The prenatal environment and its influence on maternal and child mitochondrial DNA copy number and methylation: A review of the literature
Anna R. Smith, Alejandra Hinojosa Briseño, Martin Picard, Andrés Cárdenas
Abstract
Mitochondrial DNA (mtDNA) is sensitive to environmental stressors and associated with human health. We reviewed epidemiological literature examining associations between prenatal environmental, dietary, and social exposures and alterations in maternal/child mtDNA copy number (mtDNAcn) and mtDNA methylation. Evidence exists that prenatal maternal exposures are associated with alterations in mtDNAcn for air pollution, chemicals (e.g. metals), cigarette smoke, human immunodeficiency virus (HIV) infection and treatment. Evidence for their associations with mtDNA methylation was limited. Given its potential implications as a disease pathway biomarker, studies with sufficient biological specificity should examine the long-term implications of prenatal and early-life mtDNA alterations in response to prenatal exposures.