Effects of chronic, low dose arsenic exposure on post-translational modifications of mitochondrial proteins
Arsenic is a pervasive natural element that has been known to cause toxicity in humans for centuries. Arsenic is unequally distributed throughout the Earth’s crust. This results in increased risk of human exposure in particular regions of the world. Despite lengthy awareness of the health risks from arsenic exposure, the specific mechanisms through which arsenic enacts its myriad of toxicities remains unclear. Our lab seeks to understand these mechanisms of toxicity to better understand the health risks posed to the general public. Our lab has previously shown that chronic exposure to low levels of arsenic can cause basic energy metabolism in cells to become disrupted. This disruption results in cellular aerobic glycolysis, also known as the Warburg effect, which is one of the hallmarks of cancer. My work will focus on using this model of arsenic exposed cells to study the adverse consequences of altered energy metabolism on cellular function. To accomplish this, I will be utilizing high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) to measure the amount and integrity of energy-producing proteins. Once identified, we can manipulate and study these proteins individually to narrow the field of potential targets of arsenic disruption within the cell. These studies will add to our understanding of arsenic toxicity, allowing for better treatment of arsenic exposed patients and the possibility of preventing arsenic toxicity.