The Role of Peroxide-Dependent Oxidative Stress in Zinc-Induced Toxicity (2013)
Undergraduates: Preeti Kodavanti, Phillip Wages, James Samet (PI)
Faculty Advisor: James Samet
Department: Biology
Cell signaling helps maintain a baseline homeostatic environment. Inhalation of ambient air particles is a common occurrence throughout highly populated urban areas with high levels of factory emissions and motor vehicle combustion. Oxidative stress is a major effect of many environmental agents as a result of alteration of mitochondrial activity. This project specifically focuses on zinc, an abundant metallic element present in ambient air particles, and its role in oxidative stress. In order to experimentally determine and analyze the effects of zinc cytotoxicity and its potential effects on relative oxidative stress patterns, A431 skin carcinoma cells were placed under a set concentration of zinc treatment in the presence of zinc ionophore pyrithione and this was compared to various concentration of standard triton X surfactant via an integrative approach. Exposure of cells to these conditions was controlled in a CO2 chamber. It has been determined that zinc plays a role in cell toxicity and has a greater effect on toxicity under the presence of its co-compound, pyrithione. In comparison to triton X at various concentrations, this confirmed a significant decrease in viable cells over the course of 1-2 hours post-exposure. This may potentially play a role in determining how zinc specifically (from an signal transduction standpoint) affects peroxide-dependent protein sulfenylation and other signaling cascades that result from oxidative stress patterns.