Machlin L J, Bendich A
Clinical Nutrition, Hoffmann-La Roche Inc., Nutley, New Jersey 07110.
FASEB J. 1987 Dec;1(6):441-5.
Highly reactive molecules called free radicals can cause tissue damage by reacting with polyunsaturated fatty acids in cellular membranes, nucleotides in DNA, and critical sulfhydryl bonds in proteins. Free radicals can originate endogenously from normal metabolic reactions or exogenously as components of tobacco smoke and air pollutants and indirectly through the metabolism of certain solvents, drugs, and pesticides as well as through exposure to radiation. There is some evidence that free radical damage contributes to the etiology of many chronic health problems such as emphysema, cardiovascular and inflammatory diseases, cataracts, and cancer. Defenses against free radical damage include tocopherol (vitamin E), ascorbic acid (vitamin C), beta-carotene, glutathione, uric acid, bilirubin, and several metalloenzymes including glutathione peroxidase (selenium), catalase (iron), and superoxide dismutase (copper, zinc, manganese) and proteins such as ceruloplasmin (copper). The extent of tissue damage is the result of the balance between the free radicals generated and the antioxidant protective defense system. Several dietary micronutrients contribute greatly to the protective system. Based on the growing interest in free radical biology and the lack of effective therapies for many of the chronic diseases, the usefulness of essential, safe nutrients in protecting against the adverse effects of oxidative injury warrants further study.
被称为自由基的高反应性分子可通过与细胞膜中的多不饱和脂肪酸、DNA中的核苷酸以及蛋白质中的关键巯基键发生反应,从而导致组织损伤。自由基可内源性地源自正常代谢反应,或外源性地作为烟草烟雾和空气污染物的成分,并通过某些溶剂、药物和杀虫剂的代谢以及辐射暴露间接产生。有证据表明,自由基损伤与许多慢性健康问题的病因有关,如肺气肿、心血管疾病、炎症性疾病、白内障和癌症。对抗自由基损伤的防御机制包括生育酚(维生素E)、抗坏血酸(维生素C)、β-胡萝卜素、谷胱甘肽、尿酸、胆红素以及几种金属酶,包括谷胱甘肽过氧化物酶(硒)、过氧化氢酶(铁)和超氧化物歧化酶(铜、锌、锰),还有诸如铜蓝蛋白(铜)等蛋白质。组织损伤的程度是所产生的自由基与抗氧化保护防御系统之间平衡的结果。几种膳食微量营养素对保护系统有很大贡献。鉴于对自由基生物学的兴趣日益浓厚,以及许多慢性疾病缺乏有效疗法,必需、安全的营养素在预防氧化损伤不良影响方面的效用值得进一步研究。