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Articles de revues sur le sujet « Cadmium effects on SOD1 »

Auteur : Grafiati

Publié le 10 mars 2023

Mis à jour le 31 juillet 2025

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1

Zoidis, Evangelos, George Papadomichelakis, Athanasios C. Pappas, Georgios Theodorou, and Kostas Fegeros. "Effects of Selenium and Cadmium on Breast Muscle Fatty-Acid Composition and Gene Expression of Liver Antioxidant Proteins in Broilers." Antioxidants 8, no. 5 (2019): 147. http://dx.doi.org/10.3390/antiox8050147.

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The present work was part of a project intended to evaluate whether organic selenium (Se) has the potential to protect against toxic effects exerted by cadmium (Cd). For this reason, 300 as-hatched, one-day-old broiler chickens were randomly allocated in four dietary treatments with five replicate pens per treatment. Chickens in T1 treatment, were offered a diet supplemented with 0.3 ppm Se (as Se-yeast), without added Cd; in T2 treatment, they were offered a diet with 0.3 ppm Se and 10 ppm Cd; in T3 treatment, they were offered a diet with 0.3 ppm Se and 100 ppm Cd; in T4 treatment, chickens

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Medicherla, Balasubrahmanyam, and Alfred L. Goldberg. "Heat shock and oxygen radicals stimulate ubiquitin-dependent degradation mainly of newly synthesized proteins." Journal of Cell Biology 182, no. 4 (2008): 663–73. http://dx.doi.org/10.1083/jcb.200803022.

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Accumulation of misfolded oxidant-damaged proteins is characteristic of many diseases and aging. To understand how cells handle postsynthetically damaged proteins, we studied in Saccharomyces cerevisiae the effects on overall protein degradation of shifting from 30 to 38°C, exposure to reactive oxygen species generators (paraquat or cadmium), or lack of superoxide dismutases. Degradation rates of long-lived proteins (i.e., most cell proteins) were not affected by these insults, even when there was widespread oxidative damage to proteins. However, exposure to 38°C, paraquat, cadmium, or deletio

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Bovio, Federica, Barbara Sciandrone, Chiara Urani, Paola Fusi, Matilde Forcella, and Maria Elena Regonesi. "Superoxide dismutase 1 (SOD1) and cadmium: A three models approach to the comprehension of its neurotoxic effects." NeuroToxicology 84 (May 2021): 125–35. http://dx.doi.org/10.1016/j.neuro.2021.03.007.

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Zhang, Shuai, Ruikang Li, Jing Xu, Yan Liu, and Yanjie Zhang. "The Impact of Atmospheric Cadmium Exposure on Colon Cancer and the Invasiveness of Intestinal Stents in the Cancerous Colon." Toxics 12, no. 3 (2024): 215. http://dx.doi.org/10.3390/toxics12030215.

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Background: Inhalation exposure to carcinogenic metals such as cadmium (Cd) is a significant global health concern linked to various cancers. However, the precise carcinogenic mechanism underlying inhalation exposure remains elusive. Methods: In this study, CT26 mouse colon cancer (CC) cells were implanted into BALB/c mice to establish CC mouse models. Some of the CC mice were implanted with intestinal stents. The mice were exposed to atomized oxygen and nitrogen (O2/N2) gas containing Cd. Results: Atmospheric Cd intensified inflammation in CC cells and heightened Nicotinamide Adenine Dinucleo

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Jiang, Shun Yao, and Pei Jiang Zhou. "Effects of Cadmium on the Expression of Antioxidant Enzymes, Oxidative Stress and Apoptosis in Primary Hepatocytes of Carassius Auratus." Advanced Materials Research 518-523 (May 2012): 341–46. http://dx.doi.org/10.4028/www.scientific.net/amr.518-523.341.

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The primary hepatocytes of Carassius auratus were incubated with 0, 0.01, 0.1, 1, 10 and 100 mg/l Cadmium(Cd2+) at 25°C for 8h in vitro. The results showed that the hepatocytes survival rate in the 1, 10 and 100 mg/l Cd2+ treated groups were significantly lower than that in the control, the percentage of apoptotic hepatocytes significantly increased in 0.1, 1 and 10 mg/l of Cd2+ treated groups, intracellular reactive oxygen species(ROS) and malondialdehyde (MDA) content significantly increased in 0.1, 1, 10 and 100 mg/l Cd2+ treated groups, typical DNA ladder was observed in 0.1, 1 and 10 mg/l

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A.Paritha, bhanu, and Deepak M. "The effect of Cadmium on antioxidant enzymes in the liver of fresh water fish Cyprius carpio (Linn)." Biolife 3, no. 1 (2022): 50–53. https://doi.org/10.5281/zenodo.7263050.

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<strong>ABSTRACT</strong> In the present investigation, the fresh water fish C. carpio and Cadmium were used.  Bio assays were conducted to find LC50 96hr value of the metal to the fishes and it was found to be 1.5%.  Then groups of fishes were reared in various sublethal concentrations of Cadmium for 30days.  The liver from the control and Cadmium –treated fishes was dissected out for the estimation of Superoxide Dimutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPx), and Gulutathione-S-Transferrase (GST).  In treated fishes, the liver antioxidant enzymes incre

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Nikolic-Kokic, Aleksandra, Zorana Orescanin-Dusic, Ivan Spasojevic, et al. "The effects of wild-type and mutant SOD1 on smooth muscle contraction." Archives of Biological Sciences 67, no. 1 (2015): 187–92. http://dx.doi.org/10.2298/abs141006023n.

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In this work we compared the mutated liver copper zinc-containing superoxide dismutase (SOD1) protein G93A of the transgenic rat model of familial amyotrophic lateral sclerosis (FALS), to wild-type (WT) rat SOD1. We examined their enzymatic activities and effects on isometric contractions of uteri of healthy virgin rats. G93A SOD1 showed a slightly higher activity than WT SOD1 and, in contrast to WT SOD1, G93A SOD1 did not induce smooth muscle relaxation. This result indicates that effects on smooth muscles are not related to SOD1 enzyme activity and suggest that heterodimers of G93A SOD1 form

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Yadav, Pravendra, Andrea Petrella, Francesco Todaro, et al. "Ex Situ Stabilization/Solidification Approaches of Marine Sediments Using Green Cement Admixtures." Materials 17, no. 14 (2024): 3597. http://dx.doi.org/10.3390/ma17143597.

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The routine dredging of waterways produces huge volumes of sediments. Handling contaminated dredged sediments poses significant and diverse challenges around the world. In recent years, novel and sustainable ex situ remediation technologies for contaminated sediments have been developed and applied. This review article focuses on cement-based binders in stabilizing contaminants through the stabilization/solidification (S/S) technique and the utilization of contaminated sediments as a resource. Through S/S techniques, heavy metals can be solidified and stabilized in dense and durable solid matr

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Nikolić-Kokić, Aleksandra, Zorana Oreščanin-Dušić, Marija Slavić, et al. "The Effects of Human Wild-Type and Fals Mutant L144P SOD1 on Non-Vascular Smooth Muscle Contractions / EFEKTI HUMANE NORMALNE I FALS MUTIRANE L144P SOD1 NA NEVASKULARNE KONTRAKCIJE GLATKIH MIŠIĆA." Journal of Medical Biochemistry 32, no. 4 (2013): 375–79. http://dx.doi.org/10.2478/jomb-2013-0032.

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Summary Background: Mutated copper, zinc-containing superoxide dismutase (SOD1) may self-aggregate, an event that could also be an initial cause of motor neuron malfunction leading to disease onset. The effects of human mutated SOD1 pro- tein from the blood of familial amyotrophic lateral sclerosis (FALS) patients bearing Leu144Phe (L144F) mutation were compared to wild-type (WT) human SOD1 derived from healthy examinees, for enzymatic activity and the effects on isometric contractions of non-vascular smooth muscle. Methods: We isolated WT and L144F SOD1 enzymes from eight patients with FALS,

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Sorrells, A. D., K. Corcoran-Gomez, K. A. Eckert, et al. "Effects of environmental enrichment on the amyotrophic lateral sclerosis mouse model." Laboratory Animals 43, no. 2 (2009): 182–90. http://dx.doi.org/10.1258/la.2008.005090.

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The manner in which an animal's environment is furnished may have significant implications for animal welfare as well as research outcomes. We evaluated four different housing conditions to determine the effects of what has been considered standard rodent enrichment and the exercise opportunities those environments allow on disease progression in the amyotrophic lateral sclerosis mouse model. Forty-eight copper/zinc superoxide dismutase mice (strain: B6SJL-TgN [SOD1-G931]1Gur) (SOD1) and 48 control (C) (strain: B6SJL-TgN[SOD1]2Gur) male mice were randomly assigned to four different conditions

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Ying, Weihai, Christopher M. Anderson, Yongmei Chen, et al. "Differing Effects of Copper, Zinc Superoxide Dismutase Overexpression on Neurotoxicity Elicited by Nitric Oxide, Reactive Oxygen Species, and Excitotoxins." Journal of Cerebral Blood Flow & Metabolism 20, no. 2 (2000): 359–68. http://dx.doi.org/10.1097/00004647-200002000-00018.

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Overexpression of Cu,Zn superoxide dismutase (SOD1) reduces ischemic injury in some stroke models but exacerbates injury in a neonatal stroke model and in other settings. The current study used a SOD1 transgenic (SOD1-Tg) murine cortical culture system, derived from the same mouse strain previously used for the stroke models, to identify conditions that determine whether SOD1 overexpression in neurons is protective or detrimental. The nitric oxide (NO) donors S-nitroso- N-acetylpenicillamine, spermine-NONOate, and diethylamine-NONOate produced less death in SOD1-Tg neurons than in wild-type ne

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Pereira, Gabriel Rodrigues Coutinho, Bárbara de Azevedo Abrahim Vieira, and Joelma Freire De Mesquita. "Comprehensive in silico analysis and molecular dynamics of the superoxide dismutase 1 (SOD1) variants related to amyotrophic lateral sclerosis." PLOS ONE 16, no. 2 (2021): e0247841. http://dx.doi.org/10.1371/journal.pone.0247841.

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Amyotrophic Lateral Sclerosis (ALS) is the most frequent motor neuron disorder, with a significant social and economic burden. ALS remains incurable, and the only drugs approved for its treatments confers a survival benefit of a few months for the patients. Missense mutations in superoxide dismutase 1 (SOD1), a major cytoplasmic antioxidant enzyme, has been associated with ALS development, accounting for 23% of its familial cases and 7% of all sporadic cases. This work aims to characterize in silico the structural and functional effects of SOD1 protein variants. Missense mutations in SOD1 were

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Culik, Robert M., Ashok Sekhar, Jayashree Nagesh, et al. "Effects of maturation on the conformational free-energy landscape of SOD1." Proceedings of the National Academy of Sciences 115, no. 11 (2018): E2546—E2555. http://dx.doi.org/10.1073/pnas.1721022115.

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Amyotrophic lateral sclerosis (ALS) is a devastating fatal syndrome characterized by very rapid degeneration of motor neurons. A leading hypothesis is that ALS is caused by toxic protein misfolding and aggregation, as also occurs in many other neurodegenerative disorders, such as prion, Alzheimer’s, Parkinson’s, and Huntington’s diseases. A prominent cause of familial ALS is mutations in the protein superoxide dismutase (SOD1), which promote the formation of misfolded SOD1 conformers that are prone to aberrant interactions both with each other and with other cellular components. We have shown

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Beni, Sara M., Jeanna Tsenter, Alexander G. Alexandrovich та ін. "CuZn-SOD Deficiency, Rather than Overexpression, is Associated with Enhanced Recovery and Attenuated Activation of NF-κB After Brain Trauma in Mice". Journal of Cerebral Blood Flow & Metabolism 26, № 4 (2005): 478–90. http://dx.doi.org/10.1038/sj.jcbfm.9600209.

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Superoxide-dismutases (SOD) catalyze O2− conversion to hydrogen peroxide (H2O2) and with other antioxidant enzymes and low molecular weight antioxidants (LMWA) constitute endogenous defense mechanisms. We first assessed the effects of SOD1 levels on outcome after closed head injury (CHI) and later, based on these results, the effects of SOD−/- deficiency on cellular redox homeostasis. Superoxide-dismutase 1-deficient (SOD1−/-) and -overexpressing (transgenic (Tg)) mice and matched wild-type (WT) controls were subjected to CHI and outcome (neurobehavioral and memory functions) was assessed duri

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Muratet, François, Elisa Teyssou, Aude Chiot, et al. "Impact of a frequent nearsplice SOD1 variant in amyotrophic lateral sclerosis: optimising SOD1 genetic screening for gene therapy opportunities." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 9 (2021): 942–49. http://dx.doi.org/10.1136/jnnp-2020-325921.

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ObjectiveMutations in superoxide dismutase 1 gene (SOD1), encoding copper/zinc superoxide dismutase protein, are the second most frequent high penetrant genetic cause for amyotrophic lateral sclerosis (ALS) motor neuron disease in populations of European descent. More than 200 missense variants are reported along the SOD1 protein. To limit the production of these aberrant and deleterious SOD1 species, antisense oligonucleotide approaches have recently emerged and showed promising effects in clinical trials. To offer the possibility to any patient with SOD1-ALS to benefit of such a gene therapy

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Damiano, Simona, Concetta Sozio, Giuliana La Rosa, et al. "Metabolism Regulation and Redox State: Insight into the Role of Superoxide Dismutase 1." International Journal of Molecular Sciences 21, no. 18 (2020): 6606. http://dx.doi.org/10.3390/ijms21186606.

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Energy metabolism and redox state are strictly linked; energy metabolism is a source of reactive oxygen species (ROS) that, in turn, regulate the flux of metabolic pathways. Moreover, to assure redox homeostasis, metabolic pathways and antioxidant systems are often coordinately regulated. Several findings show that superoxide dismutase 1 (SOD1) enzyme has effects that go beyond its superoxide dismutase activity and that its functions are not limited to the intracellular compartment. Indeed, SOD1 is secreted through unconventional secretory pathways, carries out paracrine functions and circulat

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Agbas, Abdulbaki, Dongwei Hui, Xinsheng Wang, Vekalet Tek, Asma Zaidi, and Elias K. Michaelis. "Activation of brain calcineurin (Cn) by Cu-Zn superoxide dismutase (SOD1) depends on direct SOD1–Cn protein interactions occurring in vitro and in vivo." Biochemical Journal 405, no. 1 (2007): 51–59. http://dx.doi.org/10.1042/bj20061202.

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Cn (calcineurin) activity is stabilized by SOD1 (Cu-Zn superoxide dismutase), a phenomenon attributed to protection from superoxide (O2•−). The effects of O2•− on Cn are still controversial. We found that O2•−, generated either in vitro or in vivo did not affect Cn activity. Yet native bovine, recombinant human or rat, and two chimaeras of human SOD1–rat SOD1, all activated Cn, but SOD2 (Mn-superoxide dismutase) did not affect Cn activity. There was also a poor correlation between SOD1 dismutase activity and Cn activation. A chimaera of human N-terminal SOD1 and rat C-terminal SOD1 had little

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Pytte, Julia, Loren L. Flynn, Ryan S. Anderton, et al. "Disease-modifying effects of an SCAF4 structural variant in a predominantly SOD1 ALS cohort." Neurology Genetics 6, no. 4 (2020): e470. http://dx.doi.org/10.1212/nxg.0000000000000470.

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ObjectiveTo test the hypothesis that rs573116164 will have disease-modifying effects in patients with superoxide dismutase 1 (SOD1) familial amyotrophic lateral sclerosis (fALS), we characterized rs573116164 within a cohort of 190 patients with fALS and 560 healthy age-matched controls to assess the variant for association with various measures of disease.MethodsUsing a previously described bioinformatics evaluation algorithm, a polymorphic short structural variant associated with SOD1 was identified according to its theoretical effect on gene expression. An 12–18 poly-T repeat (rs573116164) w

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Peggion, Caterina, Valeria Scalcon, Maria Lina Massimino, et al. "SOD1 in ALS: Taking Stock in Pathogenic Mechanisms and the Role of Glial and Muscle Cells." Antioxidants 11, no. 4 (2022): 614. http://dx.doi.org/10.3390/antiox11040614.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the loss of motor neurons in the brain and spinal cord. While the exact causes of ALS are still unclear, the discovery that familial cases of ALS are related to mutations in the Cu/Zn superoxide dismutase (SOD1), a key antioxidant enzyme protecting cells from the deleterious effects of superoxide radicals, suggested that alterations in SOD1 functionality and/or aberrant SOD1 aggregation strongly contribute to ALS pathogenesis. A new scenario was opened in which, thanks to the generation of SOD1 related m

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Ma, Delin, Jeffrey M. Shuler, Aishwarya Kumar, et al. "Effects of Tongue Force Training on Bulbar Motor Function in the Female SOD1-G93A Rat Model of Amyotrophic Lateral Sclerosis." Neurorehabilitation and Neural Repair 31, no. 2 (2016): 147–56. http://dx.doi.org/10.1177/1545968316666956.

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Background. The use of exercise in amyotrophic lateral sclerosis (ALS) is controversial. Although moderate exercise appears to be beneficial for limb muscles in ALS, the effects of exercise on bulbar muscles such as the tongue have not been studied. Objective. To determine the effects of tongue force training on bulbar motor function in the SOD1-G93A rat model of ALS. Methods. We compared the effects of tongue force training on bulbar motor function and neuromuscular junction innervation in female SOD1-G93A rats and age-matched female wild-type controls. Half of each group underwent afternoon

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Sato, Atsushi, Yasunaga Shiraishi, Toyokazu Kimura, et al. "Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet." Antioxidants 11, no. 7 (2022): 1403. http://dx.doi.org/10.3390/antiox11071403.

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Metabolic syndrome (Mets) is an important condition because it may cause stroke and heart disease in the future. Reactive oxygen species (ROSs) influence the pathogenesis of Mets; however, the types of ROSs and their localization remain largely unknown. In this study, we investigated the effects of SOD1, which localize to the cytoplasm and mitochondrial intermembrane space and metabolize superoxide anion, on Mets using SOD1 deficient mice (SOD1−/−). SOD1−/− fed on a high-fat/high-sucrose diet (HFHSD) for 24 weeks showed reduced body weight gain and adipose tissue size compared to wild-type mic

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Du, Xiaoyu, Quanxiu Dong, Jie Zhu, Lingjie Li, Xiaolin Yu, and Ruitian Liu. "Rutin Ameliorates ALS Pathology by Reducing SOD1 Aggregation and Neuroinflammation in an SOD1-G93A Mouse Model." International Journal of Molecular Sciences 25, no. 19 (2024): 10392. http://dx.doi.org/10.3390/ijms251910392.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive loss of motor neurons, with limited effective treatments. Recently, the exploration of natural products has unveiled their potential in exerting neuroprotective effects, offering a promising avenue for ALS therapy. In this study, the therapeutic effects of rutin, a natural flavonoid glycoside with neuroprotective properties, were evaluated in a superoxide dismutase 1 (SOD1)-G93A mouse model of ALS. We showed that rutin reduced the level of SOD1 aggregation and diminished glial cell activation i

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Carlström, Mattias, Russell D. Brown, Johan Sällström, et al. "SOD1 deficiency causes salt sensitivity and aggravates hypertension in hydronephrosis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 1 (2009): R82—R92. http://dx.doi.org/10.1152/ajpregu.90843.2008.

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Hydronephrosis causes renal dysfunction and salt-sensitive hypertension, which is associated with nitric oxide deficiency and abnormal tubuloglomerular feedback (TGF) response. We investigated the role of oxidative stress for salt sensitivity and for hypertension in hydronephrosis. Hydronephrosis was induced in superoxide dismutase 1-transgenic (SOD1-tg), SOD1-deficient (SOD1-ko), and wild-type mice and in rats. In mice, telemetric measurements were performed during normal (0.7% NaCl) and high-sodium (4% NaCl) diets and with chronic tempol supplementation. The 8-iso-prostaglandin-F2α (F2-IsoPs

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Maier, Marcel, Tobias Welt, Fabian Wirth, et al. "A human-derived antibody targets misfolded SOD1 and ameliorates motor symptoms in mouse models of amyotrophic lateral sclerosis." Science Translational Medicine 10, no. 470 (2018): eaah3924. http://dx.doi.org/10.1126/scitranslmed.aah3924.

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Mutations in the gene encoding superoxide dismutase 1 (SOD1) lead to misfolding and aggregation of SOD1 and cause familial amyotrophic lateral sclerosis (FALS). However, the implications of wild-type SOD1 misfolding in sporadic forms of ALS (SALS) remain unclear. By screening human memory B cells from a large cohort of healthy elderly subjects, we generated a recombinant human monoclonal antibody (α-miSOD1) that selectively bound to misfolded SOD1, but not to physiological SOD1 dimers. On postmortem spinal cord sections from 121 patients with ALS, α-miSOD1 antibody identified misfolded SOD1 in

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Wang, Xiao-lu, Liang Wang, Fo-lan Lin, Si-si Li, Ting-xuan Lin, and Ren-wang Jiang. "Protective Effect of Penetratin Analogue-Tagged SOD1 on Cisplatin-Induced Nephrotoxicity through Inhibiting Oxidative Stress and JNK/p38 MAPK Signaling Pathway." Oxidative Medicine and Cellular Longevity 2021 (August 21, 2021): 1–13. http://dx.doi.org/10.1155/2021/5526053.

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Copper/zinc superoxide dismutase (SOD1) can clear cisplatin- (CP-) induced excessive reactive oxygen species (ROS), but exogenous SOD1 cannot enter cells because of its low biomembrane permeability. Cell-penetrating peptides (CPPs) can rapidly cross plasma membranes. This study is aimed at identifying an efficient and stable CPP-SOD1 and investigating its effects on CP-induced nephrotoxicity. We recombined SOD1 with 14 different CPPs and purified them using an NTA-Ni2+ column. In in vitro experiments, CPPs-SOD1 cell membrane penetration ability and JNK/p38 MAPK signaling pathway were evaluated

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Joyce, Peter I., Philip Mcgoldrick, Rachele A. Saccon, et al. "A novel SOD1-ALS mutation separates central and peripheral effects of mutant SOD1 toxicity." Human Molecular Genetics 24, no. 7 (2014): 1883–97. http://dx.doi.org/10.1093/hmg/ddu605.

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Dayal, Sanjana, Katina M. Wilson, Ryan Hutchins, and Steven R. Lentz. "Deficiency of Superoxide Dismutase Impairs Generation of Activated Protein C and Enhances Susceptibility to Experimental Thrombosis in Mice." Blood 118, no. 21 (2011): 535. http://dx.doi.org/10.1182/blood.v118.21.535.535.

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Abstract Abstract 535 In vitro studies have suggested that reactive oxygen species such as superoxide can produce several potentially prothrombotic effects, including enhanced platelet activation, increased tissue factor (TF) expression, and an oxidative modification in thrombomodulin that impairs its capacity to enhance the generation of activated protein C (APC) by thrombin. It is not known, however, if elevated levels of superoxide accelerate susceptibility to experimental thrombosis in vivo. Using a murine model that is genetically deficient in superoxide dismutase-1 (SOD1, an antioxidant

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Bradman, Matthew J. G., Richard Morris, Anne McArdle, Malcolm J. Jackson, and Thimmasettappa Thippeswamy. "The effects of L-NAME on neuronal NOS and SOD1 expression in the DRG–spinal cord network of axotomised Thy 1.2 eGFP mice." Neuron Glia Biology 7, no. 2-4 (2011): 129–41. http://dx.doi.org/10.1017/s1740925x12000051.

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Nitric oxide (NO) plays an important role in pathophysiology of the nervous system. Copper/zinc superoxide dismutase (SOD1) reacts with superoxide, which is also a substrate for NO, to provide antioxidative protection. NO production is greatly altered following nerve injury, therefore we hypothesised that SOD1 and NO may be involved in modulating axotomy responses in dorsal root ganglion (DRG)–spinal network. To investigate this interaction, adult Thy1.2 enhanced membrane-bound green fluorescent protein (eGFP) mice underwent sciatic nerve axotomy and received NG-nitro- <l-arginine methylest

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Renzini, Alessandra, Eva Pigna, Marco Rocchi, et al. "Sex and HDAC4 Differently Affect the Pathophysiology of Amyotrophic Lateral Sclerosis in SOD1-G93A Mice." International Journal of Molecular Sciences 24, no. 1 (2022): 98. http://dx.doi.org/10.3390/ijms24010098.

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Amyotrophic Lateral Sclerosis (ALS) is a devastating adult-onset neurodegenerative disease, with ineffective therapeutic options. ALS incidence and prevalence depend on the sex of the patient. Histone deacetylase 4 (HDAC4) expression in skeletal muscle directly correlates with the progression of ALS, pointing to the use of HDAC4 inhibitors for its treatment. Contrarily, we have found that deletion of HDAC4 in skeletal muscle worsened the pathological features of ALS, accelerating and exacerbating skeletal muscle loss and negatively affecting muscle innervations in male SOD1-G93A (SOD1) mice. I

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Zhu, Cheng, Matthew V. Beck, Jack D. Griffith, Mohanish Deshmukh, and Nikolay V. Dokholyan. "Large SOD1 aggregates, unlike trimeric SOD1, do not impact cell viability in a model of amyotrophic lateral sclerosis." Proceedings of the National Academy of Sciences 115, no. 18 (2018): 4661–65. http://dx.doi.org/10.1073/pnas.1800187115.

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Aberrant accumulation of misfolded Cu, Zn superoxide dismutase (SOD1) is a hallmark of SOD1-associated amyotrophic lateral sclerosis (ALS), an invariably fatal neurodegenerative disease. While recent discovery of nonnative trimeric SOD1-associated neurotoxicity has suggested a potential pathway for motor neuron impairment, it is yet unknown whether large, insoluble aggregates are cytotoxic. Here we designed SOD1 mutations that specifically stabilize either the fibrillar form or the trimeric state of SOD1. The designed mutants display elevated populations of fibrils or trimers correspondingly,

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Davidovic-Plavsic, Biljana, Natasa Lukic, Aleksandra Nikolic-Kokic, and Biljana Kukavica. "Effects of hemazin SC 500 (terbuthylazine) on antioxidative enzymes in human erythrocytes in vitro." Journal of the Serbian Chemical Society 84, no. 5 (2019): 455–65. http://dx.doi.org/10.2298/jsc181011115d.

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The aim of this work was to investigate the effect of the commercial formulation hemazin SC 500, an herbicide containing terbuthylazine as the active compound, on the isoenzyme patterns and activities of Cu-Zn superoxide dismutase (SOD1) and catalase (CAT), as well as on the glutathione S-transferase (GST) activity, in human erythrocytes in vitro. The human erythrocytes were treated with hemazin SC 500 over a broad range of terbuthylazine concentrations (37 nmol L-1? ?37 ?mol L-1) for 1 and 3 h at a temperature of 37?C. Native electrophoresis of the control and treated samples revealed two SOD

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Bian, Xinyu, Xiaoyu Zhuang, Junpeng Xing, Shu Liu, Zhiqiang Liu, and Fengrui Song. "Native Mass Spectrometry Coupled to Spectroscopic Methods to Investigate the Effect of Soybean Isoflavones on Structural Stability and Aggregation of Zinc Deficient and Metal-Free Superoxide Dismutase." Molecules 27, no. 21 (2022): 7303. http://dx.doi.org/10.3390/molecules27217303.

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The deficiency or wrong combination of metal ions in Cu, Zn-superoxide dismutase (SOD1), is regarded as one of the main factors causing the aggregation of SOD1 and then inducing amyotrophic lateral sclerosis (ALS). A ligands-targets screening process based on native electrospray ionization ion mobility mass spectrometry (ESI-IMS-MS) was established in this study. Four glycosides including daidzin, sophoricoside, glycitin, and genistin were screened out from seven soybean isoflavone compounds and were found to interact with zinc-deficient or metal-free SOD1. The structure and conformation stabi

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Dash, Banaja P., Axel Freischmidt, Jochen H. Weishaupt, and Andreas Hermann. "Downstream Effects of Mutations in SOD1 and TARDBP Converge on Gene Expression Impairment in Patient-Derived Motor Neurons." International Journal of Molecular Sciences 23, no. 17 (2022): 9652. http://dx.doi.org/10.3390/ijms23179652.

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Amyotrophic Lateral Sclerosis (ALS) is a progressive and fatal neurodegenerative disease marked by death of motor neurons (MNs) present in the spinal cord, brain stem and motor cortex. Despite extensive research, the reason for neurodegeneration is still not understood. To generate novel hypotheses of putative underlying molecular mechanisms, we used human induced pluripotent stem cell (hiPSCs)-derived motor neurons (MNs) from SOD1- and TARDBP (TDP-43 protein)-mutant-ALS patients and healthy controls to perform high-throughput RNA-sequencing (RNA-Seq). An integrated bioinformatics approach was

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Ting, Hsiao-Chien, Hui-I. Yang, Horng-Jyh Harn та ін. "Coactivation of GSK3β and IGF-1 Attenuates Amyotrophic Lateral Sclerosis Nerve Fiber Cytopathies in SOD1 Mutant Patient-Derived Motor Neurons". Cells 10, № 10 (2021): 2773. http://dx.doi.org/10.3390/cells10102773.

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Amyotrophic lateral sclerosis (ALS) is a progressive nervous system disease that causes motor neuron (MN) degeneration and results in patient death within a few years. To recapitulate the cytopathies of ALS patients’ MNs, SOD1G85R mutant and corrected SOD1G85G isogenic-induced pluripotent stem cell (iPSC) lines were established. Two SOD1 mutant ALS (SOD1G85R and SOD1D90A), two SOD1 mutant corrected (SOD1G85G and SOD1D90D), and one sporadic ALS iPSC lines were directed toward MNs. After receiving ~90% purity for MNs, we first demonstrated that SOD1G85R mutant ALS MNs recapitulated ALS-specific

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Zhao, Zhu-fen, Ye Zhang, Yang Sun, Chun-hai Zhang, and Ming-wei Liu. "Protective effects of baicalin on caerulein-induced AR42J pancreatic acinar cells by attenuating oxidative stress through miR-136-5p downregulation." Science Progress 104, no. 2 (2021): 003685042110261. http://dx.doi.org/10.1177/00368504211026118.

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Baicalin, the main active component of Scutellaria baicalensis, has antioxidant and anti-apoptotic effects and is used to treat acute pancreatitis; however, its specific mechanism is unclear. This study aims to determine the protective effect and underlying mechanism of baicalin on AR42J pancreatic acinar cell injury. AR42J acinar cells (caerulein, 10 nmol/L) were induced in vitro to establish a cell model for acute pancreatitis. Cell relative survival was measured by thiazolyl blue tetrazolium bromide, and cell apoptosis and death were examined by flow cytometry. The expression levels of supe

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Broom, Helen R., Jessica A. O. Rumfeldt, and Elizabeth M. Meiering. "Many roads lead to Rome? Multiple modes of Cu,Zn superoxide dismutase destabilization, misfolding and aggregation in amyotrophic lateral sclerosis." Essays in Biochemistry 56 (August 18, 2014): 149–65. http://dx.doi.org/10.1042/bse0560149.

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ALS (amyotrophic lateral sclerosis) is a fatal neurodegenerative syndrome characterized by progressive paralysis and motor neuron death. Although the pathological mechanisms that cause ALS remain unclear, accumulating evidence supports that ALS is a protein misfolding disorder. Mutations in Cu,Zn-SOD1 (copper/zinc superoxide dismutase 1) are a common cause of familial ALS. They have complex effects on different forms of SOD1, but generally destabilize the protein and enhance various modes of misfolding and aggregation. In addition, there is some evidence that destabilized covalently modified w

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Shteinfer-Kuzmine, Anna, Shirel Argueti-Ostrovsky, Marcel F. Leyton-Jaimes, et al. "Targeting the Mitochondrial Protein VDAC1 as a Potential Therapeutic Strategy in ALS." International Journal of Molecular Sciences 23, no. 17 (2022): 9946. http://dx.doi.org/10.3390/ijms23179946.

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Impaired mitochondrial function has been proposed as a causative factor in neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), caused by motor neuron degeneration. Mutations in superoxide dismutase (SOD1) cause ALS and SOD1 mutants were shown to interact with the voltage-dependent anion channel 1 (VDAC1), affecting its normal function. VDAC1 is a multi-functional channel located at the outer mitochondrial membrane that serves as a mitochondrial gatekeeper controlling metabolic and energetic crosstalk between mitochondria and the rest of the cell and it is a key player in

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Apolloni, Savina, Francesca Caputi, Annabella Pignataro, et al. "Histamine Is an Inducer of the Heat Shock Response in SOD1-G93A Models of ALS." International Journal of Molecular Sciences 20, no. 15 (2019): 3793. http://dx.doi.org/10.3390/ijms20153793.

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(1) Background: Amyotrophic lateral sclerosis (ALS) is a multifactorial non-cell autonomous disease where activation of microglia and astrocytes largely contributes to motor neurons death. Heat shock proteins have been demonstrated to promote neuronal survival and exert a strong anti-inflammatory action in glia. Having previously shown that the pharmacological increase of the histamine content in the central nervous system (CNS) of SOD1-G93A mice decreases neuroinflammation, reduces motor neuron death, and increases mice life span, here we examined whether this effect could be mediated by an e

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Sakowski, Stacey A., J. Lunn, Angela S. Busta, et al. "Neuromuscular effects of G93A-SOD1 expression in zebrafish." Molecular Neurodegeneration 7, no. 1 (2012): 44. http://dx.doi.org/10.1186/1750-1326-7-44.

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Deng, Binbin, Wenjing Lv, Weisong Duan, et al. "Progressive Degeneration and Inhibition of Peripheral Nerve Regeneration in the SOD1-G93A Mouse Model of Amyotrophic Lateral Sclerosis." Cellular Physiology and Biochemistry 46, no. 6 (2018): 2358–72. http://dx.doi.org/10.1159/000489627.

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Background: Myelination, degeneration and regeneration are implicated in crucial responses to injury in the peripheral nervous system. Considering the progression of amyotrophic lateral sclerosis (ALS), we used the superoxide dismutase 1 (SOD1)-G93A transgenic mouse model of ALS to investigate the effects of mutant SOD1 on the peripheral nerves. Methods: Changes in peripheral nerve morphology were analyzed in SOD1 mutant mice at various stages of the disease by toluidine blue staining and electron microscopy (EM). Schwann cell proliferation and recruitment of inflammatory factors were detected

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Alkhaddur, A., and E. V. Mashkina. "EFFECT OF PHITOCHEMICAL EXTRACTS ON EXPRESSION OF GENES NFE2L2, JUN, SOD1 IN HUMAN CELLS." Aerospace and Environmental Medicine 56, no. 3 (2022): 40–46. http://dx.doi.org/10.21687/0233-528x-2022-56-3-40-46.

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Investigations of the effects of phitochemical compounds from extracts of pomegranate, grape seeds and garlic on expression of NFE2L2, JUN, SOD1 in cultivated cells of the human blood showed that transcription of SOD1 increased in the presence of pomegranate and grape seed extracts. Level of mRNA in NFE2L2 and JUN rose briskly only under the influence of a high concentration of the grape seed extract. Level of JUN mRNA correlated with NFE2L2 mRNA. Garlic extract had no effect on transcription of NFE2L2, JUN, SOD1. Activation of the transcription of all 3 genes under study by the grape seeds ex

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Dehdashti, Maryam, Zahra Abbasy, Hamid Zaferani Arani, et al. "Cytotoxic and Apoptotic Effects of Vanadyl Sulfate on MCF-7 Breast Cancer Cell Line." Galen Medical Journal 12 (June 21, 2023): e3050. http://dx.doi.org/10.31661/gmj.v12i.3050.

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 Background: Breast cancer (BC) is the major cause of death from cancer among women. Some studies have indicated the cytotoxic effects of vanadyl oxide sulfate (VOSO4). This study aimed to evaluate the anti-cancer effect of VOSO4 in the treatment of MCF-7 cell line. Materials and Method: The MCF-7 cell line was treated with different concentrations of VOSO4 for 24 and 48 hours. The measurement of cell death was performed by MTT assay. The cell apoptosis rate was measured using Annexin V/Propidium Iodide assay through flow cytometry. Also, the expression levels of p53, P21, Caspase8

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Noblanc, Anaīs, Alicia Klaassen, and Bernard Robaire. "The Exacerbation of Aging and Oxidative Stress in the Epididymis of Sod1 Null Mice." Antioxidants 9, no. 2 (2020): 151. http://dx.doi.org/10.3390/antiox9020151.

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There is growing evidence that the quality of spermatozoa decreases with age and that children of older fathers have a higher incidence of birth defects and genetic mutations. The free radical theory of aging proposes that changes with aging are due to the accumulation of damage induced by exposure to excess reactive oxygen species. We showed previously that absence of the superoxide dismutase 1 (Sod1) antioxidant gene results in impaired mechanisms of repairing DNA damage in the testis in young Sod1−/− mice. In this study, we examined the effects of aging and the Sod−/− mutation on mice epidi

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Giannakou, Maria, Ifigeneia Akrani, Angeliki Tsoka, et al. "Discovery of Novel Inhibitors against ALS-Related SOD1(A4V) Aggregation through the Screening of a Chemical Library Using Differential Scanning Fluorimetry (DSF)." Pharmaceuticals 17, no. 10 (2024): 1286. http://dx.doi.org/10.3390/ph17101286.

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Background: Cu/Zn Superoxide Dismutase 1 (SOD1) is a 32 kDa cytosolic dimeric metalloenzyme that neutralizes superoxide anions into oxygen and hydrogen peroxide. Mutations in SOD1 are associated with ALS, a disease causing motor neuron atrophy and subsequent mortality. These mutations exert their harmful effects through a gain of function mechanism, rather than a loss of function. Despite extensive research, the mechanism causing selective motor neuron death still remains unclear. A defining feature of ALS pathogenesis is protein misfolding and aggregation, evidenced by ubiquitinated protein i

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Vallarola, Antonio, Francesca Sironi, Massimo Tortarolo, et al. "RNS60 exerts therapeutic effects in the SOD1 ALS mouse model through protective glia and peripheral nerve rescue." Journal of Neuroinflammation 15, no. 1 (2018): 65. https://doi.org/10.1186/s12974-018-1101-0.

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<strong>Background: </strong>Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects the motor neuromuscular system leading to complete paralysis and premature death. The multifactorial nature of ALS that involves both cell-autonomous and non-cell-autonomous processes contributes to the lack of effective therapies, usually targeted to a single pathogenic mechanism. RNS60, an experimental drug containing oxygenated nanobubbles generated by modified Taylor-Couette-Poiseuille flow with elevated oxygen pressure, has shown anti-inflammatory and neuroprotective pr

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Bouldin, Samantha D., Maxwell A. Darch, P. John Hart, and Caryn E. Outten. "Redox properties of the disulfide bond of human Cu,Zn superoxide dismutase and the effects of human glutaredoxin 1." Biochemical Journal 446, no. 1 (2012): 59–67. http://dx.doi.org/10.1042/bj20120075.

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The intramolecular disulfide bond in hSOD1 [human SOD1 (Cu,Zn superoxide dismutase 1)] plays a key role in maintaining the protein's stability and quaternary structure. In mutant forms of SOD1 that cause familial ALS (amyotrophic lateral sclerosis), this disulfide bond is more susceptible to chemical reduction, which may lead to destabilization of the dimer and aggregation. During hSOD1 maturation, disulfide formation is catalysed by CCS1 (copper chaperone for SOD1). Previous studies in yeast demonstrate that the yeast GSH/Grx (glutaredoxin) redox system promotes reduction of the hSOD1 disulfi

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Kimura, Shintaro, Yuji O. Kamatari, Yukina Kuwahara, et al. "Canine SOD1 harboring E40K or T18S mutations promotes protein aggregation without reducing the global structural stability." PeerJ 8 (July 15, 2020): e9512. http://dx.doi.org/10.7717/peerj.9512.

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Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disease associated with aggregation of superoxide dismutase 1 (SOD1) protein. More than 160 mutations in human SOD1 have been identified in familial ALS and extensively characterized in previous studies. Here, we investigated the effects of T18S and E40K mutations on protein aggregation of canine SOD1. These two mutations are exclusively found in canine degenerative myelopathy (an ALS-like neurodegenerative disease in dogs), whose phenotype is unknown at the level of protein folding. Interestingly, the T18S and E4

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Lobsiger, Christian S., Séverine Boillée, and Don W. Cleveland. "Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons." Proceedings of the National Academy of Sciences 104, no. 18 (2007): 7319–26. http://dx.doi.org/10.1073/pnas.0702230104.

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Global, age-dependent changes in gene expression from rodent models of inherited ALS caused by dominant mutations in superoxide-dismutase 1 (SOD1) were identified by using gene arrays and RNAs isolated from purified embryonic and adult motor neurons. Comparison of embryonic motor neurons expressing a dismutase active ALS-linked mutant SOD1 with those expressing comparable levels of wild-type SOD1 revealed the absence of mutant-induced mRNA changes. An age-dependent mRNA change that developed presymptomatically in adult motor neurons collected by laser microdissection from mice expressing dismu

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Mouli, Karthik, Anton V. Liopo, Larry J. Suva, et al. "SOD1 Is an Integral Yet Insufficient Oxidizer of Hydrogen Sulfide in Trisomy 21 B Lymphocytes and Can Be Augmented by a Pleiotropic Carbon Nanozyme." Antioxidants 13, no. 11 (2024): 1361. http://dx.doi.org/10.3390/antiox13111361.

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Down syndrome (DS) is a multisystemic disorder that includes accelerated aging caused by trisomy 21. In particular, overexpression of cystathionine-β-synthase (CBS) is linked to excess intracellular hydrogen sulfide (H2S), a mitochondrial toxin at higher concentrations, which impairs cellular viability. Concurrent overexpression of superoxide dismutase 1 (SOD1) may increase oxidative stress by generating excess hydrogen peroxide (H2O2) while also mitigating the toxic H2S burden via a non-canonical sulfide-oxidizing mechanism. We investigated the phenotypic variability in basal H2S levels in re

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Somalinga, Balajee R., Gregory A. Miller, Hiba T. Malik, W. Christian Wigley, and Philip J. Thomas. "A Screen to Identify Cellular Modulators of Soluble Levels of an Amyotrophic Lateral Sclerosis (ALS)–Causing Mutant SOD1." Journal of Biomolecular Screening 16, no. 9 (2011): 974–85. http://dx.doi.org/10.1177/1087057111418505.

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The molecular pathology of many protein misfolding, toxic gain-of-function diseases, such as amyotrophic lateral sclerosis (ALS), is not well understood. Although protein misfolding and aggregation are common themes in these diseases, efforts to identify cellular factors that regulate this process in an unbiased fashion and on a global scale have been lacking. Using an adapted version of an extant β-gal-based protein solubility assay, an expression screen for cellular modulators of solubility of an ALS-causing mutant SOD1 was carried out in mammalian cells. Following fluorescence-activated cel

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