Acetaminophen-induced liver injury and oxidative stress: protective effect of propofol

Abstract

We evaluated the effects of propofol on oxidative stress and acute liver injury and regeneration produced by acetaminophen administration in rats. Acetaminophen (3.5 g kg(-1)) was administered by gastric tube to 50 adult male Wistar rats. One minute before acetaminophen, propofol was administered intraperitoneally (60 mg kg(-1)) to 25 rats and diethyl ether to the other 25 animals. All rats were sacrificed. Markers of oxidative stress (malondialdehyde levels, cholesterol/high-density lipoprotein cholesterol fraction and glutathione-S-transferase-pi activity), liver injury (aspartate aminotransferase alanine aminotransferase and alkaline phosphatase and histological signs of inflammation and in-situ apoptosis) and liver regeneration (rate of [3H]thymidine incorporation into hepatic DNA, activity of liver thymidine kinase and mitotic index in hepatocytes) were determined. Unpaired Student's t-test and one-way analysis of variance were used for statistical analysis and a P value of 0.05 or less was considered significant. All markers of oxidative stress were significantly decreased in propofol-treated animals. Biochemical and histological markers of liver injury and regeneration in propofol-treated animals did not show any significant decrease compared with those observed in the control group. The antioxidant capacity of propofol, verified in our study, did not manage to prevent liver injury and accelerate regeneration after acetaminophen administration in rats.