Vitamin E and tannic acid improve DNA damage in rats submitted chronic ethanol administration

摘要

Purpose - Chronic ethanol consumption induces lipid peroxidation by increasing free radicals orrnreducing antioxidants and may increase damage to hepatic DNA. Tannins are polyphenolicrnmetabolites present in various plants and one of their effects is antioxidant activity that reducesrnlipoperoxidation, as is the case for vitamin E. This paper aims to assess the role of tannic acid andrnvitamin E in lipid peroxidation and in DNA damage in rats receiving ethanol.rnDesign/methodology/approach - A total of 60 Wistar rats were divided into six groups:rncontrol + ethanol (0-24hs), tannic acid + ethanol (0-24 hs), and vitamin E + ethanol (0-24 hs). Thernanimals were sacrificed immediately (0 hour) or 24 hours after a period of four weeks of ethanolrnadministration and the following measurements were made: plasma vitamin E and liver glutathione,rnthiobarbituric acid resistant substances, and α-tocopherol. The comet test was also applied tornhepatocytes.rnFindings - Ethanol administration led to an increase in DNA damage (148.67 ± 15.45 versusrn172.63 ± 18.94) during a period of 24 hours which was not detected in the groups receiving tannic acidrnor vitamin E. Steatosis was lower in the groups receiving tannic acid.rnOriginality/value - The paper highlights that antioxidant role of vitamin E and of tannic acid inrnbiological systems submitted to oxidative stress should be reevaluated, especially regarding thernprotective role of tannic acid against hepatic steatosis.