摘要：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. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.3M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . 105 106 107 108 109 110 111 112 113
Loading...
