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

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 4 weeks 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.

► Hepatoprotective effect of PH from salmon byproduct protein was investigated. ► Administration of PH attenuated ethanol-induced oxidative stress in the rats. ► The PH inhibited lipid peroxidation in the rats. ► The PH increased GSH levels and liver antioxidant enzyme activities such as SOD and GPx.