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1,1,1-三氯乙烷对小鼠脑组织中环磷酸腺苷代谢的作用。

Actions of 1,1,1-trichloroethane on the cAMP metabolism in mouse brain.

作者信息

Nilsson K B

出版信息

Acta Pharmacol Toxicol (Copenh). 1986 Nov;59(5):362-9. doi: 10.1111/j.1600-0773.1986.tb00185.x.

Abstract

Inhalation or intraperitoneal administration of 1,1,1-trichloroethane (TCE) increased the cAMP content in the brain stem in a dose-related and time-dependent fashion. TCE had no effect on the cAMP level in the cerebellum and hippocampus, but slightly reduced that in the cerebral cortex. Following intraperitoneal administration of TCE the activity of norepinephrine- and F- -activated adenylate cyclase (AC) in a brain stem homogenate was enhanced, while the serotonin-stimulated AC activity was decreased. Neither the basal AC activity nor the guanine nucleotide- and forskolin-activated enzyme was affected by TCE. TCE had no effect on the soluble cAMP-dependent phosphodiesterase activity. It is suggested that the increased cAMP content in the brain stem induced by TCE may be mediated via adrenoreceptor interaction with the guanine nucleotide-binding regulatory component, resulting in activation of the catalytic unit of the adenylate cyclase and thereby an increase in the cAMP level.

摘要

吸入或腹腔注射1,1,1-三氯乙烷(TCE)会以剂量相关和时间依赖的方式增加脑干中的环磷酸腺苷(cAMP)含量。TCE对小脑和海马体中的cAMP水平没有影响,但会使大脑皮层中的cAMP水平略有降低。腹腔注射TCE后,脑干匀浆中去甲肾上腺素和F-激活的腺苷酸环化酶(AC)的活性增强,而5-羟色胺刺激的AC活性降低。TCE对基础AC活性以及鸟嘌呤核苷酸和福斯高林激活的酶均无影响。TCE对可溶性cAMP依赖性磷酸二酯酶活性没有影响。有人提出,TCE诱导的脑干中cAMP含量增加可能是通过肾上腺素能受体与鸟嘌呤核苷酸结合调节成分相互作用介导的,从而导致腺苷酸环化酶催化单位的激活,进而使cAMP水平升高。

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