Nilova N S, Polezhaeva L N
Vopr Med Khim. 1993 Nov-Dec;39(6):28-31.
Neurotization of rats, developed after long-term emotional-painful stress, resulted in activation of lipid peroxidation in brain both within 2 days and 8 days of stress interruption. Compensative activation of the antioxidative protective system in response to increase in lipid peroxidation rate was not observed especially in synaptosomes. Activation of glutathione peroxidase, which is involved in adaptation, was accompanied by inhibition of superoxide dismutase and glutathione transferase. Thus, the balance was impaired between the rate of lipid peroxidation and the mechanisms of antioxidative protection.
长期情绪性疼痛应激后发育的大鼠神经化，在应激中断后的2天和8天内均导致脑内脂质过氧化激活。尤其在突触体中未观察到抗氧化保护系统因脂质过氧化速率增加而产生的代偿性激活。参与适应过程的谷胱甘肽过氧化物酶的激活伴随着超氧化物歧化酶和谷胱甘肽转移酶的抑制。因此，脂质过氧化速率与抗氧化保护机制之间的平衡受到损害。
