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[通过作用于非特异性微粒体氧化酶改变呋氟尿嘧啶的毒性和抗肿瘤特性]

[Change of toxic and antineoplastic properties of ftorafur by means of action on nonspecific microsomal oxidase].

作者信息

Belitskiĭ G A, Bukhman V M, Konopleva I A

出版信息

Biull Eksp Biol Med. 1979 Oct;88(10):442-4.

PMID:387108
Abstract

The inducers of microsomal hydroxylases, phenobarbitone and methylcholanthrene, inhibited the development of neurotoxic shock provoked by high doses of ftorafur in mice, but stimulated the animal mortality on the 4th-8th day after the drug administration. The opposite effect on both toxicity manifestations has been obtained under the action of the inhibitor SKF 525-A. Pretreatment of the animals with phenobarbitone or phenobarbitone-methylcholanthrene combination markedly increased the antineoplastic activity of ftorafur determined by a loss of the spleen weight in mice infected with Rauscher's leukemia.

摘要

微粒体羟化酶诱导剂苯巴比妥和甲基胆蒽可抑制小鼠因大剂量呋喃氟尿嘧啶引发的神经毒性休克的发展,但会在给药后第4至8天增加动物死亡率。在抑制剂SKF 525 - A的作用下,对这两种毒性表现产生了相反的效果。用苯巴比妥或苯巴比妥 - 甲基胆蒽组合对动物进行预处理,显著提高了呋喃氟尿嘧啶的抗肿瘤活性,这一活性通过感染劳斯氏白血病的小鼠脾脏重量减轻来测定。

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