N-Acetylcysteine Mediated Regulation of MnSOD, UCP-2 and Cytochrome C Associated with Amelioration of Monocrotophos-Induced Hepatotoxicity in Rats

Pesticides are now a risk to the environment and public health. Monocrotophos (MCP) is known to cause organ toxicity and impart degenerative effects at cellular levels. N-acetylcysteine (NAC) is a natural antioxidant having various prophylactic properties. Male Wistar rats were given NAC (200 mg/kg b.wt), MCP (0.9 mg/kg b.wt) and NAC followed by MCP; intragastrically for 28 consecutive days. Regulation of MnSOD, UCP-2 and cytochrome c was analyzed by western blotting and polymerase chain reaction. Histology, electron microscopy and weight parameters were evaluated in the liver. MCP exposure significantly decreased body weight gain, relative liver weight, and structural changes. Altered MnSOD protein expression, decreased transcription of UCP-2 and MnSOD, and released cytochrome c indicated that oxidative stress is involved in MCP exposure. Treatment of NAC to MCP-exposed rats normalized the weight and structural changes, restored MnSOD and UCP-2 levels and prevented the release of cytochrome c. The present study suggests that the regulation of UCP-2, MnSOD and cytochrome c is involved in NAC efficacy against MCP toxicity. These findings illustrate that NAC can serve as a potential therapeutic agent for toxicity and oxidative stress in mammals.