Meydani M
Vascular Biology Program, JM USDA-Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
Mech Ageing Dev. 1999 Nov;111(2-3):123-32. doi: 10.1016/s0047-6374(99)00067-6.
Oxidative damage by free radicals, which is the basis for the free radical theory of aging, has been well investigated within the context of oxidant/antioxidant balance. Age-associated disorders are believed to be associated with the time-dependent shift in the antioxidant/prooxidant balance in favor of oxidative stress. In this brief review, the importance of dietary antioxidant intervention on longevity and age-associated changes in bodily functions and diseases are discussed. Evidence has indicated that increasing the endogenous antioxidants defense system and modulation of free radical production by dietary restrictions contribute to increased longevity in animal models. Thus, increasing dietary intake of antioxidants is believed to increase longevity. Earlier studies have shown some increase in median life span in animal models. It was found that supplementing middle-aged (18 months) C57/BL mice with various antioxidants (vitamin E, glutathione, melatonin, and strawberry extract) had no effect on longevity as measured by the average age of death. Therefore, dietary antioxidant supplementation seems unlikely to increase longevity when begun in middle age; supplementation started in early life might be more effective. However, in middle-aged mice, vitamin E was effective in reducing lung viral titer when animals were exposed to influenza virus. Vitamin E supplementation improves cell-mediated immunity in mice and in humans. In addition to modulating the oxidation of low-density lipoproteins, vitamin E can modulate immune/endothelial cells interactions, thus reducing the risk of cardiovascular disease (CVD), a major cause of morbidity and mortality in elderly. Thus, antioxidants such as vitamin E from food sources or supplements appear to be promising for successful aging by improving immune function, and reducing the risk of several age-associated chronic diseases, such as CVD.
自由基造成的氧化损伤是衰老自由基理论的基础,在氧化剂/抗氧化剂平衡的背景下已得到充分研究。与年龄相关的疾病被认为与抗氧化剂/促氧化剂平衡随时间的变化有关,这种变化有利于氧化应激。在这篇简短的综述中,讨论了饮食抗氧化剂干预对寿命以及身体功能和疾病的年龄相关变化的重要性。有证据表明,在动物模型中,增强内源性抗氧化剂防御系统以及通过饮食限制调节自由基产生有助于延长寿命。因此,增加饮食中抗氧化剂的摄入量被认为可以延长寿命。早期研究表明动物模型的平均寿命有所增加。研究发现,给中年(18个月)的C57/BL小鼠补充各种抗氧化剂(维生素E、谷胱甘肽、褪黑素和草莓提取物),以平均死亡年龄衡量,对寿命没有影响。因此,从中年开始补充饮食抗氧化剂似乎不太可能延长寿命;在生命早期开始补充可能更有效。然而,在中年小鼠中,当动物接触流感病毒时,维生素E可有效降低肺部病毒滴度。补充维生素E可改善小鼠和人类的细胞介导免疫。除了调节低密度脂蛋白的氧化外,维生素E还可调节免疫/内皮细胞相互作用,从而降低心血管疾病(CVD)的风险,CVD是老年人发病和死亡的主要原因。因此,来自食物来源或补充剂的抗氧化剂如维生素E似乎有望通过改善免疫功能并降低几种与年龄相关的慢性疾病(如CVD)的风险来实现成功衰老。