Chronic ethanol and nicotine interaction on rat tissue antioxidant defense system
Chronic ethanol and nicotine interaction on rat tissue antioxidant defense system
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DOI：
10.1016/s0741-8329(01)00176-8
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发表时间：
2001-10-01
期刊：
影响因子：
2.3
通讯作者：
Somani, SA
中科院分区：
文献类型：
--
作者：
Husain, K;Scott, BR;Somani, SA
乙醇消费和吸烟在世界各地的社会中很常见，并已被确定为对人类健康有害。本研究旨在探讨长期摄入乙醇和尼古丁对大鼠不同组织抗氧化防御系统的交互作用。雄性Fisher-344大鼠被分为4组，每组5只，治疗6.5周：（1）对照组口服生理盐水;（2）乙醇（20% [wt./卷]）以2 g/kg的剂量口服给药;（3）以0.1 mg/kg的剂量皮下给药尼古丁;和（4）通过上述途径和剂量给药乙醇加尼古丁的组合。末次给药后20 h处死动物，分离并分析肝、肺、肾和睾丸。长期摄入乙醇导致肝脏、肺和睾丸中谷胱甘肽（GSH）含量显著减少，而长期给予尼古丁则显著减少肝脏和睾丸中GSH含量。乙醇、尼古丁或乙醇与尼古丁联合作用可显著提高肝脏超氧化物歧化酶（SOD）活性，降低肾脏SOD活性。乙醇、尼古丁或乙醇+尼古丁的组合显著降低肝脏中的过氧化氢酶（CAT）活性，并增加肾脏和睾丸中的CAT活性。慢性摄入乙醇导致肝脏和肾脏中谷胱甘肽过氧化物酶（GSH-Px）活性显著降低，而乙醇加尼古丁的组合增加肝脏中GSH-Px活性，降低肾脏和睾丸中GSH-Px活性。乙醇，尼古丁，或乙醇和尼古丁的组合显着增加脂质过氧化反应，分别在肝脏中。这表明，长期暴露于乙醇和尼古丁产生类似的，在某些情况下添加剂，氧化组织损伤大鼠。(C)2001 Elsevier Science Inc. All rights reserved.
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.