Isakhanian G D, Gorkin V Z
Vopr Med Khim. 1976 May-Jun;22(3):380-8.
AMP-deaminases were isolated and partially purified from subfractions of soluble mitochondrial proteins of rat liver under normal conditions and in ethanol intoxication. Repeated freezing and thawing of the mitochondrial fractions from liver of rats, which were treated with ethanol (1 ml of 32% solution daily for 7 days, intraperitoneally), liberated into the subfraction of soluble mitochondrial proteins significantly less AMP-deaminases, as compared with the control animals. The enzyme preparations obtained from intoxicated and intact animals were quite similarly inactivated by controlled heating, deaminated at similar rates AMP, ADP, FAD and some other nitrogenous compounds (but did not deaminate adenosine and some structural analogues of AMP). However, an inhibitory effect of the structural analogues of AMP and of nucleosides was significantly higher towards the AMP-deaminase from healthy rats as compared with the corresponding enzyme preparations obtained from the ethanol-treated animals. The increase in velocity of enzymatic AMP deamination in the subfraction of soluble mitochondrial proteins apparently does not represent a suitable target for possible therapeutic approaches to control the phenomenon, observed in the experimental ethanol intoxication, of stimulation of the deaminating activity in total mitochondrial fraction of rat liver.
在正常条件下以及乙醇中毒情况下，从大鼠肝脏可溶性线粒体蛋白亚组分中分离并部分纯化了AMP脱氨酶。用乙醇处理的大鼠（每天腹腔注射1 ml 32%溶液，持续7天）肝脏线粒体组分经反复冻融后，与对照动物相比，释放到可溶性线粒体蛋白亚组分中的AMP脱氨酶明显减少。从中毒动物和正常动物获得的酶制剂在通过控制加热使其失活方面非常相似，以相似的速率对AMP、ADP、FAD和其他一些含氮化合物进行脱氨作用（但不对腺苷和一些AMP结构类似物进行脱氨）。然而，与从乙醇处理动物获得的相应酶制剂相比，AMP结构类似物和核苷对健康大鼠的AMP脱氨酶的抑制作用明显更高。可溶性线粒体蛋白亚组分中酶促AMP脱氨速度的增加显然不是控制实验性乙醇中毒中观察到的大鼠肝脏总线粒体组分脱氨活性刺激现象的可能治疗方法的合适靶点。
