ArticleMolecular and cellular biochemistry2003
Oxygen radical generation and endosulfan toxicity in Jurkat T-cells.
Article in Molecular and cellular biochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 25 citations in OpenAlex.
- Mechanistic Interplay Between Autophagy and Apoptotic Signaling in Endosulfan-Induced Dopaminergic Neurotoxicity: Relevance to the Adverse Outcome Pathway in Pesticide Neurotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Organochlorine Pesticide-Mediated Induction of NADPH Oxidase and Nitric-Oxide Synthase in Endothelial Cell.Journal of clinical and diagnostic research : JCDR · 2017Article
- Endosulfan upregulates AP-1 binding and ARE-mediated transcription via ERK1/2 and p38 activation in HepG2 cells.Toxicology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism by which endosulfan exposure causes cellular dysfunction in experimental animals and humans is not clear. In the present study, we provide experimental evidence in support of the role of oxidative stress in endosulfan toxicity. Using both cell free system and Jurkat cells as in vitro models, we demonstrate that endosulfan can generate oxygen radicals that is inhibitable by superoxide dismutase (SOD) and glutathione (GSH). In the cell culture model, oxygen radical generation in response to endosulfan was dose- (0-100 microM) and time-dependent (0-12 h). Two-color flowcytometric analysis showed that endosulfan mediated changes in delta psi(m) and generation of superoxide radicals do occur simultaneously in the affected cell population. It was hypothesized that endosulfan exerts a severe oxidative stress in Jurkat cells and this could be prevented or minimized by an antioxidant. To test this hypothesis, GSH was added exogenously and endosulfan toxicity was evaluated by alamarblue assay. In conclusion, our results demonstrate a role for reactive oxygen species (ROS) in endosulfan toxicity and that supplementation of antioxidants such as GSH may be useful in individuals who are at risk to endosulfan toxicity.
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