Mitochondrial Epigenetics and Environmental Health: Making a Case for Endocrine Disrupting Chemicals.

摘要: Recent studies implicate mitochondrial dysfunction in the development and progression of numerous chronic diseases, which may be partially due to modifications DNA (mtDNA). There is also mounting evidence that epigenetic mtDNA an additional layer regulation controls biogenesis function. Several environmental factors (eg, smoking, air pollution) have been associated with altered methylation a handful mechanistic observational human studies. However, little understood about other contaminants induce changes. Numerous toxicants are classified as endocrine disrupting chemicals (EDCs). Beyond their actions on hormonal pathways, EDC exposure elevated oxidative stress, occur through or result dysfunction. Although only few assessed impacts EDCs methylation, current review provides reasons consider disruption mechanism action reviews potential limitations related currently available evidence. First, there sufficient (including bisphenols phthalates) directly target function, more direct needed connect this methylation. Second, these potent modulators nuclear epigenetics, including histone modifications. Finally, shown disrupt several methyltransferases transcription factor A/nuclear respiratory 1 pathway. Taken together, highlight need for future research evaluating by detail specific mechanisms responsible such disruptions.