Sapolsky R M, Donnelly T M
Endocrinology. 1985 Aug;117(2):662-6. doi: 10.1210/endo-117-2-662.
Aged males rats show a delay in terminating their adrenocortical stress response and, thus, hypersecrete corticosterone during the poststress period. Because of the numerous catabolic effects of corticosterone, we hypothesized that chronic stress should induce greater pathophysiological changes in aged than in young subjects. We report that stress-induced tumor growth, associated with inoculation with fetal rats cells transformed by tumor virus, is accelerated in aged rats. Furthermore, simulation of the aged pattern of corticosterone hypersecretion in young animals using steroid administration similarly accelerates stress-induced tumor growth.
老年雄性大鼠在终止肾上腺皮质应激反应方面存在延迟，因此在应激后阶段会过度分泌皮质酮。由于皮质酮具有多种分解代谢作用，我们推测慢性应激在老年个体中比在年轻个体中应诱发更严重的病理生理变化。我们报告，与接种由肿瘤病毒转化的胎鼠细胞相关的应激诱导肿瘤生长在老年大鼠中加速。此外，在年轻动物中使用类固醇给药模拟老年皮质酮过度分泌模式同样会加速应激诱导的肿瘤生长。
