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新生大鼠暴露于铅后其大脑中的蛋白质合成

Protein synthesis in rat brain following neonatal exposure to lead.

作者信息

Kennedy J L, Girgis G R, Rakhra G S, Nicholls D M

出版信息

J Neurol Sci. 1983 Apr;59(1):57-68. doi: 10.1016/0022-510x(83)90081-3.

Abstract

(1) Suckling rats were exposed to lead through the milk of their dams who received a diet of 4% lead carbonate and weanling rats were exposed to 2 injections of 5.0 mg Pb2+/100 g body weight. The brains were used to prepare the following homogenate fractions: postmitochondrial supernatant, postmicrosomal supernatant, ribosomes, initiation factors. (2) The postmitochondrial supernatant fractions were tested in vitro for protein synthesizing activity using the incorporation of labelled phenylalanine, and phenylalanyl-tRNA into peptide. The preparations from the lead-exposed rats had a significant reduction in activity. (3) Peptide formation with the brain ribosomes was not changed in the lead-exposed rats. (4) The aminoacyl-tRNA synthetase reaction was significantly reduced and accounted for most of the reduced peptide formation with brain homogenates from lead-exposed rats. (5) The binding of methionyl-tRNAfMet to ribosomes was increased using initiation factor preparations from the brain of lead-exposed rats.

摘要

(1) 给哺乳期大鼠通过其摄入含4%碳酸铅饮食的母鼠乳汁接触铅,给断奶大鼠注射2次5.0毫克Pb2+/100克体重的铅。取大脑制备以下匀浆组分:线粒体后上清液、微粒体后上清液、核糖体、起始因子。(2) 使用标记苯丙氨酸和苯丙氨酰 - tRNA掺入肽的方法,在体外测试线粒体后上清液组分的蛋白质合成活性。来自铅暴露大鼠的制剂活性显著降低。(3) 铅暴露大鼠大脑核糖体的肽形成没有变化。(4) 氨酰 - tRNA合成酶反应显著降低,这是铅暴露大鼠大脑匀浆中肽形成减少的主要原因。(5) 使用来自铅暴露大鼠大脑的起始因体制剂时,甲硫氨酰 - tRNAfMet与核糖体的结合增加。

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