Decreased placental mitochondrial DNA-content in response to air pollution during in utero life

Abstract

Recent studies have emphasized the importance of PM, and its associated metal components, in the formation of reactive oxygen species (ROS) and inflammation. Mitochondria are the major intracellular sources and primary targets of ROS. Mitochondrial DNA (mtDNA) is particularly vulnerable to ROS-induced damage, resulting in a higher mutation rate that impacts mitochondrial function. Given its multiple essential roles in metabolic pathways, mitochondrial dysfunction (i.e. change in mtDNA-content) is important in fetal development. In utero exposure to environmental factors may influence mitochondrial function which may comprise a mechanism of earlier onset of multifactorial disease such as cardiovascular disease in later life1.