ArticleFree radical biology & medicine2021
The antioxidant role of STAT3 in methylmercury-induced toxicity in mouse hypothalamic neuronal GT1-7 cell line.
Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Nrf2 and STAT3 Pathways in Protecting Against Methylmercury-Induced Oxidative Stress in Hypothalamic Neuronal GT1-7 Cells.Neurochemical research · 2026Article
- Psoralen and Isopsoralen fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Roles of Oxidative Phosphorylation and Fatty Acid Oxidation in Neuroinflammation Induced by Lipopolysaccharide in Hypothalamic Neuronal Cells.International journal of inflammation · 2026Article
- JAK2/STAT3 Signaling Pathway Modulates Acute Methylmercury Toxicity in the Mouse Astrocyte C8-D1A Cell Line.Neurochemical research · 2025Article
- Isolation and Antioxidant Mechanism of Polyphenols fromAntioxidants (Basel, Switzerland) · 2024Article
- Cell fiber-based 3D tissue array for drug response assay.Scientific reports · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
Abstract
Oxidative stress, impairment of antioxidant defenses, and disruption of calcium homeostasis are associated with the toxicity of methylmercury (MeHg). Yet, the relative contribution and interdependence of these effects and other molecular mechanisms that mediate MeHg-induced neurotoxicity remain uncertain. The signal transducer and activator of transcription 3 (STAT3) is a transcription factor that regulates the expression of anti-apoptotic and cell cycle progression genes. In addition to its role in cell growth and survival, STAT3 regulates redox homeostasis and prevents oxidative stress by the modulation of nuclear genes that encode for electron transport complexes (ETC) and antioxidant enzymes. Here we tested the hypothesis that STAT3 contributes to the orchestration of the antioxidant defense response against MeHg injury. We show that MeHg (>1 μM) exposure induced STAT3 activation within 1 h and beyond in mouse hypothalamic neuronal GT1-7 cells in a concentration-and time-dependent manner. Pharmacological inhibition of STAT3 phosphorylation exacerbated MeHg-induced reactive oxygen species (ROS) production and antioxidant responses. Finally, treatment with the antioxidant Trolox demonstrated that MeHg-induced STAT3 activation is mediated, at least in part, by MeHg-induced ROS generation. Combined, our results demonstrated a role for the STAT3 signaling pathway as an early response to MeHg-induced oxidative stress.
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