Exposure to Chlorpyrifos and Mitochondrial Dysfunction in a Striatal Cell Model of Huntington’s Disease

Despite the genetic cause of Huntington’s disease (HD), emerging evidence suggests that potential exposure to environmental factors may contribute to the variability in the age of onset, progression, and severity of the disorder. Recognizing some of the shared similarities in the pathophysiological mechanisms in HD and pesticide neurotoxicity such as oxidative stress and mitochondrial dysfunction, we hypothesized that the commonly used pesticide chlorpyrifos would exhibit a disease-toxicant interaction and reveal the influence of CPF in HD neuropathology. Our results suggest that expression of mutant HD protein potentiates CPF neurotoxicity via oxidative stress and mitochondrial dysfunction pathways to cause striatal neuron loss