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[甲状腺切除大鼠小脑对9,10-二甲基-1,2-苯并蒽致瘤作用抵抗力增强的机制]

[Mechanism of increased resistance of thyroidectomized rats to the blastomogenous effect of 9,10-dimethyl-1,2-benzanthracene in cerebellum].

作者信息

Berezov T T, Burobina S S, Spryshkova N A, Alexeeva R I

出版信息

Vopr Med Khim. 1975 Jul-Aug;21(4):359-63.

PMID:814711
Abstract

In rat cerebellum development of tumor, induced by 9,10-dimethyl-1,2-benzanthracene, was accompanied by a gradual increase in concentration of corticosterone in peripheral blood and by a decrease in 5-hydroxytryptophane decarboxylase activity. Experimental athyreosis inhibited development of the tumor in cerebellum (the tumor developed in 80.8% of normothyreotic animals treated with the benzanthracene derivatives; in the athyreotic animals this figure did not exceed 55.7%), decreased the corticosterone concentration in blood and caused a subsequent decrease in the 5-hydroxytryptophane decarboxylase activity in cerebellum as compared with the corresponding values determined in rats with intact thyroid gland. These alterations are considered as possible determinants of increased resistance of thyroidectomized rats to the blastomogenous effect of 9,10-dimethyl-1,2-benzanthracene on cerebellum.

摘要

在由9,10 - 二甲基 - 1,2 - 苯并蒽诱导的大鼠小脑肿瘤发生过程中,外周血中皮质酮浓度逐渐升高,同时5 - 羟色氨酸脱羧酶活性降低。实验性甲状腺切除抑制了小脑肿瘤的发生(在用苯并蒽衍生物处理的正常甲状腺动物中,肿瘤发生率为80.8%;在甲状腺切除的动物中,这一数字不超过55.7%),降低了血液中皮质酮浓度,并导致与完整甲状腺大鼠相比,小脑5 - 羟色氨酸脱羧酶活性随后降低。这些改变被认为是甲状腺切除大鼠对9,10 - 二甲基 - 1,2 - 苯并蒽对小脑的致瘤作用抵抗力增强的可能决定因素。

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