Ethanol-induced hepatotoxicity and protective effect of betaine

Citation
G. Kanbak et al., Ethanol-induced hepatotoxicity and protective effect of betaine, CELL BIOC F, 19(4), 2001, pp. 281-285
Citations number
24
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL BIOCHEMISTRY AND FUNCTION
ISSN journal
02636484 → ACNP
Volume
19
Issue
4
Year of publication
2001
Pages
281 - 285
Database
ISI
SICI code
0263-6484(200112)19:4<281:EHAPEO>2.0.ZU;2-#
Abstract
The protective effects of betaine in ethanol hepatotoxicity were investigat ed in 24 female wistar albino rats. Animals were divided into three groups: control, ethanol and ethanol + betaine group. Animals were fed liquid diet s and consumed approximately 60 diet per day, Rats were fed ethanol 8 kg(-1 ) day(-1). The ethanol + betaine group were fed ethanol plus betaine (0.5% w/v). All animal were fed for 2 months. Reduced glutathione, malondialdehyd e and vitamin A were determined in the liver tissue. Alanine aminotransfera se activities were also measured on intracardiac blood samples. GSH levels in the ethanol group were significantly lower than these in the control gro up (p < 0.001). GSH was elevated in the betaine group as compared to the et hanol group (p < 0.001). MDA in the ethanol group was significantly higher than that in the control group (p < 0.05). MDA was decreased in the betaine group as compared to the ethanol group (p < 0.05). Vitamin A in the ethano l group was significantly lower than that in the control group (p < 0.01), but, in the ethanol + betaine group it was high compared with the ethanol g roup (p < 0.01). ALT in the ethanol group was higher than that in the contr ol group (p < 0.05). Oxidative stress may play a major role in the ethanol- mediated hepatotoxicity. Betaine may protect liver against injury and it ma y prevent vitamin A depletion. Therefore, it may be a useful nutritional ag ent in the prevention of clinical problems dependent on ethanol-induced vit amin A depletion and peroxidative injury in liver. Copyright (C) 2001 John Wiley & Sons, Ltd.