BACKGROUND AND OBJECTIVE: We evaluated the effects of propofol on oxidative stress and acute liver injury and regeneration produced by acetaminophen administration in rats. METHODS: 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. RESULTS: 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. CONCLUSION: The antioxidant capacity of propofol, verified in our study, did not manage to prevent liver injury and accelerate regeneration after acetaminophen administration in rats.
BACKGROUND AND OBJECTIVE: We evaluated the effects of propofol on oxidative stress and acute liver injury and regeneration produced by acetaminophen administration in rats. METHODS: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. RESULTS: 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. CONCLUSION: The antioxidant capacity of propofol, verified in our study, did not manage to prevent liver injury and accelerate regeneration after acetaminophen administration in rats.
Authors: Tahia H Saleem; Nagwa Abo El-Maali; Mohammed H Hassan; Nahed A Mohamed; Nashwa A M Mostafa; Emaad Abdel-Kahaar; Azza S Tammam Journal: Int J Hepatol Date: 2018-09-02