By Lester Packer, Midori Hiramatsu, Toshikazu Yoshikawa
Antioxidant meals vitamins in Human Health discusses new discoveries within the components of oxygen and nitric oxide metabolism and pathophysiology, redox law and mobile signaling, and the id of typical antioxidants and their mechanisms of motion on unfastened radicals and their position in healthiness and disease.
An crucial source for researchers, scholars, and execs in nutrition technological know-how and foodstuff, gerontology, body structure, pharmacology, and comparable components.
* well-being results of antioxidant nutrients
* foodstuff of supplements C and E, selenium, alpha-lipoic acid, coenzyme Q10, carotenoids, and flavonoids
* traditional resource antioxidants, together with pine bark, ginko biloba, wine, herbs,uyaku, and carica papaya
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Additional resources for Antioxidant Food Supplements in Human Health
Feskens, E. J. , Hollman, P. C. , Katan, M. , and Kromhout, D. (1993). Dietary antioxidant flavonoids and the risk of coronary heart disease: The Zuphthen elderly study. Lancet 342, 1007-1011. Hoshina, E. , Allard, J. , and Jeejebhoy, K. N. (1990). Vitamin E suppresses increased lipid peroxidation in cigarette smokers. J. Parenter. Enteral. Nutr. 14, 300-305. , (1995). Cross sectional study of the effects of drinking green tea on cardiovascular and liver diseases. Br. Med. J. 310, 693-696. , and Maatela, J.
39). 98). Thus, the risk appears to be significantly elevated at low levels of both vitamin E and selenium, suggesting that selenium and c~-tocopherol compensate for each other. , 1991b; Knekt 1993). Knekt (1993) also showed that in both nonsmokers and smokers the inverse association between simultaneously high serum levels of c~-tocopherol, /3-carotene, retinol, and selenium and lung cancer risk was stronger than the association for the single nutrients (Knekt, 1993). The present studies demonstrated that selenium and o~-tocopherol apparently compensated for each other.
Oxidative damage to DNA is extensive. It is possible to measure the amount of this damage by measuring the fragments that result from repair of that oxidative DNA damage. Based on the urinary excretion of these DNA fragments, oxidative damage to DNA occurs at an estimated rate of 10 s hits per cell per day in the rat (5) and about 10 4 hits per cell per day in the human (6). These oxidative lesions are effectively but not perfectly repaired; the normal steady-state level of oxida- 3. Nutrition in Chronic Disease Prevention 47 tive DNA lesions is about 106 per cell in the young rat and about twice this in the old rat (5, 7).