Baraboĭ V A
Fiziol Zh (1978). 1989 Sep-Oct;35(5):85-97.
A concept on the mechanism of stress response is substantiated proceeding from the data available in literature and obtained from the author's research made on the radiation stress model. The conception envisages that products of lipid peroxidation (LPO) appear as primary (under direct effect of a stress factor on tissues) and secondary (as a consequence of high- and long-term catecholamine++) mediators. Mobilization of stress-realizing systems in that process is regarded as an adequate response of the auto-oxidative++ system to the primary activation of LPO. Transformation of catecholamines into the factor of LPO stimulation (secondary) is a result of an increase in the relative role of the quinoid way to transform catecholamines in the case of their high concentration. Radical intermediates of the quinoid metabolism appear as LPO initiators. An important pathogenetic role of LPO activation in the stress mechanism substantiates expedience to use antioxidants as agents for prophylaxis and early treatment of stress-factor injuries.
基于文献中的现有数据以及作者在辐射应激模型上开展的研究成果，一种关于应激反应机制的概念得以证实。该概念设想，脂质过氧化（LPO）产物作为初级介质（在应激因素对组织的直接作用下）和次级介质（由于高浓度和长期的儿茶酚胺++）出现。在此过程中，应激实现系统的动员被视为自氧化++系统对LPO初级激活的一种适当反应。儿茶酚胺转化为LPO刺激因子（次级）是在其高浓度情况下，醌途径在儿茶酚胺转化中的相对作用增加的结果。醌代谢的自由基中间体作为LPO引发剂出现。LPO激活在应激机制中的重要发病学作用证实了使用抗氧化剂作为预防和早期治疗应激因素损伤药物的合理性。
