Journal of Undergraduate Research


birth defects, glutathione ontogeny, chick embryo model


Life Sciences


Physiology and Developmental Biology


Most chemicals known to cause birth defects have been shown to induce oxidative stress – a disruption in intracellular redox signaling. The overall purpose of this research is to better understand how environmental/chemical insults that cause oxidative stress result in specific malformations. Since the tripeptide glutathione (GSH) is an abundant antioxidant and important mediator in redox state and signaling, the goal of this project was to measure levels of glutathione during early embryonic development in order to determine when embryos are more susceptible to environmental and chemical stresses. Changes in the amount of GSH will affect the sensitivity of cells to reactive oxygen species (ROS) and resulting oxidative stress and damage. Determining which periods of development exhibit low levels of GSH will help us identify times in development when defects are more likely to occur from environmental and chemical insults. We hypothesize that GSH levels will be lower during organogenesis (days 3 and 3.5 in chick embryo) as cell differentiation is driven by a more oxidizing redox state.

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