Trapeznikova S S, Gurtovenko V M, Navasardiants D G
Vopr Med Khim. 1983 Jul-Aug;29(4):95-8.
Effects of acute and chronic alcohol intoxication on activities of arginase, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (AcDH) were studied in rat liver, brain and kidney tissues. Alcohol intoxication altered both ureotelic (liver) and non-ureothelic (brain, kidney) arginase activity. The arginase activity in all the tissues studied was increased in chronic alcohol intoxication. Elevation in the arginase activity in liver tissue indicates that the urea cycle is activated as well as that hyperproduction of glutamic acid in brain may occur. Specific inhibitory effects of ethanol and acetaldehyde might be responsible for alterations of the arginase activity in all the tissues studied in acute alcohol intoxication. In vitro acetaldehyde at 5 X 10(-6) M concentration inhibited the arginase activity in partially purified preparations of brain and kidney tissues by 40-50% and of liver tissue--by 10-15%; 10% ethanol inhibited the liver enzyme by 90% and affected only slightly the activity of brain arginase.
研究了急性和慢性酒精中毒对大鼠肝脏、大脑和肾脏组织中精氨酸酶、乙醇脱氢酶(ADH)和乙醛脱氢酶(AcDH)活性的影响。酒精中毒改变了肝脏的尿素排泄(肝脏)和非尿素排泄(大脑、肾脏)精氨酸酶活性。在慢性酒精中毒时,所有研究组织中的精氨酸酶活性均增加。肝脏组织中精氨酸酶活性的升高表明尿素循环被激活,同时大脑中谷氨酸可能会过度产生。乙醇和乙醛的特异性抑制作用可能是急性酒精中毒时所有研究组织中精氨酸酶活性改变的原因。在体外,5×10⁻⁶ M浓度的乙醛使大脑和肾脏组织部分纯化制剂中的精氨酸酶活性抑制40% - 50%,使肝脏组织中的精氨酸酶活性抑制10% - 15%;10%的乙醇使肝脏酶活性抑制90%,对大脑精氨酸酶活性的影响较小。