期刊
ANNALS OF NUTRITION AND METABOLISM
卷 61, 期 3, 页码 207-212出版社
KARGER
DOI: 10.1159/000343106
关键词
Chain-breaking antioxidant; Tocopherols; Tocotrienols; Ataxia with vitamin E deficiency
Vitamin E (alpha-tocopherol) was discovered nearly 100 years ago because it was required to prevent fetal resorption in pregnant, vitamin E-deficient rats fed lard-containing diets that were easily oxidizable. The human diet contains eight different vitamin E-related molecules synthesized by plants; despite the fact that all of these molecules are peroxyl radical scavengers, the human body prefers alpha-tocopherol. The biological activity of vitamin E is highly dependent upon regulatory mechanisms that serve to retain alpha-tocopherol and excrete the non-alpha-tocopherol forms. This preference is dependent upon the combination of the function of alpha-tocopherol transfer protein (alpha-TTP) to enrich the plasma with alpha-tocopherol and the metabolism of non-alpha-tocopherols. alpha-TTP is critical for human health because mutations in this protein lead to severe vitamin E deficiency characterized by neurologic abnormalities, especially ataxia and eventually death if vitamin E is not provided in large quantities to overcome the lack of alpha-TTP. alpha-Tocopherol serves as a peroxyl radical scavenger that protects polyunsaturated fatty acids in membranes and lipoproteins. Although specific pathways and specific molecular targets have been sought in a variety of studies, the most likely explanation as to why humans require vitamin E is that it is a fat-soluble antioxidant. Copyright (C) 2012 S. Karger AG, Basel
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