Pénzes L, Fischer H D, Noble R C
Gerontology Centre, Semmelweis University of Medicine, Budapest, Hungary.
Z Gerontol. 1993 Mar-Apr;26(2):65-9.
A relationship is discussed between free radicals, lipid metabolism, neurotransmitters, and aging. Almost all of the lipid fractions of nerve tissue are heavily exposed during aging to the deleterious effects of a continuous formation of free radicals. In comparative terms, brain tissue has less enzymatic capacity to lower or counteract the rate of lipid peroxidation. However, various defense mechanisms exist that enable phospholipid reconstitution to occur and their metabolic activity to be maintained through reutilization of products arising from their biosynthesis and turnover. The effect of hyperoxygenation or hypoxygenation in association with free radicals generation on neurone stability and neurotransmitters reveals different susceptibilities to neuronal stimuli- and release quotients related to aging. With respect to the relationship between the environment and aging, neurotransmitter mechanisms, exemplified by that of dopamine and its turnover, play an important role in coping with stress, iatrogenic and toxic factors during aging. Possible pharmacological and other ways of mitigating age-related changes by means of protective reactions, accelerated repair processes, and compensatory mechanisms are discussed.
本文探讨了自由基、脂质代谢、神经递质与衰老之间的关系。在衰老过程中，神经组织的几乎所有脂质部分都极易受到自由基持续生成所带来的有害影响。相比之下，脑组织降低或抵消脂质过氧化速率的酶活性较低。然而，机体存在多种防御机制，能够通过重新利用磷脂生物合成和周转产生的产物，实现磷脂的重构并维持其代谢活性。与自由基生成相关的高氧或低氧对神经元稳定性和神经递质的影响，揭示了与衰老相关的神经元刺激和释放商的不同敏感性。就环境与衰老的关系而言，以多巴胺及其周转机制为例的神经递质机制，在应对衰老过程中的应激、医源性和毒性因素方面发挥着重要作用。本文还讨论了通过保护反应、加速修复过程和补偿机制来减轻与年龄相关变化的可能药理学方法及其他方法。
