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Journal articles on the topic 'Toxic factors'

Author: Grafiati

Published: 3 June 2025

Last updated: 6 July 2025

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1

Charalampos, Depastas. "Toxic factors and autism." Rostrum of Asclepius 16, no. 3 (2017): 182–96. https://doi.org/10.5281/zenodo.821622.

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<strong>ABSTRACT</strong> Autism is a neurodevelopmental disorder. Today it has observed a continuing and rapid increase in its prevalence. Autism increase, in combination with unknown factors that cause it, so far, has drawn the interest of several researchers (from different scientific fields). It could be characterized as a multiple-factors disorder. In recent decades, many researchers have implicated mainly environmental, chemical, genetic, hereditary, and biological factors. The present article focuses on environmental factors that their exposure causes irreversible brain damages (toxicity) - autism. Some of these factors are (mainly) mercury, brominated, thalidomide, misoprostol, valproic acid, chloropiryfos, ethanol etc. However, according to literature review, it has not been proved a direct correlation with the factors which have been implicated for autism disorder. As a result, the question “what causes autism” is still unanswered. Today, diagnostic criteria, early diagnosis, methods for autistic education and medication (under circumstances) are continuously improving.

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2

Porter, G. A. "Risk factors for toxic nephropathies." Toxicology Letters 46, no. 1-3 (1989): 269–79. http://dx.doi.org/10.1016/0378-4274(89)90135-5.

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3

Sarafian, S. K., and S. A. Morse. "Environmental factors affecting toxic shock syndrome toxin-1 (TSST-1) synthesis." Journal of Medical Microbiology 24, no. 1 (1987): 75–81. http://dx.doi.org/10.1099/00222615-24-1-75.

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4

Miyoshi, S., E. G. Oh, K. Hirata, and S. Shinoda. "Exocellulr Toxic Factors Prowced byVibrio Vulnificus." Journal of Toxicology: Toxin Reviews 12, no. 3 (1993): 253–88. http://dx.doi.org/10.3109/15569549309014409.

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5

Bras, G., and E. McLean. "TOXIC FACTORS IN VENO-OCCLUSIVE DISEASE." Annals of the New York Academy of Sciences 111, no. 1 (2006): 392–98. http://dx.doi.org/10.1111/j.1749-6632.1963.tb36979.x.

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6

Neumann, H. G. "Toxic equivalence factors, problems and limitations." Food and Chemical Toxicology 34, no. 11-12 (1996): 1045–51. http://dx.doi.org/10.1016/s0278-6915(97)00073-2.

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7

Galelli, A., S. Anderson, B. Charlot, and J. E. Alouf. "Induction of murine hemopoietic growth factors by toxic shock syndrome toxin-1." Journal of Immunology 142, no. 8 (1989): 2855–63. http://dx.doi.org/10.4049/jimmunol.142.8.2855.

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Abstract Toxic shock syndrome toxin-1 (TSST-1), an extra-cellular 22 kDa single chain protein produced by most Staphylococcus aureus strains isolated from patients with toxic shock syndrome (TSS), induces modifications of blood cell values similar to those observed during TSS. We therefore analyzed the effects of TSST-1 on the proliferation and differentiation of murine granulocyte-macrophage progenitor cells (CFU-culture) and the eventual role of endotoxin in this response. TSST-1 had no direct effect on the proliferation of CFU-culture and was unable to influence the CSF-induced proliferation and differentiation of these progenitors. In contrast, TSST-1 was a potent inducer in spleen cell cultures of a factor with an ability to induce both colony formation by bone marrow cells and proliferation of an IL-3-dependent cell line. Nanogram amounts of TSST-1 were able to induce the release of CSF activity in spleen cell cultures from both normal and LPS-hyporesponsive mice. Cells from C3H/HeJ mice were as responsive as cells from C3H/He Pas mice. Furthermore, in spleen cell cultures from normal mice, TSST-1 and LPS did not act synergistically to induce CSF activity. Nanogram amounts of TSST-1 were also able to induce CSF activity in vivo but failed to induce IL-3 activity in the serum and organ-conditioned media from TSST-1-treated mice.

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8

Rotaru, Lilia. "Environmental toxic factors and clinical pattern of Parkinson’s disease." Moldovan Medical Journal 64, no. 4 (2021): 69–71. http://dx.doi.org/10.52418/moldovan-med-j.64-4.21.13.

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Background: Parkinson’s disease (PD) – the most common neuro-degenerative movement disorder – is considered a result of a multifactorial pathogenic process modulated by cumulative and interactive effects of genes and exposures. An environmental exposure could enhance or create dopaminergic neurons vulnerability and increase PD risk. The purpose of the study was to find if excessive exposure to toxic environmental factors may influence clinical pattern of PD. Material and methods: The study was conducted on 111 patients diagnosed with PD, study group being defined as PD exposed to toxins (33 patients), control group including PD patients without toxin exposure (78 patients). General epidemiological data and clinical data were recorded. Results: Toxin exposure was found in 33 patients (29.73%), more of them – men and rural residents. Toxin exposed PD patients had an insignificantly younger age. The most common disease phenotype in the study group was the akinetic-rigid phenotype (64.7%, p = 0.040), bradykinesia being the most common sign at the disease onset (57.6%, p = 0.008). Levodopa equivalent daily dose also was higher in the study group (659.02 ± 232.46, p = 0.042). Conclusions: Excessive exposure to toxic environmental factors may influence the clinical pattern of PD. In this study the akinetic-rigid type was the predominant disease phenotype associated with toxin exposure. Doses needed for treatment were higher in PD patients exposed to toxins, as an indicator of a more severe motor impairment in this group

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9

Jacoby, Jean M., Diane C. Collier, Eugene B. Welch, F. Joan Hardy, and Michele Crayton. "Environmental factors associated with a toxic bloom of Microcystis aeruginosa." Canadian Journal of Fisheries and Aquatic Sciences 57, no. 1 (2000): 231–40. http://dx.doi.org/10.1139/f99-234.

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Environmental factors associated with the occurrence of toxic cyanobacterial blooms and toxin production were investigated during the summers of 1994 and 1995 in Steilacoom Lake, Washington. A pronounced and prolonged toxic bloom of Microcystis aeruginosa occurred during summer 1994 but not during 1995. Lake characteristics that were associated with the toxic bloom in 1994 were higher total phosphorus, decreased water transparency, high water column stability, high surface water temperature and pH, and decreased lake flushing. Decreased water transparency during 1994 may have been due to significantly lower zooplankton abundance. We hypothesize that this decreased transparency was caused by increased planktivory by higher numbers of coho salmon (Oncorhynchus kisutch) fingerlings during 1994 and (or) inhibition of zooplankton grazing by Microcystis. The success of Microcystis over other cyanobacteria was associated with low nitrogen to phosphorus ratios and low nitrate-nitrogen with sufficient ammonium-nitrogen concentrations. Toxin production (i.e., micrograms of microcystin per gram of plankton biomass) was not constant over the duration of detectable toxicity; hence, no relationship was found between Microcystis abundance and microcystin concentration. However, microcystin concentration was positively correlated with increasing soluble reactive phosphorus concentrations between 1 and 10 µg·L-1, indicating that toxin production may have been limited by phosphorus.

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10

Menzies, F. D., A. W. Gordon, S. H. McBride, and E. A. Goodall. "Risk factors for toxic mastitis in cows." Veterinary Record 152, no. 11 (2003): 319–22. http://dx.doi.org/10.1136/vr.152.11.319.

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11

Ali, Saleem H. "Sugar: other ‘toxic’ factors play a part." Nature 482, no. 7386 (2012): 471. http://dx.doi.org/10.1038/482471b.

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12

Husain, Sohail Z., Veronique Morinville, John Pohl, et al. "Toxic-metabolic Risk Factors in Pediatric Pancreatitis." Journal of Pediatric Gastroenterology and Nutrition 62, no. 4 (2016): 609–17. http://dx.doi.org/10.1097/mpg.0000000000001035.

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13

Godoy, P., and R. Reif. "Transcription factors controlling responses to toxic chemicals." Archives of Toxicology 87, no. 1 (2012): 3–4. http://dx.doi.org/10.1007/s00204-012-0981-5.

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14

Ahlborg, UG, GC Becking, LS Birnbaum, et al. "Toxic equivalency factors for dioxin-like PCBs." Chemosphere 28, no. 6 (1994): 1049–67. http://dx.doi.org/10.1016/0045-6535(94)90324-7.

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15

Ahlborg, Ulf G., and Annika Hanberg. "Toxic equivalency factors for dioxin-like PCBs." Environmental Science and Pollution Research 1, no. 2 (1994): 67–68. http://dx.doi.org/10.1007/bf02986503.

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16

Tang, Tianjia, Michael Claggett, Joon Byun, Mike Roberts, Jessica Granell, and Dale E. Aspy. "MOBILE6.2 Modeling of Exhaust Air Toxic Emission Factors." Transportation Research Record: Journal of the Transportation Research Board 1941, no. 1 (2005): 99–106. http://dx.doi.org/10.1177/0361198105194100112.

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The newly released MOBILE6.2 has incorporated both air toxic and particulate matter emission factor modeling functions. A series of test runs were performed to gain a better understanding of the air toxic modeling function and overall model behavior. These test runs and scenarios evaluated the changes in emission factors of all six built-in air toxic compounds as affected by vehicle activities, fuel physical properties, fuel chemical compositions, oxygenated fuel additives, and environmental conditions. Results obtained indicate that exhaust emission factors for acrolein, acetaldehyde, benzene, 1,3-butadiene, formaldehyde, and methyl tertiary butyl ether are inversely proportional to freeway and arterial vehicle speeds. This phenomenon follows the trend of total organic gas emission factors. Effects from roadway facility differences indicated that the higher the percentage of vehicle miles traveled on a freeway, the lower the air toxic emission factors on a per vehicle mile traveled basis. Exhaust air toxic emission factors increase when fuel Reid vapor pressure value and sulfur content increase. Diesel sulfur content has no effect on the six toxic compound emission factors. Effects from fuel chemical compositions on all emission factors varied. However, chemical compositions do have significant effects on all air toxic compound emission factors. On the same note, both minimum and maximum temperatures affect all air toxic emissions significantly. The time series evaluation indicates that all six tested air toxic compound emissions decrease linearly from the year 2002 to 2020.

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17

FEOLA, MARIO, JAN SIMONI, RUC TRAN, CHARLES D. LOX, and PETER C. CANIZARO. "Toxic Factors in the Red Blood Cell Membrane." Journal of Trauma: Injury, Infection, and Critical Care 29, no. 8 (1989): 1065–75. http://dx.doi.org/10.1097/00005373-198908000-00003.

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18

RAJASEKARAN, MAHADEVAN, PAUL STEIN, and C. LOWELL PARSONS. "Toxic factors in human urine that injure urothelium." International Journal of Urology 13, no. 4 (2006): 409–14. http://dx.doi.org/10.1111/j.1442-2042.2006.01301.x.

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19

Safe, S. "Development, validation and limitations of toxic equivalency factors." Chemosphere 25, no. 1-2 (1992): 61–64. http://dx.doi.org/10.1016/0045-6535(92)90480-f.

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20

Goarant, C., J. Herlin, R. Brizard, AL Marteau, C. Martin, and B. Martin. "Toxic factors of Vibrio strains pathogenic to shrimp." Diseases of Aquatic Organisms 40 (2000): 101–7. http://dx.doi.org/10.3354/dao040101.

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21

Vos, Joseph G., Cees De Heer, and Henk Van Loveren. "Immunotoxic effects of TCDD and toxic equivalency factors." Teratogenesis, Carcinogenesis, and Mutagenesis 17, no. 4-5 (1997): 275–84. http://dx.doi.org/10.1002/(sici)1520-6866(1997)17:4/5<275::aid-tcm10>3.0.co;2-b.

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22

Makkar, H. P. S., A. O. Aderibigbe, and K. Becker. "Comparative evaluation of non-toxic and toxic varieties of Jatropha curcas for chemical composition, digestibility, protein degradability and toxic factors." Food Chemistry 62, no. 2 (1998): 207–15. http://dx.doi.org/10.1016/s0308-8146(97)00183-0.

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23

Moles, T. M., and D. J. Baker. "Toxic Trauma." Prehospital and Disaster Medicine 16, no. 2 (2001): 78–80. http://dx.doi.org/10.1017/s1049023x00025735.

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AbstractHazardous materials (HAZMAT) carry many inherent dangers. Such materials are distributed widely in industrial and military sites. Toxic trauma (TT) denotes the complex of systemic and organ injury caused by toxic agents. Often, TT is associated with other injuries that also require the application of life-support techniques. Rapid onset of acute respiratory failure and consequent cardiovascular failure are of primary concern. Management of TT casualties is dependent upon the characteristics of the toxic agents involved and on the demographics surrounding the HAZMAT incident.Agents that can produce TT possess two pairs of salient characteristics: (1) causality (toxicity and latency), and (2) EMS system (persistency and transmissibility). Two characteristics of presentations are important: (1) incident presentation, and (2) casualty presentation. In addition, many of these agents complicate the processes associated with anaesthesia and must be dealt with. Failure of recognition of these factors may result in the development of respiratory distress syndromes and multiorgan system failure, or even death.

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24

Masur, T. V., and O. V. Yablonska. "Suppression of cellular immunity factors by toxic fraction of supernatant of broth culture Pasteurella haemolytica." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 20, no. 83 (2018): 314–19. http://dx.doi.org/10.15421/nvlvet8363.

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In the etiology of many infectious animal diseases, Pasteurella haemolytica belongs to a specific place. An important factor in the pathogenicity of this microorganism, like the Pasteurella multocida serotype D, is the thermostable exotoxin. It can be obtained from bacterial-purified culture fluid. Although the study of toxin formation among microorganisms is quite popular, however, the features of toxin formation in hemolytic pasteurals, depending on the virulence of the pathogen, the nature of the toxic effects of these objects in vivo remain unclear. Materials for research were 16 isolates of Pasteurella haemolytica, isolated from pathological and biological material obtained during the outbreaks of respiratory pathology in farm animals. Initially, the nature of the research concerned the establishment of the potential for toxin formation in the isolates obtained. The method provided for a comparative analysis of the DNA nucleotide sequences of each of the investigated isolates P. haemolytica and information obtained from the international database. Another part of the work concerned the actual allocation of the major groups of toxic components of Pasteurella haemolytica by extraction to determine their biochemical nature. Exotoxin isolation was carried out from the Pasteurella spp. The components of the sediment and supernatant were separated by ion exchange chromatography on TSK gels. In order to detect the harmful effects of toxin hemolytic pasteurals on the body, they used the method of determining the opsonic index (the ratio of the phagocytic number in the mixture without the products of toxic fractions to the mixture with the toxin-containing fraction). It has been established that an important factor of the pathogenetic effect in Pasteurella haemolytica is the toxic fraction. Electrophoregram analysis of the results of DNA amplification in a comparative aspect with the data of standard samples helped to determine the presence of elements of the genome, which indicate the potential for toxin formation in isolated hemolytic pasteurized isolates from the test material. Toxic fractions isolated from Pasteurella haemolytica broth culture supernatant are substances of protein-carbohydrate nature. The isolated peak toxicogenic fractions of dialysate of a bacterial culture sieve contained protein and carbohydrates within the limits of 12.5–20 μg / ml and 0–20 μg/ml, respectively. In the dialysate of the broth culture supernatant, where 5 groups of toxigenic fractions were identified, the content of protein and carbohydrates in them varied, respectively, in the range from 20 to 95 μg/ml and from 3.3 to 26.62 μg/ml. At reproduction of opsono-phagocytic reaction with participation of toxigenic fractions of hemolytic pasteurel, a sufficiently expressed immunosuppressive effect of these complexes on the body of warm-blooded substances with an opsonic index of 3 ± 0.03 was established. During further research it is planned to determine the dermal necrotic and lethal effects of the isolated toxicogenic fractions of hemolytic pasteuride on the body of warm-blooded ones.

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25

Jupin, C., S. Anderson, C. Damais, J. E. Alouf, and M. Parant. "Toxic shock syndrome toxin 1 as an inducer of human tumor necrosis factors and gamma interferon." Journal of Experimental Medicine 167, no. 3 (1988): 752–61. http://dx.doi.org/10.1084/jem.167.3.752.

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We present evidence that toxic shock syndrome toxin 1 (TSST-1) induces the production of high levels of TNF by human blood monocytes. Enriched lymphocyte preparations incubated with the staphylococcal toxin produced significant levels of TNF-like activity that is not neutralized by anti-rHuTNF antibodies and is likely to be lymphotoxin (LT or TNF-beta). We demonstrate also that TSST-1 is a potent inducer of IFN-gamma. When lymphocyte preparations were costimulated with PMA, the TSST-1 effect was strongly potentiated and the levels of cytotoxic factors, IFN-gamma, and IL-2 present in supernatant fluids were comparable to those observed after treatment with PMA and PHA. Thus, TSST-1, which is also known as an inducer of IL-1 and IL-2, stimulates the production of endogenous mediators that could play a role in the physiopathological processes of toxic shock syndrome (TSS). The described results suggest that the discrepancies in the clinical features between TSS and endotoxin shock may be related to qualitative differences in cytokine production.

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26

Hoetzenecker, Wolfram, Tarun Mehra, Ieva Saulite, et al. "Toxic epidermal necrolysis." F1000Research 5 (May 20, 2016): 951. http://dx.doi.org/10.12688/f1000research.7574.1.

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Toxic epidermal necrolysis (TEN) is a rare, life-threatening drug-induced skin disease with a mortality rate of approximately 30%. The clinical hallmark of TEN is a marked skin detachment caused by extensive keratinocyte cell death associated with mucosal involvement. The exact pathogenic mechanism of TEN is still uncertain. Recent advances in this field have led to the identification of several factors that might contribute to the induction of excessive apoptosis of keratinocytes. In addition, specific human leukocyte antigen types seem to be associated with certain drugs and the development of TEN. As well-controlled studies are lacking, patients are treated with various immunomodulators (e.g. intravenous immunoglobulin) in addition to the best supportive care.

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27

Tabatabaei, Sayyed-Ali, Saba Ariafar, and Mojdeh Mohammadi. "Toxic Environmental Factors and Multiple Sclerosis: A Mechanistic View." Avicenna Journal of Pharmaceutical Research 3, no. 1 (2022): 45–54. http://dx.doi.org/10.34172/ajpr.2022.1063.

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Multiple sclerosis (MS) is an acquired inflammatory and neurodegenerative immuno-mediated disorder of the central nervous system (CNS) characterized by inflammation, demyelination, and primary or secondary axonal degeneration. Epidemiological studies have suggested that both genetic and non-genetic risk factors are involved in the etiology of MS. Non-genetic factors include infections, vaccinations, nutritional habits, hormonal factors, and physical and chemical agents. Toxic environmental factors have been proposed to play a considerable role in MS pathogenesis. This review explored pieces of evidence and potential mechanisms of action for some toxic factors such as heavy metals, organic solvents (OSs), tobacco smoking, plastic monomers, additives, and pesticides. The obtained findings provide us with the potential for prevention, especially for people at greater risk such as individuals exposed to these toxic factors. It should be noted that further investigations are needed to find precise mechanisms of causality in humans and to develop defensive approaches.

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28

Ortiz-Castillo, Fátima, Luis Enrique Salinas-Aragón, Martín Sánchez-Aguilar, et al. "Amoebic toxic colitis: analysis of factors related to mortality." Pathogens and Global Health 106, no. 4 (2012): 245–48. http://dx.doi.org/10.1179/2047773212y.0000000019.

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29

Feola, Mario, Jan Simoni, Ruc Tran, and Peter C. Canizaro. "THE TOXIC FACTORS OF THE RED BLOOD CELL MEMBRANE." Journal of Trauma: Injury, Infection, and Critical Care 28, no. 7 (1988): 1085. http://dx.doi.org/10.1097/00005373-198807000-00043.

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30

Nisbet, Ian C. T., and Peter K. LaGoy. "Toxic equivalency factors (TEFs) for polycyclic aromatic hydrocarbons (PAHs)." Regulatory Toxicology and Pharmacology 16, no. 3 (1992): 290–300. http://dx.doi.org/10.1016/0273-2300(92)90009-x.

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31

Li, Zijun. "Toxic Masculinity: Analyzing Man Standards and Sexual Inequality through Euphoria." Lecture Notes in Education Psychology and Public Media 6, no. 1 (2023): 757–64. http://dx.doi.org/10.54254/2753-7048/6/20220777.

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Toxic masculinity has been a hot topic since people's self-awareness rose, still, in large of film and television works, a lot of conversation and characterization indicated toxic masculinity implicitly. A hit American TV series, Euphoria, shows toxic masculinity and its potential impact on people around, which reveals a new perspective about the causes of toxic masculinity and how harmful it is. By coding the violent scenario and analyzing the conversations in the episodes, data shows that the main characters with toxic masculinity suffered from peer pressure, American culture and social certain expectation, and the major victims in related violent clips are the female and the queer group. The results turn out that peer pressure, American culture and people's expectation of males can be vital factors in toxic masculinity formation, and the poisonous personality will directly influence female and queer groups around them.

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Pavlova, Elena, Elena Terentyeva, and Armine Matevosyan. "Toxic communication as a risk factor when promoting Health, Safety & Environmental culture in an organization." E3S Web of Conferences 169 (2020): 05003. http://dx.doi.org/10.1051/e3sconf/202016905003.

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The study focuses on the problem of toxic communication as one of the risk factors in Health, Safety & Environmental culture development. The data obtained indicate that the effectiveness of Health, Safety & Environmental communication is reduced due to the expansion of toxic communication, which includes such phenomena as intentional confusion, topic overdiscussing, lack of dialogue on equal footing, lack of feedback, and weak corporate culture. It is also shown that in most cases, ineffective Health, Safety & Environmental leadership of managers and chiefs demonstrates the communicative behaviour of a toxic boss. The conclusion is drawn on the need for further studies of toxic communication in order to reduce its negative impact on Health, Safety & Environmental culture promotion.

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Gao, Zhuye, Siwei Li, Qinghua Shang, et al. "Complex Networks Approach for Analyzing the Correlation of Traditional Chinese Medicine Syndrome Evolvement and Cardiovascular Events in Patients with Stable Coronary Heart Disease." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/824850.

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This is a multicenter prospective cohort study to analyze the correlation of traditional Chinese medicine (TCM) syndrome evolvement and cardiovascular events in patients with stable coronary heart disease (CHD). The impact of syndrome evolvement on cardiovascular events during the 6-month and 12-month follow-up was analyzed using complex networks approach. Results of verification using Chi-square test showed that the occurrence of cardiovascular events was positively correlated with syndrome evolvement when it evolved from toxic syndrome to Qi deficiency, blood stasis, or sustained toxic syndrome, when it evolved from Qi deficiency to blood stasis, toxic syndrome, or sustained Qi deficiency, and when it evolved from blood stasis to Qi deficiency. Blood stasis, Qi deficiency, and toxic syndrome are important syndrome factors for stable CHD. There are positive correlations between cardiovascular events and syndrome evolution from toxic syndrome to Qi deficiency or blood stasis, from Qi deficiency to blood stasis, or toxic syndrome and from blood stasis to Qi deficiency. These results indicate that stable CHD patients with pathogenesis of toxin consuming Qi, toxin leading to blood stasis, and mutual transformation of Qi deficiency and blood stasis are prone to recurrent cardiovascular events.

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Smith, G. R., and Ann Turner. "Factors affecting the toxicity of rotting carcasses containingClostridium botulinumtype C." Epidemiology and Infection 98, no. 3 (1987): 345–51. http://dx.doi.org/10.1017/s0950268800062105.

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SUMMARYMice killed shortly after receiving 1300–3000 spores ofClostridium botulinumtype Cper oswere incubated at one of four chosen temperatures together with bottles of cooked meat medium seeded with a similar inoculum. After incubation the rotting carcasses were homogenized. Sterile membrane filtrates of the homogenates (10–20.8%, w/v) and pure cultures were then titrated for toxicity. A temperature of 37 °C produced less toxicity in most carcasses than in cultures. At 30 °C, however, toxicity (often 2× 105to 2× 106mouse intraperitoneal LD/g or ml) was roughly similar in both systems, and some carcasses and cultures were still toxic (2× 104to 2× 105LD/g or ml) after 349 days. Surprisingly, at 23 °C, though greatly reduced in the cultures, toxicity was high in many carcasses for at least 28 days. Little or no toxin was produced in either system at 16 °C. Unfiltered homogenates (17·8–22·5%, w/v; dose 0·25 mlper os) of toxic carcasses incubated at 30 °C for 7 days invariably produced death from botulism, often within as little as 4 h, but a 1 in 10 dilution produced less than 100% mortality.

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35

Joung, Seung-Hyun, Hee-Mock Oh, So-Ra Ko, and Chi-Yong Ahn. "Correlations between environmental factors and toxic and non-toxic Microcystis dynamics during bloom in Daechung Reservoir, Korea." Harmful Algae 10, no. 2 (2011): 188–93. http://dx.doi.org/10.1016/j.hal.2010.09.005.

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36

Roderer, Daniel, and Stefan Raunser. "Tc Toxin Complexes: Assembly, Membrane Permeation, and Protein Translocation." Annual Review of Microbiology 73, no. 1 (2019): 247–65. http://dx.doi.org/10.1146/annurev-micro-102215-095531.

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Tc toxin complexes are virulence factors of many bacteria, including insect and human pathogens. Tc toxins are composed of three subunits that act together to perforate the host membrane, similar to a syringe, and translocate toxic enzymes into the host cell. The reactions of the toxic enzymes lead to deterioration and ultimately death of the cell. We review recent high-resolution structural and functional data that explain the mechanism of action of this type of bacterial toxin at an unprecedented level of molecular detail. We focus on the steps that are necessary for toxin activation and membrane permeation. This is where the largest conformational transitions appear. Furthermore, we compare the architecture and function of Tc toxins with those of anthrax toxin and vertebrate teneurin.

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37

Peng, Lianci, Jiali Jiang, Tingting Chen, et al. "Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome." Toxins 13, no. 1 (2021): 68. http://dx.doi.org/10.3390/toxins13010068.

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Staphylococcus aureus is a Gram-positive opportunistic pathogen which causes infections in a variety of vertebrates. Virulence factors are the main pathogenesis of S. aureus as a pathogen, which induce the host’s innate and adaptive immune responses. Toxic shock syndrome toxin 1 (TSST-1) is one of the most important virulence factors of S. aureus. However, the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) in TSST-1-induced innate immune response is still unclear. Here, purified recombinant TSST-1 (rTSST-1) was prepared and used to stimulate mouse peritoneal macrophages. The results showed that under the action of adenosine-triphosphate (ATP), rTSST-1 significantly induced interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) production in mouse macrophages and the production was dose-dependent. In addition, rTSST-1+ATP-stimulated cytokine production in macrophage depends on the activation of toll like receptor 4 (TLR4), but not TLR2 on the cells. Furthermore, the macrophages of NLRP3−/− mice stimulated with rTSST-1+ATP showed significantly low levels of IL-1β production compared to that of wild-type mice. These results demonstrated that TSST-1 can induce the expression of inflammatory cytokines in macrophages via the activation of the TLR4 and NLRP3 signaling pathways. Our study provides new information about the mechanism of the TSST-1-inducing host’s innate immune responses.

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38

Olayinka, Oluwaseyi, Olaniyi O. Olayinka, Brook T. Alemu, Muge Akpinar-Elci, and George T. Grossberg. "Toxic Environmental Risk Factors for Alzheimer’s Disease: A Systematic Review." Aging Medicine and Healthcare 10, no. 1 (2019): 4–17. http://dx.doi.org/10.33879/amh.2019.1727.

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Alexopoulou, O., C. Beguin, M. Buysschaert, et al. "PREDICTIVE FACTORS OF THYROID CARCINOMA IN NON-TOXIC MULTINODULAR GOITRE." Acta Clinica Belgica 59, no. 2 (2004): 84–89. http://dx.doi.org/10.1179/acb.2004.012.

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Francisqueti, Fabiane V., Klinsmann C. Santos, Artur JT Ferron, et al. "Fructose: Toxic effect on cardiorenal risk factors and redox state." SAGE Open Medicine 4 (January 1, 2016): 205031211668429. http://dx.doi.org/10.1177/2050312116684294.

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Aim: To investigate the effects of fructose consumption on the antioxidant capacity in heart and kidney, cardiovascular disease risk factors, and evaluation of these variables after its removal. Methods: Male Wistar rats (n = 36) were divided into control group (n = 12): standard chow + water or F group: standard chow + fructose in drinking water (30%) for 15 weeks. After, F group was divided to continue receiving standard chow + fructose in drinking water (30%) (n = 12) or standard chow + water (Ex group, n = 12) for 9 weeks. Water, chow and caloric diaries intake, final body weight, adiposity index, plasma glucose and triacylglycerol, systolic blood pressure, and cardiac and renal hydrophilic antioxidant capacity were analyzed. Results: Control and Ex groups consumed less chow and water compared to F group. Caloric intake was higher in control group. There was no difference in final body weight and adiposity index. Systolic blood pressure and cardiac and renal hydrophilic antioxidant capacity were worst in F group. Conclusion: Prolonged exposure to fructose induces oxidative stress, systolic blood pressure, and increase in triacylglycerol. When stopped fructose consumption, Ex group presented improvement in these variables, suggesting the toxicity effect of fructose when consumed in high amounts and prolonged exposure.

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EASTERLY, C. E. "TOXIC EQUIVALENCY FACTORS CAN UNIFY EXPOSURE PARAMETERS IN ENVIRONMENTAL EPIDEMIOLOGY." Epidemiology 7, Supplement (1996): S88. http://dx.doi.org/10.1097/00001648-199607001-00279.

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Kemen, Christoph, Joachim Lemke, Peter H. Hoeger, et al. "Human Leukocyte Antigen-Related Risk Factors for Toxic Epidermal Necrosis." Pediatric Infectious Disease Journal 28, no. 6 (2009): 552. http://dx.doi.org/10.1097/inf.0b013e31819f3610.

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Pohl, John, Veronique Morinville, Sohail Z. Husain, and Aliye Uc. "Toxic-Metabolic Risk Factors Are Uncommon in Pediatric Chronic Pancreatitis." Journal of Pediatric Gastroenterology & Nutrition 62, no. 6 (2016): e66-e67. http://dx.doi.org/10.1097/mpg.0000000000001156.

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Claggett, Michael, and Terry L. Miller. "Variability of Mobile Source Air Toxic Emissions Factors with MOBILE6.2." Transportation Research Record: Journal of the Transportation Research Board 1987, no. 1 (2006): 103–9. http://dx.doi.org/10.1177/0361198106198700111.

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Silver, S., J. Schottel, and A. Weiss. "Bacterial resistance to toxic metals determined by extrachromosomal R factors." International Biodeterioration & Biodegradation 48, no. 1-4 (2001): 263–81. http://dx.doi.org/10.1016/s0964-8305(01)00093-2.

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Gupta, Y. P. "Anti-nutritional and toxic factors in food legumes: a review." Plant Foods for Human Nutrition 37, no. 3 (1987): 201–28. http://dx.doi.org/10.1007/bf01091786.

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Jandacek, Ronald J., and Patrick Tso. "Factors affecting the storage and excretion of toxic lipophilic xenobiotics." Lipids 36, no. 12 (2001): 1289–305. http://dx.doi.org/10.1007/s11745-001-0844-z.

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Hines, Harry B., and Ernst E. Brueggemann. "Factors affecting the capillary electrophoresis of ricin, a toxic glycoprotein." Journal of Chromatography A 670, no. 1-2 (1994): 199–208. http://dx.doi.org/10.1016/0021-9673(94)80295-5.

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Peters, Jeffrey M., and Frank J. Gonzalez. "Why Toxic Equivalency Factors Are Not Suitable for Perfluoroalkyl Chemicals." Chemical Research in Toxicology 24, no. 10 (2011): 1601–9. http://dx.doi.org/10.1021/tx200316x.

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Gorsira, Madelijne, Wim Huisman, Adriaan Denkers, and Linda Steg. "Why Dutch officials take bribes: a toxic mix of factors." Crime, Law and Social Change 75, no. 1 (2020): 45–72. http://dx.doi.org/10.1007/s10611-020-09919-w.

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AbstractThe aim of this study was to gain an in-depth understanding of the factors that underlie public officials’ engagement in corruption. Given the significant public interest, we gained permission from the Dutch Ministry of Justice to analyze multiple confidential criminal files of cases in which Dutch public officials took bribes from private companies. Extending previous research, we analyzed three types of factors, individual factors, organizational factors, and factors related to the relationships between corrupt officials and their bribers. Moreover, for the first time, we considered the interplay between these three types of factors. The results suggest that public officials’ engagement in bribery is rooted in a combination of individual, organizational and relationship variables that influence and reinforce each other, creating a toxic mix. This implies that the battle against bribery can be fought on multiple fronts, whereby changing one critical factor may cause the mix to lose its toxicity.

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