title: Copper and genomic stability in mammals.
abstract: As the free ion and in the form of some complexes, there is no doubt that copper can promote damage to cellular molecules and structures through radical formation. At the same time, and perhaps as a consequence, mammals have evolved means of minimizing levels of free copper ions and destructive copper complexes that enter the organism and its cells. These means include tight binding of copper ions to protein carriers and transporters; direct exchange of copper between protein carriers, transporters, and cuproenzymes; and mobilization of secretory mechanisms and excretory pathways, as needed. As a consequence, normally, and except under certain genetic conditions, copper is likely to be benign to most mammals and not responsible for genomic instability, including fragmentation of and/or alterations to DNA, induction of mutations or apoptosis, or other toxic events. Indeed, cuproenzymes are important members of the antioxidant system of the organism.
authors: Department of Chemistry and Biochemistry, Institute for Molecular Biology and Nutrition, California State University, 92834-6866, Fullerton, CA, USA. mlinder@fullerton.edu
authors: M C
authors: MC
authors: Linder
mesh_terms: D000818:Animals; D003300:Copper / Q000378:metabolism / Q000494:pharmacology*; D004247:DNA / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D006801:Humans; D009154:Mutation
chemical_list: D003300:Copper; D004247:DNA