ArticleMolecular medicine reports2025
MitoQ alleviates malathion‑induced hepatorenal toxicity via oxidative stress and inflammation modulation.
Article in Molecular medicine reports, 2025. 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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Who cites it
3 citing papers in PubMed.
- Pesticides Drive Liver Diseases Through Non-Apoptotic Regulated Cell Death Pathways.Diseases (Basel, Switzerland) · 2026Review
- Safety Assessment ofJournal of toxicology · 2026Article
- Mitochondrial dynamics in skin health and disease: energy, aging, and therapeutic perspectives.Burns & trauma · 2026Review
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Abstract
Malathion, a commonly used organophosphate pesticide, induces severe hepatorenal toxicity, mitochondrial dysfunction and inflammatory responses primarily through oxidative stress and apoptosis. The present study investigated the protective effects of mitoquinol (MitoQ), a mitochondria‑targeted antioxidant, against malathion‑induced toxicity in male Wistar albino rats. A total of 50 rats were divided into the following five groups: i) Control; ii) malathion‑only; iii) malathion + MitoQ; iv) MitoQ‑only; and v) vehicle. Malathion exposure significantly elevated the levels of aspartate aminotransferase, alkaline phosphatase, creatinine, urea and uric acid and decreased total protein, albumin and globulin levels. At the mitochondrial level, malathion reduced antioxidant enzyme activity (superoxide dismutase, glutathione peroxidase and glutathione) and ATP production while increasing reactive oxygen species, leading to oxidative damage. Furthermore, malathion induced upregulation of pro‑apoptotic markers such as Bax, and downregulation of the anti‑apoptotic marker, Bcl‑2. In addition, malathion increased TNF‑α, NF‑κB, Toll‑like receptor (TLR) 2 and TLR4 expression, and malathion toxicity induced severe hepatorenal damage, including vascular congestion, inflammatory infiltration and tubular degeneration. MitoQ co‑administration revealed a trend towards mitigating altered hepatorenal markers, inflammatory markers and regulated apoptotic/antiapoptotic gene markers, with partial restoration in mitochondrial function and histopathological changes. In parallel, MitoQ normalized cellular changes induced by malathion in the liver and kidneys. In conclusion, malathion toxicity in the liver and kidneys is mediated by mitochondrial oxidative stress, apoptosis and inflammation. MitoQ exerts protective effects by restoring mitochondrial homeostasis, reducing inflammatory signaling and mitigating tissue damage. Future research should explore longer treatment durations and potential synergistic effects with other antioxidants to optimize protection against pesticide‑induced toxicity.
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