Ames Bruce N, Atamna Hani, Killilea David W
Nutrition, Metabolisms and Genomics Center, Children's Hospital Oakland Research Institute, Oakland, CA 94609, U States.
Mol Aspects Med. 2005 Aug-Oct;26(4-5):363-78. doi: 10.1016/j.mam.2005.07.007.
Mitochondrial oxidative decay, which is a major contributor to aging, is accelerated by many common micronutrient deficiencies. One major mechanism is inhibition of the pathway of heme biosynthesis in mitochondria, which causes a deficit of heme-a. Heme-a, only found in Complex IV, is selectively diminished, resulting in oxidant leakage and accelerated mitochondrial decay, which leads to DNA damage, neural decay, and aging. We emphasize those deficiencies, which appear to cause damage through this mechanism, particularly minerals such as iron (25% of menstruating women ingest <50% of the RDA) or zinc (10% of the population ingest <50% of the RDA). Several vitamin deficiencies, such as biotin or pantothenic acid, also increase mitochondrial oxidants through this mechanism. Additionally, other minerals such as magnesium and manganese that play a role in mitochondrial metabolism, but do not affect heme directly, are discussed. An optimum intake of micronutrients could tune up metabolism and give a marked increase in health, particularly for the poor, elderly, and obese, at little cost.
线粒体氧化衰退是衰老的主要原因之一，许多常见的微量营养素缺乏会加速这种衰退。一个主要机制是线粒体中血红素生物合成途径受到抑制，这会导致血红素a缺乏。仅存在于细胞色素c氧化酶中的血红素a会选择性减少，导致氧化剂泄漏和线粒体衰退加速，进而导致DNA损伤、神经衰退和衰老。我们强调那些似乎通过这种机制造成损害的缺乏症，特别是矿物质，如铁（25%的经期女性摄入量低于推荐膳食摄入量的50%）或锌（10%的人口摄入量低于推荐膳食摄入量的50%）。几种维生素缺乏症，如生物素或泛酸，也通过这种机制增加线粒体氧化剂。此外，还讨论了其他在线粒体代谢中起作用但不直接影响血红素的矿物质，如镁和锰。最佳的微量营养素摄入量可以调节新陈代谢，并显著改善健康状况，特别是对穷人、老年人和肥胖者而言，成本很低。
