Shidlovskaia T E
Kosm Biol Aviakosm Med. 1985 Jul-Aug;19(4):45-8.
The intensity of lipid peroxidation in the homogenates and mitochondria of the liver, heart and skeletal muscle of hypokinetic rats was measured. The primary products of lipid peroxidation, i. e., diene conjugates, were accumulated in all tissues on hypokinesia days 3, 15, and 30. The content of the final product--malonic dialdehyde--in the mitochondria increased on hypokinesia days 15 and 30. The low level of NADPH--and ascorbate-dependent lipid peroxidation in the mitochondria at early stages of hypokinesia (up to 15 days) and diene conjugates in homogenates on hypokinesia day 7 can be attributed to an activation of the protective systems of the organism against the immobilization stress. It is suggested that at early stages of hypokinesia the process of lipid peroxidation, or to be more precise lipid hydroperoxidation can be blocked.
对运动不足大鼠肝脏、心脏和骨骼肌匀浆及线粒体中的脂质过氧化强度进行了测定。脂质过氧化的初级产物，即二烯共轭物，在运动不足第3天、第15天和第30天时在所有组织中均有积累。线粒体中最终产物丙二醛的含量在运动不足第15天和第30天时增加。运动不足早期（至15天）线粒体中NADPH和抗坏血酸依赖性脂质过氧化水平较低，以及运动不足第7天时匀浆中二烯共轭物含量较低，这可能归因于机体针对固定应激的保护系统被激活。有人提出，在运动不足的早期阶段，脂质过氧化过程，或者更确切地说是脂质氢过氧化过程可以被阻断。
