Meerson F Z, Tverdokhlib V P, Nikonorov A A
Vopr Med Khim. 1988 Nov-Dec;34(6):104-9.
Atherogenous dislipoproteinemia, involving a decrease in HDL cholesterol and 3-4-fold increase in the atherogeneity index was found to develop in rats after emotional-pain-dependent stress. Lipid peroxidation was activated in liver tissue of the animals, which was expressed as an increase in the MDA content, a decrease in SOD activity and as marked activation of fructose I-phosphate aldolase, an enzyme specific for liver tissue, in blood serum. The impairment of liver tissue caused an inhibition of 7 alpha-cholesterol hydroxylase--key enzyme of cholesterol hydroxylation into bile acids; the phenomenon may be of importance in development of dislipoproteinemias. Preadaptation of the animals to moderate hypoxia as well as administration of an antioxidant ionol prevented the activation of lipid peroxidation in liver tissue, liberation of fructose I-phosphate aldolase into blood, depression of 7 alpha-cholesterol hydroxylase and protected against the stress-dependent atherogenous dislipoproteinemia. Possible chemical and adaptational protection of liver, which is a very stress-sensitive tissue, is discussed.
发现大鼠在情绪性疼痛依赖应激后会出现致动脉粥样硬化性血脂异常,表现为高密度脂蛋白胆固醇降低以及动脉粥样硬化指数升高3 - 4倍。动物肝脏组织中的脂质过氧化被激活,表现为丙二醛含量增加、超氧化物歧化酶活性降低以及血清中肝组织特异性酶果糖1 - 磷酸醛缩酶明显激活。肝脏组织损伤导致7α - 胆固醇羟化酶(胆固醇羟化生成胆汁酸的关键酶)受到抑制;这一现象可能在血脂异常的发生发展中具有重要意义。动物预先适应中度缺氧以及给予抗氧化剂离子载体可防止肝脏组织脂质过氧化的激活、果糖1 - 磷酸醛缩酶释放入血、7α - 胆固醇羟化酶的抑制,并预防应激依赖性致动脉粥样硬化性血脂异常。文中讨论了对肝脏这种对应激非常敏感的组织可能的化学和适应性保护作用。