Protective effect of N-acetylcysteine in isoniazid induced hepatic injury in growing rats

Abstract

<span style="font-size: 13.5pt;mso-bidi-font-size:8.5pt;font-family:" times="" new="" roman","serif""="">Status of oxidative/antioxidativc profile was the mechanistic approach to inumerate the nature of protection by Nacetylcysteine (NAC) in isoniazid (INH) exposed experimental animals. Analysis of lipid peroxidation, thiol levels, cytochrome P_{<span style="mso-bidi-font-size:6.0pt;font-family:" times="" new="" roman","serif""="">450</span>}<span style="mso-bidi-font-size:6.0pt;font-family:" times="" new="" roman","serif""="">, <span style="font-size:13.5pt;mso-bidi-font-size:8.5pt;font-family:" times="" new="" roman","serif""="">superoxide dismutase (SOD), catalase, glutathione peroxidase, reductase and transferase were estimated in liver along with the body and liver weight of animals and histological observations. Isoniazid exposure to animals resulted in no change in body and liver weights. Thiols, lipid peroxidation, catalase, SOD glutathione peroxidase, reductase, transferase and cytochrome P₄₅₀<span style="mso-bidi-font-size:6.0pt;font-family:" times="" new="" roman","serif""=""> <span style="font-size:13.5pt;mso-bidi-font-size:8.5pt;font-family:" times="" new="" roman","serif""="">levels were altered with INH exposure. Supplementation of NAC with INH protected the animals against hepatotoxic reactions by minimizing the free radical induced tissue injury and overall maintenance of the endogenous scavengers of free radicals.

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