Meeting Abstract
Emerging evidence suggest that mitochondrial processes and structures are reprogrammed during vertebrate development. Developmental exposure to such stressors may alter this reprogramming process leading to persistent effects on metabolism through life. We focused on zebrafish Danio rerio to examine synergistic later life effects of developmental exposure to a chemical (polycyclic aromatic hydrocarbons -PAHs) and physical (temperature) stressor. We focused on temperature and PAHs since thermal fluctuations are common in many aquatic habitats and PAHs are ubiquitously present at low-levels in aquatic sediments. We evaluated effects of early-life exposures to PAH mixtures on embryonic mitochondrial integrity and function at 28oC and 32oC, the persistent bioenergetic effects later in life at tissue and organismal level, and the role of the aryl hydrocarbon receptor (AHR) in mediating these effects. Embryo mitochondrial function was characterized using the XFe24 Extracellular Flux Analyzer. To evaluate persistent effects, mitochondrial function in whole hearts and brains of the adult zebrafish and whole organismal swimming performance and aerobic respiration were examined. Data suggest that early-life exposure to PAH mixtures results in embryonic mtDNA damage, as well as AHR-dependent changes in mitochondrial function. Interestingly, thermal exposure had no effect on embryonic mitochondrial function, but showed altered tissue bioenergetics later in life. Overall, results indicate that low-levels of developmental exposure to multiple abiotic stressors can have persistent whole organismal metabolic effects.
