BLACK-CURRANT PROTECTION AGAINST OXIDATIVE STRESS FORMATION

The aim of this study was to investigate the influence of black-currant juice on chronic ethanol-induced oxidative stress and its consequences in liver, brain, and serum of rats. Data demonstrated that administration of black-currant juice to rats improved antioxidant abilities in the examined tissues as evidenced by measurement of activities of Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GSSG-R), as well as levels of glutathione (GSH) and vitamins C, E, and A. Ethanol intoxication produced a decrease in the activities and levels of the antioxidants just listed, and the decrease was accompanied by a reduction in levels of arachidonic acid (AA) and docosahexaenoic acid (DHA). Further results showed enhanced lipid peroxidation as determined by malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), and neuroprostanes and elevated protein levels such as carbonyl groups and dityrosine. Ethanol intoxication altered liver metabolism as evidenced by a decrease in peroxisome proliferator-activated-receptor (PPAR), AMP-dependent protein kinase (AMPK), and nuclear factor kappa B cells (NFB) and by an increase in tumor necrosis factor (TNF-) expression. Administration of black-currant juice to ethanol-intoxicated rats exerted an antioxidant response by restoring to normal quantities the antioxidant levels and enzyme activities and prevented lipid and protein oxidative effects. The activities of alanine transaminase and aspartate transaminase, biomarkers of liver damage, returned to normal after black-currant treatment of ethanol-administered animals. In addition, the expression of PPAR, AMPK, TNF-, and NFB confirmed the protective effect of the juice. Data thus indicate the extensive antioxidant metabolic effects of black-currant juice that may be beneficial for humans.