Effect of sweet grass extract against oxidative stress in rat liver and serum

Ethanol metabolism is accompanied by generation of free radicals which can damage the cell components. However, sweet grass is a source of coumarin and its derivatives have emerged as a promising group of antioxidant compounds. The aim of this study has been to investigate the influence of sweet grass on oxidative stress formation in the liver and serum of rats intoxicated with ethanol. Alcohol intoxication led to a decrease in the superoxide dismutase, catalase, glutathione peroxidase and reductase activity in the blood serum as well as in the liver, but not in the glutathione reductase activity. The decrease in the antioxidant abilities of the examined tissues after ethanol intoxication resulted in enhanced lipid peroxidation measured as malondialdehyde and 4-hydroxynonenal levels. The metabolic consequence of oxidative modifications of lipids was damage of the liver cells membrane and an increase in its permeability appeared as a leakage of alanine aminotransferase and aspartate aminotransferase into the blood. Administration of sweet grass to the ethanol-intoxicated rats remarkably prevented the significant increase in concentrations of all measured lipid peroxidation products as well as the damage of the liver cell membrane. These results indicate beneficial antioxidant effect of the sweet grass on the liver of rats intoxicated with ethanol.

► We studied the sweet grass influence on oxidative stress formation in the liver and serum of rats intoxicated with ethanol. ► Sweet grass caused an increase in the SOD, GSH-Px, GSSG-R activity and concentration of GSH, vitamins C and A in the liver. ► Alcohol intoxication led to a decrease in the SOD, CAT, GSH-Px, GSSG-R activity in the blood serum as well as in the liver. ► Administration of sweet grass to the ethanol-intoxicated rats remarkably prevented enhanced lipid peroxidation.