsenite caused a significant increase in Malondialdehyde and Myeloperoxidase but, decreased Superoxide dismutase, Catalase, Nitric oxide, Glutathione peroxidase, Glutathione, and Glutathione-S-Transferase. Tocopherol treatment reversed the changes (p<0.05) though not largely dose-dependent. Furthermore, tocopherol annulled sodium arsenite-induced increase in parietal cell mass and decrease in mucous cell density in the stomach, decrease in villus height and villus height/crypt depth ratio in the ileum, and decrease in goblets cells and increase in crypt depth in the colon. Moreover, activated inflammatory cell infiltration by sodium arsenite was mitigated by tocopherol. Sodium arsenite provokes not only marked inflammatory cellular infiltration but a focal loss of glands, hyperplasia of crypts, atrophic villi, and hypertrophy of Peyer’s patches in the intestines, which are all lessened with tocopherol treatment. These findings underscore the anti-oxidative properties of tocopherol as a potent dietary factor against sodium arsenite toxicity in the gastrointestinal tract. Keywords: Tocopherol, arsenic, stomach, ileum, colon
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Odunuga, Odutayo O., Gbolahan W. Okunade, and Olufunso O. Olorunsogo. "Reversal of Sodium Arsenite Inhibition of Rat Liver Microsomal Ca2+ Pumping ATPase by Vitamin C." Bioscience Reports 19, no. 1 (February 1, 1999): 11–15. http://dx.doi.org/10.1023/a:1020189806066.
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Sodium arsenite (NaAsO2), at 10% of its median lethal dose, was administered to rats with and without vitamin C pretreatment. Liver microsomal fraction was isolated and the activity of Ca2+-ATPase was assayed. Sodium arsenite was found to inhibit the activity of the liver microsomal Ca2+-ATPase to 50% to that of control rats. The specific activity of the enzyme in rats administered sodium arsenite with vitamin C pretreatment was not significantly different from that of control rats.
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HERSHKO, Dan D., Bruce W. ROBB, Eric S. HUNGNESS, Guangju LUO, Xialing GUO, and Per-Olof HASSELGREN. "Arsenite inhibits interleukin-6 production in human intestinal epithelial cells by down-regulating nuclear factor-κB activity." Clinical Science 103, no. 4 (September 3, 2002): 381–90. http://dx.doi.org/10.1042/cs1030381.
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Previous studies have suggested that the production of interleukin-6 (IL-6) is increased in the intestinal mucosa during inflammation, and that nuclear factor-κB (NF-κB) is an important regulator of the IL-6 gene in the enterocyte. We tested the hypothesis that sodium arsenite inhibits IL-6 production in stimulated enterocytes and that this effect of arsenite is caused by down-regulation of NF-κB activity. Cultured Caco-2 cells were treated with sodium arsenite and were then stimulated with IL-1β. IL-6 production and gene expression were determined by ELISA and reverse transcriptase–PCR respectively. NF-κB DNA binding activity was determined by electrophoretic mobility shift assay. IL-1β increased NF-κB DNA binding activity, IL-6 mRNA levels and IL-6 production. These effects of IL-1β were inhibited by treatment of the cells with sodium arsenite in a dose- and time-dependent fashion. When cells were transfected with a plasmid expressing the p65 subunit of NF-κB, the inhibitory effect of sodium arsenite on NF-κB activity and IL-6 production was blunted. These results suggest that sodium arsenite inhibits IL-6 production in enterocytes subjected to an inflammatory stimulus, and that this effect, at least in part, reflects down-regulated NF-κB activity.
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Repetto, Guillermo, Pilar Sanz, and Manuel Repetto. "Comparative in vitro effects of sodium arsenite and sodium arsenate on neuroblastoma cells." Toxicology 92, no. 1-3 (September 1994): 143–53. http://dx.doi.org/10.1016/0300-483x(94)90173-2.
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Chaineau, Eric, Stéphane Binet, Didier Pol, Gilles Chatellier, and Vincent Meininger. "Embryotoxic effects of sodium arsenite and sodium arsenate on mouse embryos in culture." Teratology 41, no. 1 (January 1990): 105–12. http://dx.doi.org/10.1002/tera.1420410111.
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Afrakhteh, Moslem, Alireza Kheirollah, Aminollah Pourshohod, Mohammad Ali Ghaffari, Mostafa Jamalan, and Majid Zeinali. "Cytotoxicity of Sodium Arsenite-loaded Anti-HER2 Immunoliposomes Against HER2-expressing Human Breast Cancer Cell Lines." Letters in Drug Design & Discovery 16, no. 5 (April 15, 2019): 556–62. http://dx.doi.org/10.2174/1570180815666180803120409.
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Background: Chemotherapy is a routine approach in treatment of patients with cancer, while side effects of chemotherapeutic drugs are inevitable. To minimize side effects, specific targeting of neoplastic cells is a promising strategy in cancer therapy. Sodium arsenite is a metalloid toxin with anti-neoplastic properties, but low selectivity and carcinogenic activity have limited its clinical usage. Methods: Targeting of HER2-overexpressing (SK-BR-3) and HER2-low expressing (MCF-7) cancerous breast cell lines by two different liposomal forms of sodium arsenite (bare liposome and trastuzumab-conjugated liposome) was investigated in the current study. Levels of HER2 expression in the above mentioned cell lines were confirmed by western blotting. Size and morphology of the constructed liposomes were characterized by atomic force microscopy (AFM) and dynamic light scattering (DLS). Viability of the cells after treatment was assessed using MTT assay. Results: Sodium arsenite in the free and liposomal forms showed growth inhibitory effects against both SK-BR-3 and MCF-7 cell lines in an examined concentration range of 1-20 µM, although this effect was more significant in SK-BR-3 cell line. Loading of sodium arsenite in anti-HER2 immunoliposomes significantly enhanced its cytotoxicity while the specificity was also improved. By encapsulation of sodium arsenite in anti-HER2 immunoliposomes, its efficacy in ablation of SKBR- 3 cells was increased about 1.4-fold compared to the free or liposomal forms. Conclusion: In conclusion, targeted delivery of sodium arsenite using anti-HER2 immunoliposomes can be considered as an alternative strategy for specific treatment of HER2-positive breast cancers.
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David, Bando Christopher, Jummai Adamu Tutuwa, Rejoice Habila Tadawus, Emmanuel Odiba Ogu, Daniel Ifraimu, Oche Gabriel Sunday, Polly Shingu Jesse, and Tsoken Danji Agbu. "Effect of Ethanolic Stem Extract of Nelsonia Canescens on Selected Biochemical Parameters in Male Wistar Rats Induced with Sodium Arsenite." Journal of Multidisciplinary Science: MIKAILALSYS 2, no. 1 (February 29, 2024): 110–27. http://dx.doi.org/10.58578/mikailalsys.v2i1.2777.
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Medicinal plants are those that have curative qualities or have positive pharmacological effects on the human body. The effect of ethanolic stem extracts from Nelsonia canescens was studied in relation to Sodium arsenite-induced toxicity in wistar rats. Fresh stem extract of Nelsonia canescens were obtained behind rice mill area, Wukari, Taraba state and was shade dried at room temperature and was homogenized into powder and measured at 300g into 100ml of absolute ethanol for 72 hours. 15 healthy male rats of 70g to 90g weight were obtained from animal house Makurdi, Benue state. Animals from Group 1 were used as control. 5mg/kg body weight of Sodium arsenite was administered to Group 2 animals while animals in Groups 3, 4 and 5 were administered with Nelsonia canescens ethanolic stem extracts 50 mg/kg, 100mg/kg and 200 mg/kg as well. At the end of 3 weeks the animals were sacrificed and serum sample were collected and analysed using standard methods. The results indicate that, when compared to those who received Sodium arsenite, those who received ethanol stem extracts of Nelsonia canescens showed a comparatively considerable liver protection against Sodium arsenite -induced damage. The levels of biochemical parameters: Albumin, Total protein, Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Alkaline phosphatase (ALP), Total bilirubin, Urea, Creatinine of rats administered with Sodium arsenite only was also observed. The Nelsonia canescens extract’s activity at 200mg/kg bw (higher dose) give a reasonable decrease in the amount of these liver enzymes. Deducing from study results, it indicates that Nelsonia canescens leaf extracts could be an effective agent in Sodium arsenite mediated liver toxicity in adult wistar rats and drug development.
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Khorasgani, Elham Moghtadaei, and Shiva Mahdian. "Protective Role of Rosa damascena Miller hydroalcoholic extract on Oxidative Stress Parameters and Testis Tissue in Rats Treated with Sodium Arsenite." World's Veterinary Journal 13, no. 2 (June 25, 2023): 324–31. http://dx.doi.org/10.54203/scil.2023.wvj35.
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Regarding the strong antioxidant properties of Rosa damascene extract, this study aimed to investigate the protective role of Rosa damascene Miller hydroalcoholic petal extract on oxidative stress parameters and testis tissue in rats treated with sodium arsenite. To this end, 30 male rats were divided into five groups, including control, positive control (treated with arsenite), and three groups of patients affected by sodium arsenite with 150 mg/kg, 300 mg/kg, and 450 mg/kg Rosa damascene extract for 34 days by gavage. The animals were then anesthetized, and the blood samples were collected from the heart. The left testis was removed for histopathological studies. The findings revealed that Sodium arsenite in the positive group caused a significant reduction in TAC, testosterone, and serum Luteinizing hormone (LH) and a significant increase in serum Malondialdehyde. In addition, there was no statistically significant difference among the groups regarding the amount of Follicle-stimulating hormone (FSH). Moreover, the consumption of Rosa damascene extract with sodium arsenite caused a significant increase in testosterone, LH, and FSH compared to the positive control group. Histopathological results showed that in the experimental group receiving a dosage of 300 mg/kg b.w and the control group, the number of sperm tubes increased, and the germinal epithelium’s thickness was appropriate. Daily treatment with Rosa damascene extract with a dosage of 300 mg/kg b.w for 34 days could improve the changes caused by sodium arsenite and reduce Malondialdehyde levels. Thus, it seems that Rosa damascene hydroalcoholic extract can effectively improve the male reproductive system’s function.
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Deepthi Yada, Sivakkumar T, and Nimmagadda Srinivas. "Hepatoprotective Activity of Ethanolic extract Tanacetum parthenium L in Sodium arsenite-induced Hepatotoxicity in Wistar Albino Rats." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (December 21, 2020): 2598–603. http://dx.doi.org/10.26452/ijrps.v11ispl4.4519.
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This study assessed the probable effects of Ethanolic extract of Tanacetum parthenium (EETP) whole plant as hepatoprotective compound that acts on damaged liver due to administration of Sodium arsenite (NaAsO2 — 3mg/kg) in Wistar albino rats for a period of 28 days which results in alteration in Lipid peroxidation, antioxidant enzymes, biochemical factors, and liver enzyme. 30 animals were utilized for the study and are divided into five groups containing 6 rats each. Group –I treated as control received water, Group II-V were treated with sodium arsenite. Group-III received Vitamin-E (reference drug), Group IV treated with EETP 200 mg/kg dose and Group V treated with 400 mg/kg dose after hepatotoxicity induced by Sodium arsenite. Safeguarding effects of Ethanolic extract of Tanacetum parthenium whole plant were screened by analysis of the parameters like alanine transaminase, aspartate transaminase, alkaline phosphatase and total bilirubin, malondialdehyde, antioxidant enzymes. It was explored that administration of EETP at different doses could significantly decrease the enzymatic measures of AST, ALP, ALT, and TB concentration and increase catalase, GSH, GR and GPx levels in comparison with Sodium arsenite-induced control group. The data obtained from this experimental study prefigured the antioxidant potential of EETP and its potential hepatoprotective effects, and its beneficiary therapeutic effects on vandalization or disfigurement of liver due to Sodium arsenite induction in experimental animals.
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Achummantakath, Hashim, Krishnan Subhadra Prasanna, and A. S. Nizamudeen. "Effect of Phyllanthus amarus in sodium arsenite-induced tissue damage." Bangladesh Journal of Pharmacology 17, no. 3 (September 6, 2022): 79–83. http://dx.doi.org/10.3329/bjp.v17i3.59819.
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This study aims to evaluate the effect of alcoholic extract of Phyllanthus amarus leaves on arsenic-induced histological changes in Wistar rats. Rats were divided into 4 groups: Group I: normal control; Group II: rats received sodium arsenite (40 mg/kg); Group III: rats received sodium arsenite (40 mg/kg) + P. amarus extract (100 mg/kg); Group IV: rats received sodium arsenite (40 mg/kg) + extract (200 mg/kg). All groups were treated by oral gavage with sodium arsenite for 28 days and the animals were subsequently administered (oral) with 100 and 200 mg/kg extract, once daily for two weeks. Animals were sacrificed 24 hours after the last treatment and different organs were collected for histopathological analysis. Results revealed mild to severe type of necrosis and degenerative changes in brain, kidney, and liver of arsenic fed animals. In rats administered with extract showed significant improvements, and the normal histological feature of the cells was almost restored in rats. These suggest that P. amarus can be used to treat arsenic-induced multi-organ damages.
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Roses, O. E., J. C. García Fernández, E. C. Villaamil, N. Camussa, S. A. Minetti, M. Martínez de Marco, P. N. Quiroga, et al. "Mass Poisoning By Sodium Arsenite." Journal of Toxicology: Clinical Toxicology 29, no. 2 (January 1991): 209–13. http://dx.doi.org/10.3109/15563659109038613.
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MOON, Ryan, Timothy A. PRITTS, Alexander A. PARIKH, Josef E. FISCHER, Andrew L. SALZMAN, Marnie RYAN, Hector R. WONG, and Per-Olof HASSELGREN. "Stress response decreases the interleukin-1β-induced production of complement component C3 in human intestinal epithelial cells." Clinical Science 97, no. 3 (July 21, 1999): 331–37. http://dx.doi.org/10.1042/cs0970331.
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Interleukin-1β (IL-1β) increases the production of complement component C3 in enterocytes. Heat shock regulates the response to cytokines and other inflammatory mediators in various cell types. We tested the hypothesis that the heat-shock response regulates IL-1β-induced C3 production in the enterocyte. Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with sodium arsenite (10–500 µM) for 1 h or subjected to hyperthermia (43 °C) for 1–4 h, and allowed to recover for 1 h. The cells were then treated with IL-1β (0.5 ng/ml) for up to 24 h, whereafter C3 levels were measured by ELISA and C3 mRNA by Northern blot analysis. Heat-shock protein of 72 kDa (hsp72) was determined by Western blot analysis. Treatment of the cells with sodium arsenite or subjecting them to hyperthermia induced the expression of hsp72. The IL-1β-induced expression of C3 mRNA and C3 production were down-regulated by hyperthermia and sodium arsenite in a dose-dependent fashion. The results suggest that the stress response induced by hyperthermia or sodium arsenite decreases IL-1β-induced C3 production in human enterocytes.
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Wang, J. H., H. P. Redmond, R. W. Watson, and D. Bouchier-Hayes. "Induction of human endothelial cell apoptosis requires both heat shock and oxidative stress responses." American Journal of Physiology-Cell Physiology 272, no. 5 (May 1, 1997): C1543—C1551. http://dx.doi.org/10.1152/ajpcell.1997.272.5.c1543.
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Endothelial cell (EC) death may play an important role in the development of increased vascular permeability and capillary leak syndrome during systemic inflammatory response syndrome. However, the mode of EC death and the mechanisms involved remain unclear. In this study we employed the proinflammatory mediators lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha), the chemical reagent sodium arsenite, and heat shock to trigger the stress gene responses. Human ECs were used as surrogates of the microvasculature to test the hypothesis that the induction of the heat shock response and the oxidative stress response might combine to induce apoptosis rather than necrosis in human ECs. Sodium arsenite at 80-320 microM, which induced heat shock protein 72 (HSP72) expression and reactive oxygen intermediate (ROI) generation in ECs, resulted in EC apoptosis. TNF-alpha alone (5-75 ng/ml) increased EC ROI generation but did not induce EC apoptosis. Heat shock alone (42 degrees C, 45 min) or sodium arsenite (40 microM) alone, each of which induced HSP72 expression, did not result in EC apoptosis. However, the combination of TNF-alpha with heat shock or 40 microM sodium arsenite led to EC apoptosis as HSP72 expression and ROI were induced. Furthermore, sodium arsenite (80 microM) in the presence of antioxidants failed to induce EC apoptosis. Apoptotic ECs also exhibited functional disturbances as represented by the depression of intercellular adhesion molecule-1 expression as well as the disruption of EC monolayer integrity. These results indicate that the simultaneous induction of a heat shock response and an oxidative stress response is responsible for human EC apoptosis.
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Chupis, V. N., E. A. Luschay, I. N. Larin, A. A. Zagrekov, E. V. Il’ina, and D. E. Ivanov. "Test Organisms Sodium Arsenit Sensitivity in the Environment Quality Multicomponent Biotesting System." Theoretical and Applied Ecology, no. 1 (May 10, 2007): 69–73. https://doi.org/10.25750/1995-4301-2007-1-037-41.
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The results of an estimation of influence of natrium arsenite in solutions of various concentration on intensity of bioluminocity of bacteria, mortality of daphnia and ceriodaphnia, chemotaxic reaction of infusoria, impellent activity of daphnia, growth of chlorella and scenedesmus alga chlorophyll fluorescence are given. The greatest sensitivity to natrium arsenite is found for daphnia and ceriodaphnia. The conclusion about expediency of use lowest crayfishes in ecological monitoring of the enterprises on natrium arsenite processing is made.
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Darasch, S., D. D. Mosser, N. C. Bols, and J. J. Heikkila. "Heat shock gene expression in Xenopus laevis A6 cells in response to heat shock and sodium arsenite treatments." Biochemistry and Cell Biology 66, no. 8 (August 1, 1988): 862–70. http://dx.doi.org/10.1139/o88-098.
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Continuous exposure of a Xenopus laevis kidney epithelial cell line, A6, to either heat shock (33 °C) or sodium arsenite (50 μM) resulted in transient but markedly different temporal patterns of heat-shock protein (HSP) synthesis and HSP 70 and 30 mRNA accumulation. Heat-shock-induced synthesis of HSPs was detectable within 1 h and reached maximum levels by 2–3 h. While sodium arsenite induced the synthesis of some HSPs within 1 h, maximal HSP synthesis did not occur until 12 h. The pattern of HSP 70 and 30 mRNA accumulation was similar to the response observed at the protein level. During recovery from heat shock, a coordinate decline in HSPs and HSP 70 and 30 mRNA was observed. During recovery from sodium arsenite, a similar phenomenon occurred during the initial stages. However, after 6 h of recovery, HSP 70 mRNA levels persisted in contrast to the declining HSP 30 mRNA levels. Two-dimensional polyacrylamide gel electrophoresis revealed the presence of 5 HSPs in the HSP 70 family, of which two were constitutive, and 16 different stress-inducible proteins in the HSP 30 family. In conclusion, heat shock and sodium arsenite induce a similar set of HSPs but maximum synthesis of the HSP is temporally separated by 12–24 h.
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Nuntharatanapong, Nopparat, Kai Chen, Palarp Sinhaseni, and John F. Keaney. "EGF receptor-dependent JNK activation is involved in arsenite-induced p21Cip1/Waf1 upregulation and endothelial apoptosis." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H99—H107. http://dx.doi.org/10.1152/ajpheart.00901.2004.
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Arsenic exposure is associated with an increased risk of atherosclerosis and vascular diseases. Although endothelial cells have long been considered to be the primary targets of arsenic toxicity, the underlying molecular mechanism remains largely unknown. In this study, we sought to explore the signaling pathway triggered by sodium arsenite and its implication for endothelial phenotype. We found that sodium arsenite produced time- and dose-dependent decreases in human umbilical vein endothelial cell viability. This effect correlated with the induction of p21Cip1/Waf1 (up to 10-fold), a regulatory protein of cell cycle and apoptosis. We also found that arsenite-stimulated EGF (ErbB1) and ErbB2 receptor transactivation, manifest as receptor tyrosine phosphorylation, appeared to be a proximal signaling event leading to p21Cip1/Waf1 induction, because both pharmacological inhibitors and knockdown of receptors by RNA interference blocked arsenite-induced p21Cip1/Waf1 upregulation. Arsenite-induced activation of JNK and p38 MAPK was distinct, with only JNK as a downstream target of the EGF receptor. Moreover, inhibition of JNK with SP-600125 or dominant negative MKK7 inhibited only p21Cip1/Waf1 induction, whereas the p38 MAPK inhibitor SB-203580 or dominant negative MKK4 inhibited both p21Cip1/Waf1 and p53 induction. Functionally, inhibition of p21Cip1/Waf1 induction prevented endothelial apoptosis due to arsenite treatment. Insofar as endothelial dysfunction promotes vascular disease, these data provide a mechanism for the increased incidence of cardiovascular disease due to arsenite exposure.
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ASHRAF, S., A. TAHIR, A. AMJAD, S. HAMEED, R. IMTIAZ, A. SHABBIR, and R. SHEHZADI. "SYSTEMIC HEALTH EFFECTS ASSOCIATED WITH SODIUM ARSENITE EXPOSURE: A REAPPRAISAL." Biological and Clinical Sciences Research Journal 2023, no. 1 (December 19, 2023): 601. http://dx.doi.org/10.54112/bcsrj.v2023i1.601.
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Sodium Arsenite is a potent toxic mutagenic and xenobiotic metalloid that has been increasing in the environment as a significant pollutant. Contamination of drinking water by chemicals containing arsenic is still a serious public health issue. Prolonged exposure to sodium arsenite can lead to several health problems, including irregularities in the cardiovascular system, diabetes, nephrotoxicity, neurotoxicity, hearing loss, haematological diseases, hepatotoxicity, and infertility. Sodium arsenite is a multi-site carcinogen that can cause cancers in the skin, kidney, colon, lung, and uterus, among other tissues. Numerous research investigations have demonstrated that the toxicity of arsenic is contingent upon various elements such as exposure level, frequency, duration, biological species, age, gender, genetic susceptibilities, and nutritional status. Arsenic exposure has been linked to several consequences, such as apoptosis, cell growth, and alteration of signal transduction pathways. This implies that Arsenite might have incredibly wide impacts rather than targeted effects. Furthermore, several epidemiological studies have documented the exposure sources and the worldwide impacts of arsenic, but the exact method by which it affects various systems, including cancer, is still unknown. More research is needed to give a more precise knowledge of the underlying mechanism.
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Shack, Sonsoles, Xian-Tao Wang, Gertrude C. Kokkonen, Myriam Gorospe, Dan L. Longo, and Nikki J. Holbrook. "Caveolin-Induced Activation of the Phosphatidylinositol 3-Kinase/Akt Pathway Increases Arsenite Cytotoxicity." Molecular and Cellular Biology 23, no. 7 (April 1, 2003): 2407–14. http://dx.doi.org/10.1128/mcb.23.7.2407-2414.2003.
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ABSTRACT The inhibitory effect of caveolin on the cellular response to growth factor stimulation is well established. Given the significant overlap in signaling pathways involved in regulating cell proliferation and stress responsiveness, we hypothesized that caveolin would also affect a cell's ability to respond to environmental stress. Here we investigated the ability of caveolin-1 to modulate the cellular response to sodium arsenite and thereby alter survival of the human cell lines 293 and HeLa. Cells stably transfected with caveolin-1 were found to be much more sensitive to the toxic effects of sodium arsenite than either untransfected parental cells or parental cells transfected with an empty vector. Unexpectedly, the caveolin-overexpressing cells also exhibited a significant activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, which additional studies suggested was likely due to decreased neutral sphingomyelinase activity and ceramide synthesis. In contrast to its extensively documented antiapoptotic influence, the elevated activity of Akt appears to be important in sensitizing caveolin-expressing cells to arsenite-induced toxicity, as both pretreatment of cells with the PI3K inhibitor wortmannin and overexpression of a dominant-negative Akt mutant markedly improved the survival of arsenite-treated cells. This death-promoting influence of the PI3K/Akt pathway in caveolin-overexpressing cells appeared not to be unique to sodium arsenite, as wortmannin pretreatment also resulted in increased survival in the presence of H2O2. In summary, our results indicate that caveolin-induced upregulation of the PI3K/Akt signaling pathway, which appears to be a death signal in the presence of arsenite and H2O2, sensitizes cells to environmental stress.
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Wang, Quan, and Per-Olof Hasselgren. "Heat shock response reduces intestinal permeability in septic mice: potential role of interleukin-10." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 3 (March 1, 2002): R669—R676. http://dx.doi.org/10.1152/ajpregu.00606.2001.
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Sepsis and other critical illnesses are associated with increased permeability of the intestinal mucosa. Loss of mucosal integrity may lead to multiple organ failure in these conditions. We tested the hypothesis that induction of the heat shock response reduces sepsis-induced increase in intestinal permeability. The heat shock response was induced in mice by intraperitoneal injection of 10 mg/kg sodium arsenite. Two hours later, at which time mucosal heat shock protein 72 levels were increased, sepsis was induced by cecal ligation and puncture (CLP) or sham operation was performed. Sixteen hours after sham operation or CLP, intestinal permeability was determined by measuring the appearance in blood of 4.4-kDa fluorescein isothiocyanate-conjugated dextran and 40-kDa horseradish peroxidase administered by gavage. Sepsis resulted in increased mucosal permeability for both markers, and this effect of sepsis was substantially reduced in mice treated with sodium arsenite. Plasma levels of the anti-inflammatory cytokine interleukin (IL)-10 were increased in septic mice pretreated with sodium arsenite, and the protective effect of sodium arsenite on intestinal permeability in septic mice was reversed by treatment with anti-IL-10 antibody. The present results suggest that sepsis-induced increase in mucosal permeability can be reduced by the heat shock response and that increased IL-10 levels may be involved in the protective effects of the heat shock response.
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Mandal, Samir, Nabanita Chatterjee, Subhadip Das, Krishna Das Saha, and Keya Chaudhuri. "Magnetic core–shell nanoprobe for sensitive killing of cancer cells via induction with a strong external magnetic field." RSC Adv. 4, no. 39 (2014): 20077–85. http://dx.doi.org/10.1039/c4ra01407c.
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The title system, composed of a highly magnetic core surrounded by a thin arsenite shell, has been synthesized and applied to the magnetically facilitated targeting of anticancer agent (sodium arsenite) at lower dose with minimal side effects and higher efficacy in a biocompatible manner.
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Li, Yan, Qiaoshi Zhao, Jinyin Yao, Chunpeng Lv, Yanhui Gao, Dianjun Sun, and Yanmei Yang. "MiR-96-5p Suppresses Progression of Arsenite-Induced Human Keratinocyte Proliferation and Malignant Transformation by Targeting Denticleless E3 Ubiquitin Protein Ligase Homolog." Toxics 11, no. 12 (December 1, 2023): 978. http://dx.doi.org/10.3390/toxics11120978.
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Long-term exposure to arsenic has been linked to a variety of cancers, among which skin cancer is the most prevalent form. However, the mechanism underlying arsenic carcinogenesis is unclear, and there is still limited information on the role of miRNAs in arsenic-induced skin cancer. This study aims to explore the role of miR-96-5p in the arsenite-induced proliferation and malignant transformation of human HaCaT keratinocytes. The GEO database (accession numbers GSE97303, GSE97305, and GSE97306) was used to extract mRNA and miRNA expression profiles of HaCaT cells treated with or without 0.1 μmol/L sodium arsenite for 3 and 7 weeks. In this paper, according to the CCK8 assay result, HaCaT cells exposed to 0.1 μmol/L sodium arsenite for 48 h were finalized. CCK8, MTT, EdU incorporation, and colony formation assays were used to determine the viability and proliferation of HaCaT cells and transformed HaCaT (T-HaCaT) cells. The subcellular localization and relative expression levels of DTL, as well as miR-96-5p in HaCaT cells induced by arsenite, were determined via immunofluorescence, RT-qPCR, and Western blot. Dual-luciferase reporter assay was performed to identify miR-96-5p bound directly to DTL. Transfection of miR-96-5p mimics or DTL siRNA was conducted to verify the arsenite-induced viability of HaCaT cells and T-HaCaT cells. T-HaCaT cells and nude mice were used to construct arsenite-induced malignant transformation and an in vivo xenograft model to demonstrate the over-expressed effect of miR-96-5p. The results showed that DTL was the target gene of miR-96-5p. Meanwhile, we also found that 0.1 μmol/L sodium arsenite upregulated DTL by decreasing the miR-96-5p level, leading to the proliferation and malignant transformation of HaCaT cells. MiR-96-5p agomir treatment slowed the growth of transplanted HaCaT cells transformed by arsenite in a manner associated with DTL downregulation in the nude mice xenograft model. Taken together, we confirmed that miR-96-5p, as a potent regulator of DTL, suppressed arsenite-induced HaCaT cell proliferation and malignant transformation, which might provide a novel therapeutic target for the treatment of arsenic-induced skin cancer.
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Magar, Lil Budha, Binod Rayamajhee, Sujan Khadka, Gaurab Karki, Alina Thapa, Muhammad Yasir, Sandeep Thapa, Om Prakash Panta, Suprina Sharma, and Pramod Poudel. "Detection of Bacillus Species with Arsenic Resistance and Plant Growth Promoting Efficacy from Agricultural Soils of Nepal." Scientifica 2022 (July 19, 2022): 1–10. http://dx.doi.org/10.1155/2022/9675041.
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Arsenic contamination in soil and water is one of the major environmental problems in multiple countries including Nepal imposing a serious threat to the ecosystem and public health. Many soil bacteria can detoxify arsenic, including genus Bacillus. With an objective to gauge the plant growth-promoting activities of arsenic-resistant Bacillus species, 36 samples (soil, rice, cauliflower, and beans) were collected from the Terai region of Nepal. For selective isolation of Bacillus species, each sample was heated at 80°C for 15 min before the inoculation into nutrient agar (NA). Following the standard protocol, arsenic-resistant Bacillus species were screened using NA supplemented with 100 ppm sodium arsenate and sodium arsenite. Among 158 randomly selected isolates, only five isolates were able to tolerate sodium arsenite concentration up to 600 ppm. Notably, all five isolates were able to produce indole acetic acid (IAA), a plant hormone, and solubilize phosphate. Based on biochemical analysis and 16S rRNA gene sequencing, isolates N4-1, RW, KR7-12, Bhw1-4, and BW2-2 were identified as B. subtilis subsp. stercosis, B. flexus, B. licheniformis, B. cereus, and B. flexus, respectively. To the best of our knowledge, this is the first study showing the presence of arsenic-resistant B. flexus in Nepalese soil with plant growth-promoting traits. Possible utilization of these Bacillus strains could facilitate the novel bioremediation pathway to reduce the toxic effect of arsenic from the soil and water in the Terai region of Nepal.
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Jha, D. K., and N. Yashvardhini. "Assessment of arsenic induced physiological and lipid peroxidation response in two indica rice cultivars." Journal of Environmental Biology 44, no. 3 (May 15, 2023): 390–95. http://dx.doi.org/10.22438/jeb/44/3/mrn-5054.
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Aim: To investigate the potential of sodium arsenite to induce physiological as well as oxidative stress at its low level exposure in tolerant and sensitive indica rice cultivars. Methodology: Rice seeds were surface sterilized using 0.1% HgCl2 for 15 min, followed by washing with distilled water. Twelve days after germination, the seedlings in one tray was kept aside as control and other trays were exposed to 50, 100, 150 and 200 μM of sodium arsenite. After treatment for 24 and 48hr, leaves were harvested and washed with distilled water to estimate the level of lipid peroxidation as well as physiological stress parameters. Results: The oxidative damage increased with corresponding increase in the sodium arsenite concentration in both the succeptible IR-64 and tolerant Nonabokra cultivars, the effect being more prononced in IR-64 than Nonabokra. The status of lipid peroxidation was assessed through quantification of its secondary product malondialdehyde by TBARS assay (P≤0.05). Significant increase in lipid peroxidation levels were observed in all the arsenic exposed groups of rice plants. Interpretation: The detrimental effect of arsenic was reflected as more chlorophyll loss, decrease in water content and significant reduction in the length of root as well as shoot of rice plants. Besides, significant elevated levels of LPO indicated drastic cellular damage in all the arsenic exposed groups of rice plants. Key words: Chlorophyll loss, Indica rice, Lipid peroxidation, Sodium arsenite, Water content
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Budd, K., J. R. Casey, and J. D. MacArthur. "Arsenite toxicity and arsenite tolerance in the cyanobacterium Synechococcus leopoliensis." Canadian Journal of Botany 64, no. 11 (November 1, 1986): 2433–40. http://dx.doi.org/10.1139/b86-324.
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Sodium arsenite at concentrations above 50 μM inhibited the growth of Synechococcus leopoliensis UTEX 625 in a defined culture medium. Inhibition was transitory, with growth resuming after a lag period the duration of which depended on the arsenite concentration. Cells grown for several hours in the presence of 10 μM arsenite became tolerant to concentrations of arsenite that inhibited the growth of untreated cells. Neither sensitive nor tolerant cells chemically modified the external arsenite detectably within the experimental period. At a concentration of 200 μM, arsenite temporarily halted growth of sensitive cells but did not affect that of tolerant cells. This concentration of arsenite inhibited net photosynthesis in both sensitive and tolerant cells. At the same time it selectively decreased the incorporation of carbon in the light into α-amino acids, especially glutamate, in sensitive but not in tolerant cells. Simultaneously, incorporation of carbon into pyruvic acid markedly increased. The activity of the partially purified pyruvate dehydrogenase complex of S. leopoliensis was abolished by 45 μM arsenite. It is concluded that inhibition of pyruvate dehydrogenase by arsenite is sufficient to explain its inhibition of growth in this organism.
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Fung, Hua, Pingfang Liu, and Bruce Demple. "ATF4-Dependent Oxidative Induction of the DNA Repair Enzyme Ape1 Counteracts Arsenite Cytotoxicity and Suppresses Arsenite-Mediated Mutagenesis." Molecular and Cellular Biology 27, no. 24 (October 15, 2007): 8834–47. http://dx.doi.org/10.1128/mcb.00974-07.
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ABSTRACT Arsenite is a human carcinogen causing skin, bladder, and lung tumors, but the cellular mechanisms underlying these effects remain unclear. We investigated expression of the essential base excision DNA repair enzyme apurinic endonuclease 1 (Ape1) in response to sodium arsenite. In mouse 10T½ fibroblasts, Ape1 induction in response to arsenite occurred about equally at the mRNA, protein, and enzyme activity levels. Analysis of the APE1 promoter region revealed an AP-1/CREB binding site essential for arsenite-induced transcriptional activation in both mouse and human cells. Electrophoretic mobility shift assays indicated that an ATF4/c-Jun heterodimer was the responsible transcription factor. RNA interference targeting c-Jun or ATF4 eliminated arsenite-induced APE1 transcription. Suppression of Ape1 or ATF4 sensitized both mouse fibroblasts (10T½) and human lymphoblastoid cells (TK6) to arsenite cytotoxicity. Expression of Ape1 from a transgene did not efficiently restore arsenite resistance in ATF4-depleted cells but did offset initial accumulation of abasic DNA damage following arsenite treatment. Mutagenesis by arsenite (at the TK and HPRT loci in TK6 cells) was observed only for ATF4-depleted cells, which was strongly offset by Ape1 expression from a transgene. Therefore, the ATF4-mediated up-regulation of Ape1 and other genes plays a key role against arsenite-mediated toxicity and mutagenesis.
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Pant, Niraj, R. C. Murthy, and S. P. Srivastava. "Male reproductive toxicity of sodium arsenite in mice." Human & Experimental Toxicology 23, no. 8 (August 2004): 399–403. http://dx.doi.org/10.1191/0960327104ht467oa.
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The effect of chronic oral exposure to arsenic on male mouse testicular and accessory sex organ weights, sperm parameters and testicular marker enzymes was studied. In addition, the distribution of arsenic in reproductive organs was measured using atomic absorption spectrophotometry. Sodium arsenite administered to mice (Mus musculus) via drinking water at a dose of 53.39 βmol/L (4 ppm As) for 365 days caused a decrease in the absolute and relative testicular weight. However, epididymal and accessory sex organ weight was similar to control. The activities of marker testicular enzymes such as sorbitol dehydrogenase, acid phosphatase and 17β-hydroxysteroid dehydrogenase (17β-HSD) were significantly decreased, but those of lactate dehydrogenase and γ-glutamyl transpeptidase (γ-GT) were significantly increased. A decrease in sperm count and sperm motility, along with an increase in abnormal sperm, was observed in arsenite-exposed mice. A significant accumulation of arsenic in testes, epididymis, seminal vesicle and prostate gland was observed in treated animals. Thus long term exposure (365 days) at the dose level of 53.39 μmol/L sodium arsenite (4 ppm As), to which human beings are likely to be exposed via drinking water, may cause testicular and spermatotoxic effect.
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Kapoor, M., and J. Lewis. "Alteration of the protein synthesis pattern in Neurospora crassa cells by hyperthermal and oxidative stress." Canadian Journal of Microbiology 33, no. 2 (February 1, 1987): 162–68. http://dx.doi.org/10.1139/m87-028.
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Neurospora crassa cells, grown at 28 °C for 14 h and heat shocked at 48 °C for 45 min, showed the synthesis of 11 heat-shock proteins (nHSPs) in one-dimensional electrophoretic profiles. Treatment with sodium arsenite induced the synthesis of two heat-shock proteins, nHSP70 and nHSP80, and a third, arsenite-specific protein, not induced by hyperthermia. Exposure to 0.5 or 1.0 mM H2O2 led to the induction of two of the heat-inducible nHSP70 family polypeptides. Sodium selenite, used in concert with H2O2, and arsenite were observed to modulate that heat-shock response. In addition, H2O2, menadione, and the glutathione depleters diamide and diethyl maleate promoted the synthesis of another protein, designated oxidative stress-responsive protein (OSP). A DNA-binding protein, specific for Neurospora DNA, was also demonstrated in extracts of heat-shocked cells.
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Imran, Muhammad Asif, Feroza Hamid Wattoo, Muhammad Nawaz Chaudhry, Muhammad Hamid Sarwar Wattoo, and Khan Rass Masood. "Impact of Inorganic Arsenicals on Vegetative Growth of Two Pakistani Origins Sunflower Cultivars." Journal of Chemistry 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/275830.
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Inorganic arsenicals impact on vegetative growth of two sunflower (Helianthus annuusL.) cultivars (FH-385 as Hybrid 1 and FH-405 as Hybrid 2) was monitored. Various levels of two different sodium salts of arsenic, namely, sodium arsenate (Na2HAsO4·7H2O) as source of As5+and sodium arsenite (NaAsO2) as source of As3+, were used to evaluate the effect of arsenic on plant water relation parameters. Significant stress effects were found when arsenic was higher in concentrations (>60 mg/kg soil of both salts) as compared to control plants. Genotype FH-405 showed higher levels for shoot and root length, water contents, number of leaves, and leaf area, which indicates well adaptation of this cultivar in arsenic contaminated environment. T5 (100 mg/kg) of both salts showed notable stressful impacts as compared to low arsenic concentrations (20, 40 mg/kg) and especially control plants in case of all morphophysiological parameters of sunflower cultivars.
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Bilszta, Justin L. C., Gregory J. Dusting, and Fan Jiang. "Arsenite Increases Vasoconstrictor Reactivity in Rat Blood Vessels: Role of Endothelial Nitric Oxide Function." International Journal of Toxicology 25, no. 4 (July 2006): 303–10. http://dx.doi.org/10.1080/10915810600746130.
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Arsenite has been shown to inhibit endothelium-dependent, nitric oxide-mediated vasodilation in vitro. This study investigated the effects of arsenite on vascular reactivity in vivo. Saline or sodium arsenite (6 mg kg−1) was administered intravenously in Wistar-Kyoto rats for 4 h. As compared to saline, arsenite significantly increased vasoconstrictor responses to phenylephrine in both rat isolated aorta and renal arteries examined in tissue bath. This change was diminished after preincubation of the tissues with the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester, which increased phenylephrine-induced vasoconstriction to a similar extent as arsenite. In contrast, acetylcholine-induced vasodilation, mediated by nitric oxide in the aorta and by an endothelium-derived hyperpolarizing factor in renal arteries, was not affected by arsenite. Arsenite induced expression of heat shock proteins Hsp72, Hsp32, and Hsp90, but endothelial nitric oxide synthase expression was not changed. The effects of arsenite on vasoreactivity were unlikely to be mediated by heat shock protein induction, because blockade of heat shock protein induction had little effect on the increased vasoconstriction in vessels from arsenite-treated animals. Our study suggests that in vivo arsenic treatment increases vasoconstrictor reactivity by compromising basal endothelial nitric oxide function, which is not caused by altered endothelial nitric oxide synthase expression.
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Souza, Ana Cláudia Ferreira, Sarah Cozzer Marchesi, Rafael Penha Ferraz, Graziela Domingues de Almeida Lima, Juraci Alves de Oliveira, and Mariana Machado-Neves. "Effects of sodium arsenate and arsenite on male reproductive functions in Wistar rats." Journal of Toxicology and Environmental Health, Part A 79, no. 6 (March 18, 2016): 274–86. http://dx.doi.org/10.1080/15287394.2016.1150926.
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BARIRAH REHMAN TALPUR, ZAHEER AHMED NIZAMANI, MANSOOR TARIQ, IMDAD HUSSAIN LEGHARI, and AYAZ ALI MEMON. "Toxicopathological Effects of Oral Sodium Arsenite on Production of Layers." University of Sindh Journal of Animal Sciences (USJAS) 7, no. 1 (March 31, 2023): 32–37. http://dx.doi.org/10.57038/usjas.v7i1.6225.
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Arsenic is a highly toxic metal found in surface as well ground water in many areas of South Asia and can affect humans, animals as well as commercial poultry industry. The present study aimed to assess toxico-pathological effects of arsenic on egg production, quality and health of layers. Seventy-five Hy-Line W-36 layers were divided into four treatment groups (B, C, D, E) which were daily given 1mg, 5mg, 10mg, and 20 mg/kg/bw respectively of sodium arsenite in drinking water for three weeks while one group (A) served as control. The groups were examined weekly for determination of body weight. Further, egg production, weight and quality parameters like albumin, yolk, shell weight, thickness and Haugh unit were assessed. Deleterious effects of sodium arsenite were found to be dose and time dependent. There was a significant decrease in egg production, egg weight, albumin weight, yolk weight, shell weight, shell thickness and Haugh unit. There was decreased feed intake, increased water intake and reduced body weight. In conclusion, the sodium arsenite in drinking water produces adverse effects on egg production and quality of layers in time and dose dependent manner.
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Xu, Shiqing, Zhida Hu, Yujie Wang, Qiyao Zhang, Zhi Wang, Teng Ma, Suhua Wang, Xiaohui Wang, and Li Wang. "Circ_0000284 Is Involved in Arsenite-Induced Hepatic Insulin Resistance Through Blocking the Plasma Membrane Translocation of GLUT4 in Hepatocytes via IGF2BP2/PPAR-γ." Toxics 12, no. 12 (December 4, 2024): 883. https://doi.org/10.3390/toxics12120883.
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Arsenic exposure can induce liver insulin resistance (IR) and diabetes (DM), but the underlying mechanisms are not yet clear. Circular RNAs (circRNAs) are involved in the regulation of the onset of diabetes, especially in the progression of IR. This study aimed to investigate the role of circRNAs in arsenic-induced hepatic IR and its underlying mechanism. Male C57BL/6J mice were given drinking water containing sodium arsenite (0, 0.5, 5, or 50 ppm) for 12 months. The results show that sodium arsenite increased circ_0000284 expression, decreased insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) and peroxisome proliferator-activated receptor-γ (PPAR-γ), and inhibited cell membrane protein levels of insulin-responsive glucose transporter protein 4 (GLUT4) in the mouse livers, indicating that arsenic exposure causes liver damage and disruptions to glucose metabolism. Furthermore, sodium arsenite reduced glucose consumption and glycogen levels, increased the expression of circ_0000284, reduced the protein levels of IGF2BP2 and PPAR-γ, and inhibited GLUT4 protein levels in the cell membranes of insulin-treated HepG2 cells. However, a circ_0000284 inhibitor reversed arsenic exposure-induced reductions in IGF2BP2, PPAR-γ, and GLUT4 levels in the plasma membrane. These results indicate that circ_0000284 is involved in arsenite-induced hepatic insulin resistance through blocking the plasma membrane translocation of GLUT4 in hepatocytes via IGF2BP2/PPAR-γ. This study provides a scientific basis for finding early biomarkers for the control of arsenic exposure and type 2 diabetes mellitus (T2DM), and discovering new prevention and control measures.
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Fouad, Amr A., Waleed H. Albuali, Abdulruhman S. Al-Mulhim, and Iyad Jresat. "Protective effect of telmisartan treatment against arsenic-induced testicular toxicity in rats." Zeitschrift für Naturforschung C 70, no. 7-8 (July 1, 2015): 175–81. http://dx.doi.org/10.1515/znc-2015-5031.
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Abstract Oxidative/nitrosative stress, inflammation, and apoptosis play a crucial role in the pathogenesis of arsenic-induced testicular injury. Telmisartan, the angiotensin II-receptor antagonist, possesses antioxidant and anti-inflammatory activities. The protective effect of telmisartan against arsenic-induced testicular damage was investigated in rats. Testicular damage was induced by sodium arsenite (10 mg kg–1/day, p.o., for 2 consecutive days). Telmisartan (10 mg kg–1/day, i.p.) was given for 3 consecutive days, starting 1 day before sodium arsenite administration. Telmisartan significantly attenuated the arsenic-induced decrease in the levels of serum testosterone and testicular reduced glutathione, and significantly decreased the elevation of the levels of testicular malondialdehyde, nitric oxide, and arsenic levels, as well as myeloperoxidase activity resulting from sodium arsenite administration. Histopathological and immunohistochemical examination revealed that telmisartan markedly attenuated testicular tissue changes, and decreased the arsenic-induced expression of vascular endothelial growth factor, inducible nitric oxide synthase, tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB, and caspase-3. Telmisartan, via its antioxidant and/or anti-inflammatory effects, may represent a potential candidate to protect against the deleterious effects of arsenic on testicular tissue.
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Altoé, LS, IB Reis, MLM Gomes, H. Dolder, and JC Monteiro Pirovani. "Could vitamin C and zinc chloride protect the germ cells against sodium arsenite?" Human & Experimental Toxicology 36, no. 10 (November 24, 2016): 1049–58. http://dx.doi.org/10.1177/0960327116679714.
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Arsenic (As) is commonly associated with natural and human processes such as volcanic emissions, mining and herbicides production, being an important pollutant. Several studies have associated As intake with male fertility reduction, thus the aim of the present study was to evaluate whether vitamin C and/or zinc would counteract As side effects within the testicles. Adult male Wistar rats were divided into six experimental groups: control, sodium arsenite (5 mg/kg/day), vitamin C (100 mg/kg/day), zinc chloride (ZnCl2; 20 mg/kg/day), sodium arsenite + vitamin C and sodium arsenite + ZnCl2. Testicles and epididymis were harvested and either frozen or routinely processed to be embedded in glycol methacrylate resin. As reduced the seminiferous epithelium and tubules diameter due to germ cell loss. In addition, both the round spermatids population and the daily sperm production were reduced. However, ZnCl2 and vitamin C showed to be effective against such side effects, mainly regarding to sperm morphology. Long-term As intake increased the proportions of abnormal sperm, whereas the concomitant intake of As with zinc or vitamin C enhanced the proportions of normal sperm, showing that such compounds could be used to protect this cell type against morphological defects.
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Ferreira, Mónica, Rita Cerejeira Matos, Helena Oliveira, Bruno Nunes, and Maria de Lourdes Pereira. "Impairment of mice spermatogenesis by sodium arsenite." Human & Experimental Toxicology 31, no. 3 (April 13, 2011): 290–302. http://dx.doi.org/10.1177/0960327111405862.
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Pachnanda, Reema, and Shiv Pal Singh. "Histopathological alterations in testicular tissue of male rats exposed to arsenic." Journal of Applied and Natural Science 4, no. 2 (December 1, 2012): 247–51. http://dx.doi.org/10.31018/jans.v4i2.258.
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The present study was designed to investigate the adverse effect of arsenic on testicular tissue of Swiss albino male rats. Sodium arsenite was administered to adult male rats by gavage at the doses 1, 2 and 3 mg/kg body weight for 30 days. After the treatment, the testis were processed for histopathological observations. Sodium arsenite caused remarkable reduction in testicular weight (P<0.05), while the body weight of experimental animals were reduced but not significantly (P<0.05). Histological evaluation revealed dose-dependent, gradual destruction in histoarchitecture of testicular tissue. Sodium arsenite exposure caused complete arrest of spermatogenesis with disfigured seminiferous tubules in the testes .The lumens of the tubules were devoid of spermatids and were in places filled with cellular debris. The germinal epithelium was distorted. At places interstitial odema was also evident. Sertoli and Leydig cells were damaged. Along with structural alterations, fertility rate in experimental animals was significantly decreased at higher doses i.e. 2 and 3 mg/kg, as 100% infertility was observed. After withdrawal of the treatment over a period of 30 days, recovery was observed in low dose groups as few female rats became pregnant. The study concluded that exposure of arsenic causes testicular toxicity in male albino rat.
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Che, Xiao-Fang, Chun-Lei Zheng, Satsuki Owatari, Masato Mutoh, Takenari Gotanda, Hei-Cheul Jeung, Tatsuhiko Furukawa, et al. "Overexpression of survivin in primary ATL cells and sodium arsenite induces apoptosis by down-regulating survivin expression in ATL cell lines." Blood 107, no. 12 (June 15, 2006): 4880–87. http://dx.doi.org/10.1182/blood-2005-08-3423.
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AbstractPatients with acute- or lymphoma-type adult T-cell leukemia (ATL) have a poor outcome because of the intrinsic drug resistance to chemotherapy. Protection from apoptosis is a common feature involved in multidrug-resistance of ATL. IAP (inhibitor of apoptosis) family proteins inhibit apoptosis induced by a variety of stimuli. In this study, we investigated the expression of IAP family members (survivin, cIAP1, cIAP2, and XIAP) in the primary leukemic cells from patients with ATL. We found that survivin was overexpressed in ATL, especially in acute-type ATL. Sodium arsenite was shown to down-regulate the expression of survivin at both the protein and RNA levels in a time- and dose-dependent manner, thus inhibiting cell growth, inducing apoptosis, and enhancing the caspase-3 activity in ATL cells. Nuclear factor-κB (NF-κB) enhances the transcriptional activity of survivin. Sodium arsenite suppressed the constitutive NF-κB activation by preventing the IκB-α degradation and the nuclear translocation of NF-κB. These findings suggest that survivin is an important antiapoptotic molecule that confers drug resistance on ATL cells. Sodium arsenite was shown to down-regulate the expression of survivin through the NF-κB pathway, thus inhibiting cell growth and promoting apoptosis of ATL cells.
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Mir, Amaidah, Hammad Ahmed Butt, Maria Yasmeen, Anber Saleem, Ruqqia Shafi Minhas, and Sumaira Abbasi. "Histomorphological effects of sodium arsenite on uterus of rats." International Journal of Basic & Clinical Pharmacology 9, no. 11 (October 21, 2020): 1641. http://dx.doi.org/10.18203/2319-2003.ijbcp20204454.
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Background: Arsenic is highly toxic agent and a risk factor for disease and disability. Arsenic is present in drinking water of many developing and developed countries including Pakistan and due to rapid industrialization its quantity in soil and water is increasing day by day.Methods: In an 18 month study in which we took two principal groups, labelled as control group A and experimental group B. The animals of experimental group B were administered 4 µg of sodium arsenite dissolved in 10 ml of distilled water by oral gavage daily for 14 days. The uterus was removed and processed for paraffin embedding and stained with hematoxylin and eosin (H and E). The histological parameters; uterine luminal diameter, height of uterine luminal epithelium, area occupied by epithelial component of uterine glands and the thickness of myometrium were measured and evaluated by civil AutoCAD 2013 software. The data was analyzed statistically with the statistical package for social sciences (SPSS).Results: Histological results showed the degenerative effects. The luminal diameter of uterine horns was reduced in experimental animals. The height of uterine epithelium was reduced. Area occupied by epithelial component of uterine glands was reduced along the reduction in the thickness of myometrium.Conclusions: The histological abnormalities observed in uterus showed that the degenerative effects may be due to oxidative stress produced by the exposure to sodium arsenite. As sodium arsenite produces the oxidative stress by the formation of free radicals and by the denaturation of proteins.
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Adeyi, Olubisi E., Oluwatobi T. Somade, Emmanuel I. Ugwor, Olayinka A. Oladimeji, Happiness O. Ozoemena, and Akindele O. Adeyi. "Assessments of the Safety of Arsenicals on Dyslipidaemia and Reproductive Organ Morphology of Albino Rats." Nigerian Journal of Biochemistry and Molecular Biology 39, no. 2 (August 2, 2024): 49–56. http://dx.doi.org/10.4314/njbmb.v39i2.3.
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Epidemiological studies have implicated Arsenic (As) an environmental toxicant in the etiology of many diseases which have been associated with dyslipidaemia and cardiovascular abnormalities. This study investigated the comparative effect of sub-chronic exposure to two arsenicals on the lipid profiles and morphology of the reproductive organs. Fifty albino rats were divided into five groups of 10 animals each (5 male and 5 female) were exposed to different doses of arsenic (As) either as sodium arsenite or sodium arsenate for 5 weeks. Lipids [triacylglycerol (TAG), cholesterol (CHOL) and phospholipids (PHOS)] concentrations were determined in the plasma, lipoprotein fractions, hepatic, renal, cardiac and brain tissues. In the male rats’ tissues, both arsenicals generally elicited a hormetic response, while in the tissues of female rats; both arsenicals increased the CHOL concentration. Furthermore, the perturbations in TAG concentration in female animals did not follow any regular pattern; although, depletion of TAG characterized these arsenic-induced perturbations in male rats except in the kidney, where TAG was accumulated. The arsenicals generally increased PHOS concentration in exposed animals irrespective of the sex. While HDL-TAG and HDL-CHOL concentrations were significantly reduced in As-exposed groups, changes observed in VLDL+LDL-TAG and VLDL+LDL-CHOL varied with no regular pattern. Histopathology of the sex organs revealed altered morphology in arsenite-exposed rats. Results from this study further associated these arsenicals as potential agents that can cause dyslipidaemia in tissues and also possess the ability to alter the architecture of sex organs in albino rats