Smoking and vitamin

NT268 Uejima, Y., Y. Fukuchi, T., Nagase, T. Matsuse, M. Yamaoka, and H. Orimo. Influences of tobacco smoke, and vitamin E depletion on the distal lung of weanling rats. Exp Lung Res 1995 21(4) 631-642. 

Some osteoporosis risk factors (see Table 53-1) are non-modifiable, including family history, age, ethnicity, sex, and concomitant disease states. However, certain risk factors for bone loss may be minimized or prevented by early intervention, including smoking, low calcium intake, poor nutrition, inactivity, heavy alcohol use, and vitamin D deficiency. 

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). 

Persons with a metabolic disturbance in the conversion of cyanide to thiocyanate may be at greater risk. A defect in the rhodanese system and vitamin B12 deficiency have been associated with tobacco amblyopia and Leber s hereditary optic atrophy in persons exposed to cyanide in tobacco smoke (Wilson 1983). 

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

Dorough. Effects of cigarette smoke and dietary vitamin E levels on selected lung and hepatic biotransformation enzymes in mice. Drug Nutr Interact 1985 3(4) 213-222. 

The current RDA for vitamin C is 60 mg/day for a healthy non-smoking adult, Vitamin C is a cofactor for several enzymes involved in the biosynthesis of collagen, neurotransmitters, carnitine (45), hydroxylation of cholesterol (to form bile acids). It is also an important water-soluble antioxidant, which scavenges most of the RS and acts as a coantioxidant by regenerating a-tocopheryl radicals (46). 

The functional interrelationship between vitamin C and vitamin E has been known for a number of years (LL). While dietary vitamin E appears to play a role in determining the levels of vitamin C in the plasma and lungs of cigarette smoked rats, the levels of vitamin E in plasma were not significantly altered by the smoke exposure (31). 

Kune, G.A., Bannerman, S., Field, B. et al., Diet, alcohol, smoking, serum /3-carotene, and vitamin A in male nonmelanocytic skin cancer patients and controls, Nutr. Cancer, 18, 237, 1992. 

The Effect of Smoking on Vitamin C Requirements There is evidence that smokers have a higher requirement for vitamin C than nonsmokers. A number of studies have shown lower plasma and leukocyte concentrations of vitamin C in smokers, but many also report lower intake of the vitamin by smokers. The rate of catabolism of ascorbate is up to 40% greater in smokers than nonsmokers (Kallner et al., 1981), and therefore their vitamin C requirement may be almost twice that of nonsmokers. 

SAFETY PROFILE Moderately toxic by ingestion. Experimental teratogenic and reproductive effects. Questionable carcinogen with experimental neoplastigenic data. Mutation data reported. When heated to decomposition it emits acrid smoke and irritating fumes. See also VITAMIN A. 

Ascorbic acid is required for the synthesis of collagen. It is also a powerful reducing agent (antioxidant) and plays a part in intracellular oxidation-reduction systems, and in mopping up oxidants (free radicals) produced endogenously or in the environment, e.g. cigarette smoke (see Vitamin E). 

Polysorbates are widely used in cosmetics, food products, and oral, parenteral, and topical pharmaceutical formulations and are generally regarded as nontoxic and nonirritant materials. There have, however, been occasional reports of hypersensitivity to polysorbates following their topical and intramuscular use. Polysorbates have also been associated with serious adverse effects, including some deaths, in low-birthweight infants intravenously administered a vitamin E preparation containing a mixture of polysorbates 20 and 80. When heated to decomposition, the polysorbates emit acrid smoke and irritating fumes. 

Scottish Schizophrenia Research Group (2000) Smoking habits and plasma hpid peroxidation and vitamin E levels in neuro-treated first-episode schizophrenia patients. Br. J Psychiatry, 176 290-293. 

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