Korobov V P, Raev A B
Farmakol Toksikol. 1977 Jan-Feb;40(1):41-4.
The development of thyrotoxin intoxication is attended by a sharply increased activity of aminopherases localized in the nuclei, mitochondria and hyaloplasm. The molecular pattern of the study enzymes undergoes a substantial change and is supplemented with new isoforms in the cathod portion of the spectrum embracing the alanine-aminotranspherase of the nuclei and hyaloplasm, and that of the aspartate-aminotranspherase of the nuclei and mitochondria. Actinomycin D, an inhibitor of transcription, abolishes the effect of thyrotoxin stimulating the aminopherase activity and induction of the hormones of new molecular forms of the aminopherases.
甲状腺毒素中毒的发展伴随着定位于细胞核、线粒体和透明质中的氨基转移酶活性急剧增加。所研究酶的分子模式发生了显著变化，并且在谱图的阴极部分出现了新的同工型，包括细胞核和透明质中的丙氨酸氨基转移酶以及细胞核和线粒体中的天冬氨酸氨基转移酶。转录抑制剂放线菌素D消除了甲状腺毒素刺激氨基转移酶活性以及诱导氨基转移酶新分子形式激素的作用。
