Ascorbic acid supplementation causes faster restoration of reduced glutathione content in the regression of alcohol-induced hepatotoxicity in male guinea pigs

被引:14
作者
Abhilash, P. A. [1 ]
Harikrishnan, R. [1 ]
Indira, M. [1 ]
机构
[1] Univ Kerala, Dept Biochem, Thiruvananthapuram 695581, Kerala, India
关键词
Alcohol; Ascorbic acid; Glutathione; Hepatotoxicity; Oxidative stress; INDUCED OXIDATIVE STRESS; CHRONIC ETHANOL INGESTION; ANTIOXIDANT; MEDICINES; SELENIUM; TISSUES; RISK; RATS;
D O I
10.1179/1351000212Y.0000000010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alcoholic liver disease is caused mainly by free radicals. Ascorbic acid (AA) and glutathione (GSH) are the major water-soluble antioxidants in the liver. The impact of AA supplementation on GSH, AA and activities of GSH-dependent enzymes in alcoholic guinea pigs was studied and was compared with alcohol abstention. Guinea pigs were administered ethanol at a dose of 4 g/kg body weight (b.wt)/day for 90 days. After 90 days, alcohol administration was stopped and one-half of the ethanol-treated animals were supplemented with AA (25 mg/100 g b.wt) for 30 days and the other half was maintained as the abstention group. There was a significant increase in the activities of alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transpeptidase in the serum of the ethanol group. In addition, a significant decrease in the GSH content, activities of GSH peroxidase, GSH reductase, and increased activity of GSH-S-transferase were observed in the liver of the ethanol group. Histopathological analysis and triglycerides content in the liver of the ethanol group showed induction of steatosis. But AA supplementation and abstention altered the changes caused by ethanol. However, maximum protective effect was observed in the AA-supplemented group indicating the ameliorative effect of AA in the liver.
引用
收藏
页码:72 / 79
页数:8
相关论文
共 38 条
  • [1] Oxidative mechanisms in the pathogenesis of alcoholic liver disease
    Albano, Emanuele
    [J]. MOLECULAR ASPECTS OF MEDICINE, 2008, 29 (1-2) : 9 - 16
  • [2] Bergmeyer HU., 1983, METHODS ENZYMATIC AN, VVI., P258
  • [3] ENDOTOXIN INDUCED HEPATIC-NECROSIS IN RATS ON AN ALCOHOL DIET
    BHAGWANDEEN, BS
    APTE, M
    MANWARRING, L
    DICKESON, J
    [J]. JOURNAL OF PATHOLOGY, 1987, 152 (01) : 47 - 53
  • [4] Chronic ethanol ingestion and the risk of acute lung injury: a role for glutathione availability?
    Brown, LAS
    Harris, FL
    Ping, XD
    Gauthier, TW
    [J]. ALCOHOL, 2004, 33 (03) : 191 - 197
  • [5] ASCORBATE PROTECTS GUINEA-PIG TISSUES AGAINST LIPID-PEROXIDATION
    CHAKRABORTY, S
    NANDI, A
    MUKHOPADHYAY, M
    MUKHOPADHYAY, CK
    CHATTERJEE, IB
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1994, 16 (04) : 417 - 426
  • [6] Das SK, 2005, INDIAN J CLIN BIOCHE, V20, P24, DOI 10.1007/BF02867396
  • [7] Alcohol and oxidative liver injury
    Dey, A
    Cederbaum, AI
    [J]. HEPATOLOGY, 2006, 43 (02) : S63 - S74
  • [8] Herbal medicines for liver diseases
    Dhiman, RK
    Chawla, YK
    [J]. DIGESTIVE DISEASES AND SCIENCES, 2005, 50 (10) : 1807 - 1812
  • [9] Hepatoprotective effect of stem of Musa sapientum Linn in rats intoxicated with carbon tetrachloride
    Dikshit, Piyush
    Tyagi, Moot Kumar
    Shukla, Kirtikar
    Sharma, Sonal
    Gambhir, Jasvindar Kaur
    Shukla, Rimi
    [J]. ANNALS OF HEPATOLOGY, 2011, 10 (03) : 333 - 339
  • [10] EFFECT OF ACUTE AND CHRONIC ETHANOL INGESTION ON THE CONTENT OF REDUCED GLUTATHIONE OF VARIOUS TISSUES OF THE RAT
    FERNANDEZ, V
    VIDELA, LA
    [J]. EXPERIENTIA, 1981, 37 (04): : 392 - 394