Liver fibrosis is the result of imbalance between extracellular matrix (ECM) synthesis and breakdown. Ethanol-induced increase in redox state is a sign of major change in hepatic metabolism and this inhibits tricarboxylic acid cycle activity and, fatty acid oxidation and increases fatty acid uptake, thus predisposing fatty liver. Fibrotic changes induced by alcohol are provoked by diets rich in PUFA. Heating of oils rich in PUFA produces toxic volatile and nonvolatile compounds, which aggravate liver damage. Hepatotoxicity was induced in male Wistar rats by administering alcohol (20%) and thermally oxidized sunflower oil (Delta PUFA) (15%). When N-acetyl cyteine (NAC) (150 mg/kg body weight), an ROS scavenger, was administered, there was a reversal of liver damage, which was demonstrated biochemically. Matrix metalloproteinases (MMPs), being potential biochemical indicators of fibroproliferation, were estimated in the present study, which were found to be altered in alcohol, Delta PUFA, and alcohol + Delta PUFA. The altered activities of MMPs in these groups were effectively modulated by treatment with NAC. Thus, in this study, NAC was found to modulate the effect of alcohol and Delta PUFA-induced liver damage.