Aqueous extract of black tea (Camellia sinensis) prevents chronic ethanol toxicity

Oxidants have been shown to be involved in alcohol-induced liver injury. High-fat diet may be an additional factor for more acute alcohol-induced liver injury. Moreover, black tea extract (BTE), a phytocompound has been attributed with a plethora of health-promoting actions. This study was designed to test the hypothesis that BTE protects against early ethanol and ethanol + high-fat liquid diet-induced liver injury in rats. Results show that BTE was effective in blunting both ethanol and ethanol + high-fat diet-induced enhanced activities of enzymes like aspartate aminotransferase, alanine aminotransferase and acid phosphatase. BTE was also effective in blunting ethanol and ethanol + high-fat-induced increase in production of malondialdehyde and nitric oxide. Furthermore, BTE could blunt ethanol and ethanol + high-fat diet-induced suppressed activities of superoxide dismutase and catalase. Additionally, BTE was found effective in blunting ethanol + high-fat diet-induced enhanced activity of gamma-glutamyl-transpeptidase as well as to recover lower glutathione content. Ethanol with or without high-fat diet-induced histopathological and inflammatory damages could be blunted by BTE. Results of pathology scores of hepatocellular damage caused by ethanol with or without high-fat diet and its recovery by BTE, suggest that BTE also was effective against more intense damaging effects caused by ethanol + high-fat diet BTE also could blunt body weight loss because of ethanol + high-fat diet. This study demonstrates that BTE prevents chronic ethanol toxicity developed by ethanol with or without high-fat diet, presumably by blunting oxidative stress.