Developmental toxicology, oxidative stress, Nrf and Ahr transcription factors, glutathione
637 N. Pleasant Street
Amherst, MA 01003
Many environmental pollutants, such as PAHs, PCBs, metals, and pesticides, can alter cellular redox state and cause oxidative stress. Oxidative stress during embryonic development can cause birth defects, and may also contribute to the developmental origins of adult disease. However, very little is known about how embryos respond to oxidative stress, or what antioxidant defenses exist during early life stages. How and when do these defenses develop? How are they regulated? And how do these impact developmental toxicity? Could embryonic redox state at the time of chemical exposure be a key factor in determining later-life consequences of early life stage exposures?
Using the zebrafish as a model system, Alicia Timme-Laragy's research aims to elucidate cellular and molecular mechanisms of toxicant-induced oxidative stress in embryonic development, and identify later-life consequences of embryonic exposure to oxidative stress. Of particular interest is understanding how transcription factors, such as Ahr and Nrf2, play a role in the ontogeny and adaptive response of antioxidant defenses during embryonic development.