DNA adducts and chronic degenerative diseases. Pathogenetic relevance and implications in preventive medicine.
Copyright (c) 1997 Elsevier Science B.V. All rights reserved.
Chronic degenerative diseases are the leading causes of death in developed countries.
Their control is exceedingly difficult due to their multiplicity and diversity, the interconnection with a network of multiple risk factors and protective factors, the long latency and multistep pathogenesis, and the multifocal localization.
Adducts to nuclear DNA are biomarkers evaluating the biologically effective dose, reflecting an enhanced risk of developing a mutation-related disease more realistically than the external exposure dose.
The localization and accumulation of these promutagenic lesions in different organs are the composite result of several factors, including (a) toxicokinetics (first-pass effect) ; (b) local and distant metabolism ; (c) efficiency and fidelity of DNA repair ; and (d) cell proliferation rate.
The last factor will affect not only the dilution of DNA adducts but also the possible evolution towards either destructive processes, such as emphysema or cardiomyopathies, or proliferative processes, such as benign or malignant tumors at various sites.
They also include heart tumors affecting fetal myocytes after transplacental exposure to DNA-binding agents, blood vessel tumors, and atherosclerotic plaques. (...)
Mots-clés Pascal : Homme, DNA, Adduit moléculaire, Lésion, Toxicité, Toxicocinétique, Métabolisme, Epidémiologie, Tumeur, Article synthèse, Athérosclérose, Cardiomyopathie, Appareil circulatoire pathologie, Vaisseau sanguin pathologie, Cardiopathie, Myocarde pathologie
Mots-clés Pascal anglais : Human, DNA, Molecular adduct, Lesion, Toxicity, Toxicokinetics, Metabolism, Epidemiology, Tumor, Review, Atherosclerosis, Cardiomyopathy, Cardiovascular disease, Vascular disease, Heart disease, Myocardial disease
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 97-0365473
Code Inist : 002B30A01A1. Création : 12/09/1997.