金黄地鼠肾（BHK）细胞的腺苷敏感突变体中腺苷毒性的多种机制。

Multiple mechanisms of adenosine toxicity in an adenosine sensitive mutant of baby hamster kidney (BHK) cells.

作者信息

Chan V L, Ho H J

出版信息

Basic Life Sci. 1985;31:103-16. doi: 10.1007/978-1-4613-2449-2_6.

Abstract

A class of arabinosyladenine-resistant baby hamster kidney (BHK) cell mutants, isolated in our laboratory, shows cross-resistance to deoxyadenosine, alteration of adenosine kinase, elevation of spontaneous mutation rate, and extreme sensitivity to adenosine. One of these adenosine sensitive mutants, ara-s10d, was isolated spontaneously and studies with Ador revertants suggest the involvement of a single pleiotropic mutation. The enhanced adenosine toxicity in ara-s10d cells can be attributed to pyrimidine nucleotide starvation and to at least one other mechanism, which is associated with a 200-fold elevation of IMP, 3-5 fold elevation of ATP, GTP, S-adenosylmethionine (AdoMet) and methylthioadenosine (MeSAdo).

摘要

我们实验室分离出的一类对阿拉伯糖基腺嘌呤具有抗性的幼仓鼠肾（BHK）细胞突变体，对脱氧腺苷表现出交叉抗性，腺苷激酶发生改变，自发突变率升高，并且对腺苷极度敏感。其中一个腺苷敏感突变体ara-s10d是自发分离得到的，对腺嘌呤核苷脱氨酶（Ador）回复突变体的研究表明涉及单个多效性突变。ara-s10d细胞中增强的腺苷毒性可归因于嘧啶核苷酸饥饿以及至少一种其他机制，这与肌苷一磷酸（IMP）升高200倍、三磷酸腺苷（ATP）、三磷酸鸟苷（GTP）、S-腺苷甲硫氨酸（AdoMet）和甲基硫代腺苷（MeSAdo）升高3至5倍有关。