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用蛋白质合成抑制剂处理后大鼠组织中前列腺素15-羟基脱氢酶活性迅速降低。

Rapid reduction of prostaglandin 15-hydroxy dehydrogenase activity in rat tissues after treatment with protein synthesis inhibitors.

作者信息

Blackwell G J, Flower R J, Vane J R

出版信息

Br J Pharmacol. 1975 Oct;55(2):233-8. doi: 10.1111/j.1476-5381.1975.tb07633.x.

Abstract

1 The capacity of rat kidneys to metabolize prostaglandins is rapidly lost when de novo protein synthesis is reduced by cycloheximide and puromycin. Enzyme activity declines to about half control values 45-75 min after a single dose of cycloheximide. Prostaglandin metabolism by the lung is also diminished. 2 These inhibitors apparently act by preventing the synthesis of new prostaglandin 15-hydroxy dehydrogenase enzyme. 3 The RNA synthesis actinomycin D has no effect on metabolism. 4 It is concluded that prostaglandin dehydrogenase is a short-lived enzyme in the cell whose replacement depends upon de novo protein (but not RNA) synthesis. The implications of this finding are discussed.

摘要

1 当用环己酰亚胺和嘌呤霉素降低蛋白质从头合成时,大鼠肾脏代谢前列腺素的能力会迅速丧失。单次给予环己酰亚胺后45 - 75分钟,酶活性降至对照值的约一半。肺对前列腺素的代谢也会减弱。2 这些抑制剂显然是通过阻止新的前列腺素15 - 羟基脱氢酶的合成而起作用的。3 RNA合成放线菌素D对代谢没有影响。4 得出的结论是,前列腺素脱氢酶是细胞中的一种短命酶,其更新依赖于蛋白质从头合成(而非RNA合成)。讨论了这一发现的意义。

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