Volume 5, Issue 5, October 2017, Page: 88-91
Oxidative Damage in Rats Receiving Ethanol and Supplemented with Vitamin E
Alceu Afonso Jordao, Division of Nutrition, Department of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil
Thais Helena Monteiro, Division of Nutrition, Department of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil
Raquel Alves dos Santos, Nucleus of Research in Sciences and Technology, University of Franca, Franca, Brazil
Guilherme Vannucchi Portari, Department of Nutrition, Federal University of Triangulo Mineiro, Uberaba, Brazil
Received: Apr. 11, 2017;       Accepted: May 23, 2017;       Published: Oct. 18, 2017
DOI: 10.11648/j.ajbls.20170505.11      View  1991      Downloads  191
Abstract
The metabolism of ethanol is directly related to oxidative stress, and its ingestion leads to the formation of reactive oxygen species (ROS) such as hydroxyl radicals, superoxide and hydrogen peroxide. Vitamin E has been widely used as an antioxidant; when administered in large doses it is deposited in the liver and then excreted in the bile, urine and feces. The objective of the present study was to evaluate the rate of excretion of fecal vitamin E in relation to its concentrations in serum and liver, and its role as a protective antioxidant against DNA damage induced by acute ethanol consumption. Wistar rats were divided into four groups receiving food and water ad libitum for 4 days plus the following treatments: Control (CG, n = 10 ) no treatment; Ethanol (ET, n = 10 ), receiving an acute ethanol dose intraperitoneally in the amount of 5 g/kg; vitamin E (VE, n = 10) receiving a high oral dose of vitamin E within the first three days in the amount of 100 tocopherol mg/kg body weight; ethanol plus vitamin E (VE + ET, n = 10 ) receiving both the ethanol and vitamin E doses. Higher concentrations of vitamin E were observed in the blood and liver of the animals in the groups that received vitamin E supplementation, independent of the presence or absence of ethanol. Concomitantly, these groups were also those with the highest concentration of the vitamin in the stool. The rate of DNA damage was higher in the groups that received ethanol with or without supplemental vitamin E. However, the rate of damage was lower in the group that received vitamin E supplementation than in the group that did not. The present results show that vitamin E has a protective effect against DNA damage induced by ethanol by reducing the extent of DNA damage.
Keywords
Vitamin E, Ethanol, Antioxidants, DNA Damage, Supplementation
To cite this article
Alceu Afonso Jordao, Thais Helena Monteiro, Raquel Alves dos Santos, Guilherme Vannucchi Portari, Oxidative Damage in Rats Receiving Ethanol and Supplemented with Vitamin E, American Journal of Biomedical and Life Sciences. Vol. 5, No. 5, 2017, pp. 88-91. doi: 10.11648/j.ajbls.20170505.11
Copyright
Copyright © 2017 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Reference
[1]
Das SK & Vasudevan DM. Alcohol-induced oxidative stress. Life Sciences 2007; 81: 177-87.
[2]
Lieber CS. Ethanol, metabolism, cirrhosis and alcoholism. Clin Chim Acta 1997; 257: 59-84.
[3]
Lieber CS. Metabolism of alcohol. Clinics in Liver Disease 2005; 9: 1-35.
[4]
Song BJ & Cederbaum AI. Ethanol-inducible cytochrome P450 (CYP4502E1): biochemistry, molecular biology and clinical relevance: 1996 update. Alcohol Clin Exp Res 1996; 20: 138A-46A.
[5]
Brooks PJ. DNA damage, DNA repair, and alcohol toxicity: a review. Alcohol Clin Exp Res 1997; 21: 1073-82.
[6]
Singh NP, Khan A. Acetaldehyde: genotoxicity and cytotoxicity in human lymphocytes. Mutat Res 1995; 337: 9-17.
[7]
Nordmann R, Ribiere C, Rouach H. Implication of free radical mechanism of ethanol-induced cellular injury. Free Radical Biol Med 1992; 12: 219-40.
[8]
Kuykendall JR, Bogdanffy M. Reaction kinetics of DNA-histone crosslinking by vinyl acetate and acetaldehyde. Carcinogenesis 1992; 13: 2095-2100.
[9]
Baraona E, Liu W, Ma XL, Svegliati-Baroni G, Lieber CS. Acetaldehyde-collagen addcuts in N-nitrosodimethylamine-induced liver cirrhosis in rats. Life Sci 1993; 52: 1249-55.
[10]
McDonough KH. Antioxidant nutrients and alcohol. Toxicology 2003; 189: 89-97.
[11]
Jordão Jr AA, Meirelles MSS, Chiarello PG, Vannucchi H. Efeito da administração crônica de etanol sobre a peroxidação lipídica em ratos. Medicina Ribeirão Preto 2002; 35: 48-52.
[12]
Traber MG & Atkinson J. Vitamin E, antioxidant and nothing more. Free Radic Biol Med 2007; 43 (1): 4-15.
[13]
Jordão Jr AA, Chiarello PG, Arantes MR, Meirelles MS, Vannucchi H. Effect of an acute dose of ethanol on lipid peroxidation in rats: action of vitamin E. Food and Chemical Toxicology 2004; 42: 459-64.
[14]
Lauzon DA, Johnston SL, Southern LL, Xut Z. The effect of carrier for vitamin E on liver concentrations of vitamin E and vitamin E excretion in broilers. Metabolism and Nutrition 2008; 87: 934-9.
[15]
Jordão Jr AA, Silveira S, Figueiredo JFC, Vannucchi H. Urinary excretion and plasma vitamin E levels in patients with AIDS. Nutrition 1998; 14: 423-6.
[16]
Clarke MW, Burnett JR, Croft KD. Vitamin E in human health and disease. Critical Reviews in Clinical Laboratory Sciences 2008; 45(5): 417-50.
[17]
Kayden HJ & Traber MG. Absorption, lipoprotein transport, and regulation of plasma concentrations of vitamin E in humans. Journal of Lipid Research 1993; 34: 343-58.
[18]
Santos RA, Jordao Junior AA, Vannucchi H, Takahashi CS. Protection of doxorubicin-induced DNA damage by sodium selenite and selenomethionine in Wistar rats. Nutrition Research (Los Angeles), v. 27, p. 343-348, 2007.
[19]
Tavares DC, Cecchi AO, Jordão Jr AA, Vannucchi H, Takahashi CS. Cytogenetic study of chronic ethanol consumption in rats. Teratogenesis, Carcinogenesis, and Mutagenesis 2001; 21: 361-8.
[20]
Lee SJ, Kim SY, Min H. Effects of vitamin C and E supplementation on oxidative stress and liver toxicity in rats fed a low-fat ethanol diet. Nutr Res Pract. 2013; 7: 109-114.
[21]
Shirpoor A1, Salami S, Khadem-Ansari MH, Minassian S, Yegiazarian M. Protective effect of vitamin E against ethanol-induced hyperhomocysteinemia, DNA damage, and atrophy in the developing male rat brain. Alcohol Clin Exp Res. 2009; 33 (7): 1181-6.
[22]
Sato K, Gosho M, Yamamoto T, Kobayashi Y, Ishii N, Ohashi T, Nakade Y, Ito K, Fukuzawa Y, Yoneda M. Vitamin E has a beneficial effect on nonalcoholic fatty liver disease: a meta-analysis of randomized controlled trials. Nutrition. 2015; 31 (7-8): 923-30.
[23]
Ozkol H, Bulut G, Balahoroglu R, Tuluce Y, Ozkol HU. Protective effects of selenium, N-acetylcysteine and Vitamin E against acute ethanol intoxication in rats. Biol Trace Elem Res. 2017; 175 (1): 177-185.
Browse journals by subject