Mutagens: Some possible health impacts beyond carcinogenesis
1983; Wiley; Volume: 5; Issue: 2 Linguagem: Inglês
10.1002/em.2860050204
ISSN1930-238X
Autores Tópico(s)DNA Repair Mechanisms
ResumoEnvironmental MutagenesisVolume 5, Issue 2 p. 139-152 Research Paper Mutagens: Some possible health impacts beyond carcinogenesis Philip E. Hartman, Corresponding Author Philip E. Hartman Department of Biology, The Johns Hopkins University, BaltimoreDepartment of Biology, The Johns Hopkins University, Baltimore, MD 21218Search for more papers by this author Philip E. Hartman, Corresponding Author Philip E. Hartman Department of Biology, The Johns Hopkins University, BaltimoreDepartment of Biology, The Johns Hopkins University, Baltimore, MD 21218Search for more papers by this author First published: 1983 https://doi.org/10.1002/em.2860050204Citations: 33AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Considerable attention is currently being given to the roles of environmental and endogenous mutagens in tumor induction and in tumor progression through the abilities of mutagens to induce one or another kind of somatic mutation. It is proposed here that mutagens, also through induction of somatic mutations, initiate a spectrum of additional, much more common, focal lesions that are important to the human condition. While individually they are of relative insignificance and thus neglected by many clinicians, the functional attributes of these focal lesions have important impacts on human physiology and thus contribute substantially to the process of aging. Additionally, one individual focus may progress to an extent that it produces clinically recognizible symptoms and may even jeopardize the carrier's life. The ultimate and developed expression of these lesions is heterogeneous, is far removed in time from initial induction, and relies on additional host and environmental factors for expression; therefore, the possible role of somatic mutation is readily overlooked. The focal lesions reviewed are fibrous atherosclerotic plaques, senile cataracts, and metaplasias. Literature that implicates metaplasias as precursor or as predisposing lesions in the ultimate formation of gallstones, duodenal ulcers, and adenocarcinomas is summarized. References Albert RE, Vanderlaan M, Burns FJ, Nishizumi M (1977): Effect of carcinogens on chicken atherosclerosis. Cancer Res 37: 2232–2235. Albores-Saavedra J, Cruz-Ortiz H, Alcantara-Vazques A, Hensen DE (1981): Usual types of gallbladder carcinoma. Arch Pathol Lab Med 105: 287–293. Antonius JI, Gump FE, Lattes R, Lepore M (1960): A study of certain microscopic features in regional enteritis, and their possible significance. Gastroenterol 38: 889–905. 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