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线粒体内膜蛋白生物合成中与年龄相关的衰退。

Age-related decline in the biosynthesis of mitochondrial inner membrane proteins.

作者信息

Marcus D L, Ibrahim N G, Freedman M L

出版信息

Exp Gerontol. 1982;17(5):333-41. doi: 10.1016/0531-5565(82)90033-x.

Abstract

Isolated mitochondria from rat livers of various ages show a gradual decline in the rate of inner membrane-matrix protein synthesis with advancing age of the animal. Rats at 112-120 weeks synthesize these proteins at only 40% of the rate of 2-8-week-old animals. The initial rates of incorporation of label were 145 cpm/mg/minute for the "old" animals, and 320 cpm/mg/minute for the "young" animal. No difference in either amino acid pool size or leakage of label through the mitochondrial membrane was detected in the two age groups. Treatment of the mitochondria with ferrous ammonium sulphate produced a 1.62 fold increase in mitochondrial protein synthesis in the young animal but not in the old. Hemin treatment produced a similar effect. These results suggest that the decrease in delta-aminolevulinic acid synthase activity seen with age (Paterniti et al., 1978) may be due to a decrease in the synthesis of mitochondrial inner membrane proteins.

摘要

从不同年龄大鼠肝脏中分离出的线粒体显示,随着动物年龄的增长,线粒体内膜 - 基质蛋白合成速率逐渐下降。112 - 120周龄的大鼠合成这些蛋白质的速率仅为2 - 8周龄动物的40%。“老年”动物的标记物初始掺入速率为145 cpm/mg/分钟,“年轻”动物为320 cpm/mg/分钟。在两个年龄组中,未检测到氨基酸池大小或标记物通过线粒体膜的泄漏有差异。用硫酸亚铁铵处理线粒体,年轻动物的线粒体蛋白合成增加了1.62倍,而老年动物则没有。血红素处理也产生了类似的效果。这些结果表明,随着年龄增长而出现的δ-氨基乙酰丙酸合酶活性下降(Paterniti等人,1978年)可能是由于线粒体内膜蛋白合成减少所致。

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