Arsenic-Induced, Mitochondria-Mediated Apoptosis Is Associated with Decreased Peroxisome Proliferator-Activated Receptor γ Coactivator α in Rat Brains

Chronic exposure to arsenic in drinking water damages cognitive function, and nerve cell apoptosis is one of the primary characteristics. The damage mitochondrial structure and/or function main characteristics apoptosis. Peroxisome proliferator-activated receptor γ coactivator α (PGC-1α) involved regulation biogenesis, energy metabolism, In this study, we aimed study role PGC-1α sodium arsenite (NaAsO2)-induced rat hippocampal cells. We discovered that increased arsenic-induced hippocampus with NaAsO2 (0, 2, 10, 50 mg/L, orally via for 12 weeks) by TUNEL assay, mitochondria was incomplete swollen had lysosomes, lipofuscins, nuclear membrane shrinkage observed transmission electron microscopy. Furthermore, reduced levels Bcl-2 Bax cytochrome C expression. Moreover, correlation analysis showed brain content negatively correlated ATP content; were rate; positively levels, but no significant between has been study. Taken together, results indicate NaAsO2-induced pathway related reduction PGC-1α, accompanied depletion.