Developmental toxicology of copper deficiency and excess

摘要

Copper plays a role in several critical processes in the body, including energy production, immune function, oxidative defense, iron mobilization and trafficking, red and white blood cell maturation, neuropeptide synthesis, vessel and bone integrity, and myocardial contractility. Copper deficiency during pregnancy can result in early embryonic death, and gross structural abnormalities of the skeletal, pulmonary, cardiovascular, and central nervous systems. Perinatal copper deficiency can result in persistent immunological and behavioral abnormalities even after the correction of the deficiency. Copper deficiency can arise through low dietary copper intakes, or genetic abnormalities, nutritional interactions, drug interactions, and disease-induced alterations in copper metabolism. The teratogenicity of copper can be attributed in part to excessive oxidative damage, altered angiogenesis, altered composition of extracellular matrix, and low activities of several copper enzymes. Herein we describe the teratogenic effects of copper deficiency on growth and development in humans and animal models. Potential mechanisms that underlie the teratogenecity of copper deficiency are also discussed.