Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9893155 | Molecular Aspects of Medicine | 2005 | 16 Pages |
Abstract
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.
Keywords
δ-aminolevulinic acid synthetaseα-KGDHRDAflavin adenine dinucleotideδ-ALAPDHferrochelataseTCAPPOPLPCOAα-ketoglutarate dehydrogenaseδ-Aminolevulinate dehydrataseAdenosine TriphosphateATPδ-aminolevulinic acidOxidantsFADrecommended daily allowanceAgingMitochondriaNADnicotinamide adenine dinucleotideHemeprotoporphyrinogen oxidasepyruvate dehydrogenasepyridoxal 5′-phosphatetricarboxylic acid cyclecoenzyme A
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Authors
Bruce N. Ames, Hani Atamna, David W. Killilea,