Kravchenko L V, Kranauskas A E, Dzhaparidze L M, Avren'eva L I, Spirichev V B
Vopr Med Khim. 1986 Nov-Dec;32(6):99-103.
Maintainance of rats within 3 months on a ration with low content of vitamin E (6 mg/kg as compared with 100 mg/kg in control) did not alter distinctly the enzymatic activity in mitochondria, lysosomes and the activity of the enzymes, metabolizing xenobiotics as well as did not affect the permeability of lysosomal and plasmatic membranes. In subacute T-2 mycotoxicosis of rats kept on control ration the following alterations were noted: decrease in activity of lysosomal enzymes, aniline hydroxylase, carboxyl esterase and in content of cytochrome P-450 in liver tissue simultaneously with two-fold activation of epoxide hydrolase and UDP-glucuronosyl transferase; decrease in non-sedimented activity of lysosomal enzymes; decrease in activity of alkaline phosphatase and of lysosomal enzymes in blood serum. After administration of the toxin into vitamin E deficient rats, its effect was increased, hemorrhagic syndrome was distinctly developed, permeability of lysosomal and plasmatic membranes was increased. Subnormal consumption of vitamin E appears to cause destabilization of biological membranes structure, which is manifested under conditions of stress.
用维生素E含量低的日粮(6毫克/千克,而对照组为100毫克/千克)饲养大鼠3个月,并未明显改变线粒体、溶酶体中的酶活性以及代谢外源性物质的酶的活性,也未影响溶酶体膜和质膜的通透性。在以对照日粮饲养的大鼠亚急性T-2霉菌毒素中毒时,观察到以下变化:肝脏组织中溶酶体酶、苯胺羟化酶、羧酸酯酶的活性以及细胞色素P-450的含量降低,同时环氧化物水解酶和UDP-葡糖醛酸基转移酶的活性增加两倍;溶酶体酶的非沉降活性降低;血清中碱性磷酸酶和溶酶体酶的活性降低。给维生素E缺乏的大鼠注射毒素后,其作用增强,明显出现出血综合征,溶酶体膜和质膜的通透性增加。维生素E摄入不足似乎会导致生物膜结构不稳定,这在应激条件下会表现出来。