Guliaeva N V, Luzina N L, Levshina I P, Kryzhanovskiĭ G N
Biull Eksp Biol Med. 1988 Dec;106(12):660-3.
Stress is shown to induce at first the generalized inhibition of lipid peroxidation (LPO), and then the activation of LPO. In brain and blood serum of rats subjected to continuous footshock as well as to restraint stress LPO products decreased and superoxide scavenging activity increased during the initial period of stress, after 1 hour of footshock LPO indices nearly reached normal values, and after 2 hours of footshock the accumulation of LPO products and decrease of superoxide scavenging activity were seen. LPO inhibition was accompanied by accumulation of easy oxidizable brain phospholipids and by depletion of brain cholesterol, during LPO activation brain cholesterol content and cholesterol-phospholipid ratio increased. The content of LPO products--fluorescent Schiff bases in blood plasma of women suffering from algomenorrhea at first decreased (O-12 h) and then dramatically increased (12-24 h) after a onset of pain at the beginning of menstruation. The data suggest that the stage of LPO inhibition precedes its activation during stress.
研究表明，应激首先会引发脂质过氧化（LPO）的普遍抑制，随后则是LPO的激活。在遭受连续足部电击以及束缚应激的大鼠的大脑和血清中，应激初期LPO产物减少，超氧化物清除活性增加；足部电击1小时后，LPO指标几乎达到正常值；足部电击2小时后，可见LPO产物积累以及超氧化物清除活性降低。LPO抑制伴随着易氧化脑磷脂的积累以及脑胆固醇的消耗，而在LPO激活过程中，脑胆固醇含量和胆固醇-磷脂比率增加。痛经女性血浆中LPO产物——荧光席夫碱的含量在月经开始疼痛发作后起初降低（0 - 12小时），然后急剧增加（12 - 24小时）。这些数据表明，在应激过程中，LPO抑制阶段先于其激活阶段。
