Lungs vitamin

Adams et al. 1952). After 5 weeks of an exposure sufficient to induce liver cirrhosis and altered vitamin A concentration in several tissues of the rat, wet lung weight was increased by 10%, but lung vitamin A content remained normal (Chapman et al. 1992). As it appears that lung injury is secondary to renal injury, then the absence of lung effects in animals may be because animals are also less susceptible to the renal injury produced by carbon tetrachloride than are humans. 

Georgieff MK, Radmer WJ, Sowell AL, Yeager PR, Blaner WS, Gunter EW, Johnson DE (1991) The effect of glucocorticoids on serum, liver and lung vitamin A and retinyl ester concentrations. J Pediat Gastroenterol Nutr 13 376-382... 

The American Dietetic Association, the American Heart Association, and the National Heart, Lung and Blood Institute recommend 142—198 g (5—7 02) of lean, trimmed meat daily. It was also pointed out that trimmed meat, especially red meat, provides large amounts of essential nutrients such as iron, 2inc, vitamin balanced protein. The idea that the risk of CHD and cancer can be greatiy reduced by avoiding a meat-centered diet have prompted... 

Vitamins and lipids are often required for animal cells to grow in serum-free medium. Phosphoethanolamine and ethanolamine are key additives that facilitate the growth of the mammary tumor cell line 64024 (Kano-Sueoka and Errick, 1981). In addition, ethanolamine promotes the growth of human lymphocytes and mouse hybridoma cells. Short-term cultures of human diploid lung and foreskin fibroblasts grow in medium that includes among its supplements soybean lecithin, cholesterol, sphingomyelin, and vitamin E. 

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). 

One other study deserves a mention. The Cancer Prevention Study 11 was a prospective investigation using a very large cohort of over one million adult Americans, in which the effects of commercial multivitamin supplements and vitamins A, C or E on mortality were studied, during a follow-up period of seven years. The results were complex in that the use of multivitamins plus vitamins A, C and/or E significantly reduced the risk of lung cancer in both former smokers and life-long non-smokers, but vitamins A, C and E apparently increased the risk in current smokers. 

ALPHA-TOCOPHEROL BETA-CAROTENE (ATBC) CANCER PREVENTION STUDY GROUP (1994) The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers , New Engl J Med, 330, 1029. 

OMENN G S, GOODMAN G E, THORNQUIST M D, BALMES J, CULLEN M R, GLASS A, KEOGH J P, MEYSKENS F L, VALANIS B, WILLIAMS J H, BARNHART S and HAMMAR S (1996) Effects of a combination of beta-carotene and vitamin A on lung cancer and cardiovascular disease. N EnglJ Med 1150-1155. 

SCHMITZ H H, POOR c L, WELLMAN R B and ERDMAN J w Jr (1991) Concentrations of selected carotenoids and vitamin A in human liver, kidney and lung tissue. J Nutr 121(10) 1613-21. 

Maximizing nutritional status through pancreatic enzyme replacement and vitamin and nutritional supplements is necessary for normal growth and development and for maintaining long-term lung function. 

A somewhat related situation can be used to explain the well-publicized lung-cancer inducing effects of P-carotene in heavy smokers. This subpopulation will have low vitamin C levels and hence damage due to smoke components, such as N02 can produce P-CAR which will reach the lung and initiate damage. In nonsmokers, the vitamin C (or other water-soluble antioxidant) is likely to be present in sufficient concentration to preclude this damaging process. Indeed, this speculation has been promoted by the American Chemical Society as the subject of a press release in 1997 (Bohm et al. 1997). 

No information is available on the adverse health effects of hexachloroethane in humans. Animal studies revealed that hexachloroethane primarily causes liver and kidney toxicity. Effects on the nervous system and lungs have also been reported. The mechanism by which these effects are mediated is not well characterized. Reductive metabolism by cytochrome P-450 and production of a free radical intermediate have been suggested as factors in hexachloroethane-induced hepatotoxicity (Nastainczyk et al. 1982a Thompson et al. 1984 Town and Leibman 1984). Accordingly, one possible approach may be to reduce free radical injury. To that end, oral administration of N-acetylcysteine can be used as a means of reducing free radical injury. Also, oral administration of vitamin E and vitamin C may be of value since they are free radical scavengers. 

Carotenoids are of physiological interest because some of them are precursors of vitamin A. They have been in the news recently because many exhibit radical or single oxygen trapping ability and as such have potential antioxidant activity in vivo. They may reduce the risk of cardiovascular disease, lung cancer, cervical... 

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