Environmental Toxin Exposure and Its Impact on Mitochondrial DNA Mutations_ An Epidemiological Study

Abstract

The mitochondria are the main participants of cellular respiration and energy generation, as well as apoptosis. The mitochondrial DNA (mtDNA), a miniature circular chromosome with no histone protection, is extremely susceptible to oxidative stress when generated by reactive oxygen species (ROS). Air pollution and other environmental toxins like heavy metals and pesticides have been reported to cause mitochondrial dysfunction and damage to the mtDNA. These changes can cause dysfunction of the oxidative phosphorylation, decreased production of ATP and the development of chronic illness, such as neurodegenerative, cardiovascular, and metabolic diseases. Although there is an excellent experimental evidence, population-based research has been limited and inconsistent because of the variation on measures of exposure and methods of analysis. To explore the correlation between a chronic exposure to environmental toxins and the burden of mutations and copy number of the mtDNA by means of an epidemiological framework, this study is aimed to examine the two variables. It also investigates the dose response trend as well as the mediating effect of oxidative stress biomarkers. The knowledge of these molecular alterations will help establish a sensitive biomarker of environmental stress (mtDNA). The results will improve the detection of diseases in their early stages, the design of public health policies, and the regulation of health hazards associated with toxins