Khakimov Z Z, Rakhmanov A Kh, Shaĭkhova G I
Vopr Pitan. 1988 Nov-Dec(6):62-5.
Young rats aged 14 days were subjected to malnutrition during 3.7 and 14 days. Activity of the main microsomal enzymes and lipid peroxidation (LPO) products in the microsomal cytosol fraction of the liver was studied in the test and control (aged 17.21 and 28 days) animals. It has been found that constant malnutrition leads to elevation of amidopyrine demethylase activity and inhibition of c-reductase and aniline hydrolase NADP.H cytochrome activities, as well as to a decreased content of protein and cytochrome P-450 in the liver. At the same time the levels of conjugated dienes and diene-ketones in the microsomal-cytosol fraction of the liver significantly rise that denotes activation of LPO in the microsomal membranes. It has been suggested that the suppression of the monooxygenase system function during malnutrition induces inhibition of the intensity of biotransformation of xenobiotics, including drugs which is responsible for intensification of pharmacodynamics and toxicity of the latter. These conditions should be taken into consideration during drug therapy in patients with malnutrition.
对14日龄的幼鼠进行3至7天及14天的营养不良处理。研究了试验组和对照组(17、21和28日龄)动物肝脏微粒体胞质溶胶部分中主要微粒体酶的活性以及脂质过氧化(LPO)产物。结果发现,持续的营养不良会导致氨基比林脱甲基酶活性升高,c - 还原酶和苯胺水解酶NADP.H细胞色素活性受到抑制,同时肝脏中蛋白质和细胞色素P - 450的含量降低。与此同时,肝脏微粒体胞质溶胶部分中共轭二烯和二烯酮的水平显著升高,这表明微粒体膜中LPO被激活。有人提出,营养不良期间单加氧酶系统功能的抑制会导致包括药物在内的外源性物质生物转化强度的抑制,这会导致药物药效动力学增强和毒性增加。在对营养不良患者进行药物治疗时应考虑这些情况。