GENE EXPRESSION ANALYSIS TO UNDERSTAND THE ROLE OF ZINC STATUS ON ARSENIC-INDUCED OXIDATIVE STRESS RESPONSE
Sandra Alvarez, Vanessa De La Rosa, Laurie G. Hudson, Jim Liu.
The University of New Mexico College of Pharmacy, Albuquerque, NM.
Groundwater contamination by inorganic arsenic is a global health concern. Within the Navajo tribal community, legacy uranium mining in the area has resulted in groundwater contamination by several toxic metals including arsenic. Long-term exposure to arsenic has been shown to cause an increased risk of cancer, developmental effects, cardiovascular disease, neurotoxicity, and diabetes. Previous studies have shown zinc deficiency and arsenic exposure alter the oxidative stress response, independently. The synergistic effect of zinc deficiency and arsenic exposure on oxidative stress remains unknown and has implications for exacerbating adverse health effects associated with arsenic exposure. The present study aims to investigate how zinc deficiency alters arsenic-induced oxidative stress. Changes in gene expression of key oxidative stress response genes will be measured using qPCR in arsenic treated control THP-1 cells and arsenic treated zinc deficient THP-1 cells. We expect to see increased expression of oxidative stress genes in arsenic-treated zinc deficient cells as compared to normal THP-1 cells, suggesting an increase in cellular oxidative stress as a result of zinc status. An understanding the role of zinc status lays the foundation for developing a zinc supplementation regimen for zinc-deficient populations at high risk for arsenic exposure.