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孕期小鼠摄入乙醇对化学诱导腭裂的增强作用。

Potentiation of chemically induced cleft palate by ethanol ingestion during gestation in the mouse.

作者信息

Lee M

出版信息

Teratog Carcinog Mutagen. 1985;5(6):433-40. doi: 10.1002/tcm.1770050606.

Abstract

The influence of ethanol consumption on cleft palate induction by methylmercury, cortisone, and retinyl acetate was investigated in Swiss white mice. Consumption of 20% ethanol throughout gestation significantly increased the incidence of cleft palate compared to water-fed mice, when methylmercury was given on four consecutive days (days 9-12, 5 mg/kg of body weight). Ethanol also increased the incidence of cleft palate in mice given retinyl acetate (3,400 or 5,100 IU) on day 12, compared to retinol acetate-treated mice given water, but did not affect cleft palate induction by cortisone (2.5 mg/d, days 8-11). Ethanol significantly reduced fetal weight in the presence or absence of the three teratogens, but the results do not support a hypothesis that growth retardation is directly responsible for the potentiating action of ethanol. It may be that ethanol acts to increase cleft palate induction by some teratogens by retarding fetal developmental processes.

摘要

在瑞士小白鼠身上研究了乙醇摄入对甲基汞、可的松和醋酸视黄酯诱发腭裂的影响。与饮用自来水的小鼠相比,在整个妊娠期饮用20%乙醇的小鼠,当连续四天(第9 - 12天,5毫克/千克体重)给予甲基汞时,腭裂发生率显著增加。与给予自来水的醋酸视黄醇处理小鼠相比,在第12天给予醋酸视黄酯(3400或5100国际单位)的小鼠中,乙醇也增加了腭裂发生率,但不影响可的松(2.5毫克/天,第8 - 11天)诱发腭裂。无论是否存在三种致畸剂,乙醇均显著降低胎儿体重,但结果不支持生长迟缓直接导致乙醇增强作用这一假说。可能是乙醇通过延缓胎儿发育过程,作用于增加某些致畸剂诱发腭裂的几率。

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