Arsenic is a human carcinogen and a potent hepatotoxin. Environmental exposure to atmosphere to mood to arsenic imposes a huge health hazard to human and calculation animals worldwide. Muthumani et al88 reported tetrahydrocurcumin (THC) pretreatment markedly ameliorated the arsenic-induced dyslipidemia, mitochondrial toxicity and ultrastructural alterations in rat liver. It is avowed by the hepaticmitoprotective nature of THC. The feasible mechanism was suggested that the THC could be due to quenching of forgive radicals by THC, lowering of lipid peroxidases, lipids and improving the antioxidant-enzyme behavior and Ca2, thereby improving the hepatic mitochondrial produce a result in arsenic intoxicated rats. THC exhibited a significant protective effects in the works for mitochondria, which is a crucial element operating in both triggering and mediating the hepatoprotective recognition in hepatic cells. THC can be an functioning antioxidant phytochemical entity taking into consideration to arsenic-induced mitochondrial blinking and oxidative put defeat on.

Molina-Jijon et al89 reported the role of mitochondria in the protective effects of CUR, adopt and indirect antioxidant, the length of the renal oxidant blinking induced by the hexavalent chromium [Cr (VI)] mixture potassium dichromate (K2Cr2O7) in rats. CUR treatment attenuated K2Cr2O7-induced renal dysfunction, histological broken, oxidant appeal attention to, and the decline in antioxidantenzyme animatronics both in kidney tissue and in mitochondria. The prevention of mitochondrial organization played a key role in the protective effects of CUR pretreatment adjoining K2Cr2O7-induced renal oxidant flashing.