Hepatoprotective effect of peptic hydrolysate from salmon pectoral fin protein byproducts on ethanol-induced oxidative stress in Sprague–Dawley rats

Abstract

Bioactive peptides were generated by pepsin hydrolysis from salmon pectoral fin protein byproduct, and the hepatoprotective effect of the peptic hydrolysate (PH) on ethanol-induced oxidative stress was investigated in Sprague–Dawley rats. Administration of ethanol for 4weeks significantly (p<0.05) increased serum markers of liver damage, such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase; however, these activities decreased significantly (p<0.05) after PH administration. Elevated thiobarbituric acid reactive substance levels in liver tissue and serum decreased significantly (p<0.05) following administration of PH. Ethanol exposure significantly (p<0.05) decreased glutathione contents in liver and serum, and hepatic antioxidant enzyme activities such as superoxide dismutase and glutathione peroxidase, while the PH treatment significantly (p<0.05) increased these altered parameters. These results indicate that the PH had a protective effect against ethanol-induced hepatotoxicity that was comparable to that of silymarin, which was supported by evaluating liver histopathology in the rats.