Abstract
Monocrotophos (MCP) is an organophosphate pesticide with well known toxicity in mammals. Exposure of MCP is associated with altered molecular physiology at sub-cellular levels. The present study investigated the efficacy of N-acetylcysteine (NAC) against MCP exposure mediated mitochondrial dysfunctions in hepatic tissue of rats. Exposure of MCP (0.9 mg/kg b.wt, intragastrically, 28 days) decreased mitochondrial complexes activities and gene expression of complexes subunits. The expression of PGC-1α, NRF-1, NRF-2 and Tfam was also reduced significantly. The administration of NAC (200 mg/kg b.wt, intragastrically, 28 days) significantly increased mitochondrial complexes activities and gene expression of complexes subunits. Additionally, NAC also maintained mitochondrial functions, enhanced the gene expression of PGC-1α and its downstream regulators. The results of the present study indicate that NAC prevents hepatic mitochondrial dysfunctions and maintains PGC-1α signalling. In conclusion, NAC might be speculated as a therapeutic agent for mitochondrial dysfunctions following toxic exposures.
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