Chlorpyrifos triggers mitochondrial dysfunction in mouse striatal neurons

Student Name: Viran Batth
UCD Department: Molecular Biosciences (Vet Med)
UCD Mentor: Dr. Cecilia Giulivi

Chlorpyrifos (CPF) is an organophosphate found in common pesticides that inhibits the enzyme acetylcholinesterase. Chronic exposure of CPF in humans results in neurological defects, developmental and autoimmune disorders, probably due to the generation of reactive oxygen species (ROS). Furthermore, CPF has been shown to have an effect on the dynamics and movement of mitochondria in rat cortical neurons and to decrease the activity of Complex I in PC12 cells. In this study, precursor neural cells from mouse brain were treated with 10 and 80 µM CPF for 24 hours. ATPase activity was found to be 20% lower on average compared to non-CPF-treated cells, with no changes in citrate synthase activity. Mitochondrial morphology and distribution were also analyzed through confocal microscopy. CPF-treated cells showed a significant decrease in the amount of tubular mitochondria (9% of untreated cells) accompanied by an 80% increase in the number of circular and fragmented mitochondria. Our results demonstrate that CPF exposure affects mitochondrial function suggesting its potential to produce oxidative stress and its involvement in oxidative stress-related neurodegenerative disease.