Yamane Y, Sakai K, Kojima S
Gan. 1976 Apr;67(2):295-302.
The rate of ethylation of t-RNA in vivo by L-ethionine[ethyl-1-14C] markedly lowered in the liver of rats fed a diet containing copper than that of control. In corporation of the labeled compound into the t-RNA of liver by a single injection. of L-ethionine[ethyl-1-14C] was inhibited as much as 50% by the preceding concurrent administration of copper and ethionine added in the diet to rats. Direct interaction of copper ion with ethylation by ethione in the specific t-RNA of the rat liver was examined as an important biochemical explanation in molecular level for the inhibitory mechanism of copper on rat liver carcinogenesis by ethionine. Profiles of normal t-RNA on methylated albumin-kieselguhr column chromatography revealed three components for leucine, two of which were found at the tube number 40 to 50 and disappeared in the leucyl t-RNA treated with ethionine. The components for leucine that disappeared were normalized in the liver of rats by the concurrent administration of copper.
用L-乙硫氨酸[乙基-1-¹⁴C]在体内对t-RNA进行乙基化的速率，在喂食含铜饲料的大鼠肝脏中比对照组显著降低。通过单次注射L-乙硫氨酸[乙基-1-¹⁴C]将标记化合物掺入肝脏的t-RNA中，在大鼠饮食中预先同时给予铜和乙硫氨酸时，掺入量被抑制高达50%。作为铜对乙硫氨酸诱导大鼠肝癌发生抑制机制的分子水平重要生化解释，研究了铜离子与大鼠肝脏特定t-RNA中乙硫氨酸乙基化的直接相互作用。正常t-RNA在甲基化白蛋白-硅藻土柱色谱上的图谱显示亮氨酸有三个组分，其中两个出现在第40至50管，在用乙硫氨酸处理的亮氨酰t-RNA中消失。通过同时给予铜，在大鼠肝脏中消失的亮氨酸组分恢复正常。
