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慢性乙醇摄入与A品系小鼠中尿烷诱导的肺肿瘤减少

Chronic ethanol intake and reduction of lung tumours from urethane in strain A mice.

作者信息

Kristiansen E, Clemmensen S, Meyer O

机构信息

Institute of Toxicology, National Food Agency, Søborg, Denmark.

出版信息

Food Chem Toxicol. 1990 Jan;28(1):35-8. doi: 10.1016/0278-6915(90)90133-8.

Abstract

Combinations of ethanol and urethane were added to the drinking-water of female strain A/Ph mice for 12 wk, at the end of which the animals were killed. Urethane concentrations were 0, 200, 500 and 1000 ppm and ethanol concentrations, 0, 5, 10 and 20% (v/v). All possible combinations of these urethane and ethanol concentrations were tested. Urethane induced primary lung adenomas in all treated mice in a dose-dependent manner. An average of 71 +/- 15 tumours/mouse were found, when the animals were killed, after treatment with 1000 ppm urethane for 12 wk. Ethanol alone did not alter the background incidence of tumours and produced only marginal hepatotoxicity. The tumour yields induced by urethane treatment were greatly reduced by simultaneous treatment with ethanol. The effect of ethanol was independent of urethane dose. When the concentrations of ethanol in the drinking-water were 20 and 10% the incidences of lung adenomas induced by urethane were reduced by about two-thirds and one-half, respectively. The effect of 5% ethanol, if any, was not statistically significant.

摘要

将乙醇和氨基甲酸乙酯的混合物添加到雌性A/Ph品系小鼠的饮用水中,持续12周,实验结束时处死动物。氨基甲酸乙酯的浓度分别为0、200、500和1000 ppm,乙醇浓度分别为0、5%、10%和20%(v/v)。对这些氨基甲酸乙酯和乙醇浓度的所有可能组合进行了测试。氨基甲酸乙酯以剂量依赖的方式在所有接受治疗的小鼠中诱发原发性肺腺瘤。在用1000 ppm氨基甲酸乙酯处理12周后处死动物时,平均每只小鼠发现71±15个肿瘤。单独使用乙醇不会改变肿瘤的背景发生率,仅产生轻微的肝毒性。同时用乙醇处理可大大降低氨基甲酸乙酯治疗诱导的肿瘤产量。乙醇的作用与氨基甲酸乙酯剂量无关。当饮用水中乙醇浓度为20%和10%时,氨基甲酸乙酯诱导的肺腺瘤发生率分别降低约三分之二和二分之一。5%乙醇的作用(如果有)在统计学上不显著。

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