Nutritional needs in environmental intoxication: vitamin E and air pollution, an example.
Dietary vitamin E affects the susceptibility of mice and rats to ozone and nitrogen dioxide, suggesting a free radical mechanism of toxicity. Conventional peroxidation does not completely explain the effects of alterations of lung fatty acid composition on both nitrogen dioxide and ozone toxicity. A new scheme is proposed based on the cyclization of beta, gamma-allylic peroxyl free radicals to monocyclic and bicyclic peroxides to explain the relationship between diet and toxicity. Similar results are likely with other toxicants producing peroxidation as a mechanism of toxicity. Such cyclic peroxides may mimic or interfere with the prostaglandin system. Several chronic diseases may be exacerbated through such a subtle toxic mechanism. The level of vitamin E needed for protection against peroxidation toxicity may be much greater than the present U. S. dietary intake.
D000393:Air Pollutants / Q000633:toxicity; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D004785:Environmental Pollutants / Q000633:toxicity*; D005227:Fatty Acids / Q000378:metabolism; D005609:Free Radicals; D008168:Lung / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D051379:Mice; D009585:Nitrogen Dioxide / Q000633:toxicity; D009747:Nutritional Physiological Phenomena; D010126:Ozone / Q000633:toxicity; D051381:Rats; D014810:Vitamin E / Q000494:pharmacology*
D000393:Air Pollutants; D004785:Environmental Pollutants; D005227:Fatty Acids; D005609:Free Radicals; D014810:Vitamin E; D010126:Ozone; D009585:Nitrogen Dioxide