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高氧性肺损伤与多胺生物合成。年龄相关差异。

Hyperoxic lung injury and polyamine biosynthesis. Age-related differences.

作者信息

Hacker A D, Tierney D F, O'Brien T K, Witschi H R

出版信息

Am Rev Respir Dis. 1985 Aug;132(2):354-7. doi: 10.1164/arrd.1985.132.2.354.

Abstract

To determine if lung cell replication and repair might be different between younger (30-day-old) and older (60-day-old) rats, we studied polyamine and DNA biosynthesis in rats exposed to 1.0 atm oxygen for 24, 48, 56, or 72 h. By 24 h, no statistically significant changes were observed, but by 48 h, ornithine decarboxylase and putrescine increased; S-adenosylmethionine decarboxylase activity increased by 56 h in the younger rats but not in the older rats. By 72 h, spermidine, [3H]thymidine incorporation, and the labeling index of cells in the alveolar zone had increased only in the younger rats. During the first 56 h, hyperoxia inhibited DNA synthesis. We conclude that hyperoxia initially suppresses lung cell replication but subsequently, if the rat survives, there are increases in polyamine biosynthesis and cell replication that may be important for the development of oxygen tolerance.

摘要

为了确定年轻(30日龄)和年老(60日龄)大鼠的肺细胞复制和修复是否存在差异,我们研究了暴露于1.0个大气压氧气24、48、56或72小时的大鼠体内的多胺和DNA生物合成情况。到24小时时,未观察到统计学上的显著变化,但到48小时时,鸟氨酸脱羧酶和腐胺增加;年轻大鼠中S-腺苷甲硫氨酸脱羧酶活性在56小时时增加,而年老大鼠未增加。到72小时时,仅年轻大鼠的精胺、[3H]胸苷掺入量和肺泡区细胞的标记指数增加。在最初的56小时内,高氧抑制DNA合成。我们得出结论,高氧最初会抑制肺细胞复制,但随后,如果大鼠存活下来,多胺生物合成和细胞复制会增加,这可能对氧耐受性的发展很重要。

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