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母体摄入乙醇对胎鼠和新生鼠肝脏蛋白质合成的影响。

Effect of maternal ethanol consumption on foetal and neonatal rat hepatic protein synthesis.

作者信息

Rawat A K

出版信息

Biochem J. 1976 Dec 15;160(3):653-61. doi: 10.1042/bj1600653.

Abstract

Effects of maternal ethanol consumption were investigated on the rates of protein synthehsis by livers of foetal and neonatal rats both in vivo and in vitro, and on the activities of enzymes involved in protein synthesis and degradation. The rates of general protein synthesis by ribosomes in vitro studied by measuring the incorporation of [14C]leucine into ribosomal protein showed that maternal ethanol consumption resulted in an inhibition of the rates of protein synthesis by both foetal and neonatal livers from the ethanol-fed group. The rates of incorporation of intravenously injected [14C]leucine into hepatic proteins were also significantly lower in the foetal, neonatal and adult livers from the ethanol-fed group. Incubation of adult-rat liver slices with ethanol resulted in an inhibition of the incorporation of [14C]leucine into hepatic proteins; however, this effect was not observed in the foetal liver slices. This effect of externally added ethanol was at least partially prevented by the addition of pyrazole to the adult liver slices. Pyrazole addition to foetal liver slices was without significant effect on the rates of protein synthesis. Cross-mixing experiments showed that the capacity of both hepatic ribosomes and pH5 enzyme fractions to synthesize proteins was decreased in the foetal liver from the ethanol-fed group. Maternal ethanol consumption resulted in a decrease in hepatic total RNA content, RNA/DNA ratio and ribosomal protein content in the foetal liver. Foetal hepatic DNA content was not significantly affected. Ethanol consumption resulted in a significant decrease in proteolytic activity and the activity of tryptophan oxygenase in the foetal, neonatal and adult livers. It is possible that the mechanisms of inhibition of protein synthesis observed here in the foetal liver after maternal ethanol consumption may be responsible for at least some of the changes observed in 'foetal alcohol syndrome'.

摘要

研究了母体摄入乙醇对胎鼠和新生鼠肝脏蛋白质合成速率的影响,包括体内和体外实验,以及对参与蛋白质合成和降解的酶活性的影响。通过测量[14C]亮氨酸掺入核糖体蛋白来研究体外核糖体的总蛋白质合成速率,结果表明,母体摄入乙醇会导致乙醇喂养组胎鼠和新生鼠肝脏的蛋白质合成速率受到抑制。乙醇喂养组的胎鼠、新生鼠和成年鼠肝脏中,静脉注射的[14C]亮氨酸掺入肝脏蛋白质的速率也显著降低。成年大鼠肝脏切片与乙醇孵育会导致[14C]亮氨酸掺入肝脏蛋白质受到抑制;然而,在胎鼠肝脏切片中未观察到这种效应。向成年肝脏切片中添加吡唑可至少部分阻止外源性添加乙醇的这种效应。向胎鼠肝脏切片中添加吡唑对蛋白质合成速率无显著影响。交叉混合实验表明,乙醇喂养组胎鼠肝脏中肝脏核糖体和pH5酶组分合成蛋白质的能力均下降。母体摄入乙醇会导致胎鼠肝脏中肝脏总RNA含量、RNA/DNA比值和核糖体蛋白含量降低。胎鼠肝脏DNA含量未受到显著影响。摄入乙醇会导致胎鼠、新生鼠和成年鼠肝脏中的蛋白水解活性和色氨酸加氧酶活性显著降低。母体摄入乙醇后胎鼠肝脏中观察到的蛋白质合成抑制机制可能至少部分导致了“胎儿酒精综合征”中观察到的一些变化。

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The half-life-time of induced tryptophan peroxidase in vivo.体内诱导型色氨酸过氧化物酶的半衰期。
Arch Biochem Biophys. 1959 Dec;85:478-82. doi: 10.1016/0003-9861(59)90514-4.
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Studies on the nature of polysomes.多核糖体性质的研究。
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