ArticleToxicological sciences : an official journal of the Society of Toxicology2017
Editor's Highlight: Glutathione S-Transferase Activity Moderates Methylmercury Toxicity During Development in Drosophila.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Transcriptomic analysis identifies muscle-specific mitochondrial and vesicular transport genes as methylmercury toxicity targets in a Drosophila model of congenital Minamata disease.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Acute exposure to mercury drives changes in gene expression in Drosophila melanogaster.BMC research notes · 2024Article
- KEAP1 polymorphisms and neurodevelopmental outcomes in children with exposure to prenatal MeHg from the Seychelles Child Development Study Nutrition Cohort 2.Neurotoxicology · 2023Article
- Evolution of chemosensory and detoxification gene families across herbivorous Drosophilidae.G3 (Bethesda, Md.) · 2023Article
- Perspectives on the Drosophila melanogaster Model for Advances in Toxicological Science.Current protocols · 2023Review
- Evolution of chemosensory and detoxification gene families across herbivorous Drosophilidae.bioRxiv : the preprint server for biology · 2023Article
- Targeted Intracellular Demethylation of Methylmercury Enhances Elimination Kinetics and Reduces Developmental Toxicity in Transgenic Drosophila.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- The Role of Human LRRK2 in Acute Methylmercury Toxicity in Caenorhabditis elegans.Neurochemical research · 2021Article
- Tissue-specific Nrf2 signaling protects against methylmercury toxicity in Drosophila neuromuscular development.Archives of toxicology · 2020Article
- Article
- Chronic exposure to methylmercury induces puncta formation in cephalic dopaminergic neurons in Caenorhabditis elegans.Neurotoxicology · 2020Article
- High level of methylmercury exposure causes persisted toxicity in Nauphoeta cinerea.Environmental science and pollution research international · 2020Article
- Simultaneous exposure to vinylcyclohexene and methylmercury in Drosophila melanogaster: biochemical and molecular analyses.BMC pharmacology & toxicology · 2019Article
- Glutathione antioxidant system and methylmercury-induced neurotoxicity: An intriguing interplay.Biochimica et biophysica acta. General subjects · 2019Review
- Drosophotoxicology: Elucidating Kinetic and Dynamic Pathways of Methylmercury Toxicity in a Drosophila Model.Frontiers in genetics · 2019Article
- Maternal polymorphisms in glutathione-related genes are associated with maternal mercury concentrations and early child neurodevelopment in a population with a fish-rich diet.Environment international · 2018Article
- Zinc Detoxification: A Functional Genomics and Transcriptomics Analysis inG3 (Bethesda, Md.) · 2018Article
- Editor's Highlight: Variation in Methylmercury Metabolism and Elimination Status in Humans Following Fish Consumption.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Glutathione (GSH) pathways play a central role in methylmercury (MeHg) metabolism and elimination, largely due to formation of a more readily transported MeHg-GSH conjugate. Glutathione S-transferases (GSTs) have therefore been proposed to facilitate MeHg elimination by catalyzing MeHg-GSH conjugation. A role for human GSTP1 in MeHg disposition is suggested by the association of two common polymorphisms in the coding region (Ile105Val and Ala114Val) with Hg levels in either blood or hair. In this study, we investigated a functional role for GSTs in modulating MeHg toxicity during development. Using the Drosophila model to execute targeted manipulations of both endogenous GSTs and introduced human GSTP1 variants we correlate gene and protein expression levels with GST activity and also with MeHg body burden and developmental outcomes. RNAi knockdown of endogenous GSTD1, GSTE1, or GSTS1, individually, increased susceptibility to MeHg during pupal development resulting in a reduced rate of adult eclosion. Exogenous expression of human GSTP1 in developing flies resulted in increased MeHg tolerance relative to control flies as seen with elevated eclosion rates when reared on MeHg containing food. Furthermore, the GSTP1105 and GSTP1114 variants showed a reduced enzyme activity relative to wild-type GSTP1 (GSTP1wt). Finally, we observed a trend whereby Hg body burden was inversely related to the levels of GST activity. However, in some instances GSTP1 expression resulted in increased eclosion rates without reducing Hg body burden suggesting that GSTs interact with MeHg via both toxicokinetic and toxicodynamic mechanisms. These findings indicate that GSTs moderate MeHg toxicity during development in our experimental model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.