Chronic ethanol and nicotine interaction on rat tissue antioxidant defense system

被引：196

作者：

Husain, K ^{[1
]}

Scott, BR ^{[1
]}

Reddy, SK ^{[1
]}

Somani, SA ^{[1
]}

机构：

[1] So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA

来源：

ALCOHOL | 2001年 / 25卷 / 02期

关键词：

ethanol; nicotine; antioxidant enzymes; glutathione; lipid peroxidation;

D O I：

10.1016/S0741-8329(01)00176-8

中图分类号：

R194 [卫生标准、卫生检查、医药管理];

学科分类号：

摘要：

Ethanol consumption and cigarette smoking are common in societies worldwide and have been identified as injurious to human health. This study was undertaken to examine the interactive effects of chronic ethanol and nicotine consumption on the antioxidant defense system in different tissues of rat, Male Fisher-344 rats were divided into four groups of five animals each and treated for 6.5 weeks as follows: (1) Control rats were administered normal saline orally; (2) ethanol (20% [wt./vol.]) was given orally at a dose of 2 g/kg; (3) nicotine was administered subcutaneously at a dose of 0.1 mg/kg; and (4) a combination of ethanol plus nicotine was administered by the route and at the dose described above. The animals were killed 20 h after the last treatment, and liver, lung, kidney, and testes were isolated and analyzed. Chronic ingestion of ethanol resulted in a significant depletion of glutathione (GSH) content in liver, lung, and testes, whereas chronic administration of nicotine significantly depleted GSH content in liver and testes. The combination of ethanol plus nicotine resulted in a significant depletion of GSH content in liver, lung, and testes, Ethanol, nicotine, or a combination of ethanol plus nicotine significantly increased superoxide dismutase (SOD) activity in liver and decreased SOD activity in kidney. Ethanol, nicotine, or a combination of ethanol plus nicotine significantly decreased catalase (CAT) activity in liver and increased CAT activity in kidney and testes. Chronic ingestion of ethanol resulted in a significant decrease in glutathione peroxidase (GSH-Px) activity in liver and kidney, whereas a combination of ethanol plus nicotine increased GSH-Px activity in liver and decreased GSH-Px activity in kidney and testes. Ethanol, nicotine, or a combination of ethanol plus nicotine significantly increased lipid peroxidation, respectively, in liver. It is suggested that prolonged exposure to ethanol and nicotine produce similar, and in some cases additive, oxidative tissue injuries in rat. (C) 2001 Elsevier Science Inc. All rights reserved.

引用

页码：89 / 97

页数：9

共 66 条

[1]

AEBI H, 1984, METHOD ENZYMOL, V105, P121

[2] OXIDANTS, ANTIOXIDANTS, AND THE DEGENERATIVE DISEASES OF AGING [J].

AMES, BN ;

SHIGENAGA, MK ;

HAGEN, TM .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :7915-7922

[3] THE CHRONIC ADMINISTRATION OF NICOTINE INDUCES CYTOCHROME-P450 IN RAT-BRAIN [J].

ANANDATHEERTHAVARADA, HK ;

WILLIAMS, JF ;

WECKER, L .

JOURNAL OF NEUROCHEMISTRY, 1993, 60 (05) :1941-1944

[4] INDUCTION OF BRAIN CYTOCHROME-P-450IIE1 BY CHRONIC ETHANOL TREATMENT [J].

ANANDATHEERTHAVARADA, HK ;

SHANKAR, SK ;

BHAMRE, S ;

BOYD, MR ;

SONG, BJ ;

RAVINDRANATH, V .

BRAIN RESEARCH, 1993, 601 (1-2) :279-285

[5]

ASHAKUMARY L, 1991, J ECOTOXICOL ENV MON, V1, P283

[6] Preferential effects of nicotine and 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone on mitochondrial glutathione S-transferase A4-4 induction and increased oxidative stress in the rat brain [J].

Bhagwat, SV ;

Vijayasarathy, C ;

Raza, H ;

Mullick, J ;

Avadhani, NG .

BIOCHEMICAL PHARMACOLOGY, 1998, 56 (07) :831-839

[7] ETHANOL TOXICITY AND OXIDATIVE STRESS [J].

BONDY, SC .

TOXICOLOGY LETTERS, 1992, 63 (03) :231-241

[8]

BONDY SC, 1994, ALCOHOL ALCOHOLISM, V29, P375

[9] OXIDIZED GLUTATHIONE IS INCREASED IN THE ALVEOLAR FLUID OF PATIENTS WITH THE ADULT-RESPIRATORY-DISTRESS-SYNDROME [J].

BUNNELL, E ;

PACHT, ER .

AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 148 (05) :1174-1178

[10] LIVER ANTIOXIDANT DEFENSES IN MICE FED ETHANOL AND THE AIN-76A DIET [J].

CHEN, LH ;

XI, S ;

COHEN, DA .

ALCOHOL, 1995, 12 (05) :453-457

← 1 2 3 4 5 6 7 →