INVESTIGATING THE EFFECT OF LIGHT CYCLE ALTERATION ON REACTIVE OXYGEN SPECIES PRODUCTION IN ZEBRAFISH BRAIN**

Evidence from human and animal studies indicate that exposure to disrupted light cycles leads to alterations of the sleep state, poor cognition, neuromediocrity, poor cognitive function, and the risk of developing neuroinflammatory disorders. Zebrafish, with a diurnal circadian rhythm similar to humans, are increasing in popularity as a model in neurophysiology and neuropathophysiology studies. Previous findings from our lab indicated that exposure to chronic unpredictable light cycles resulted in significant alterations to the cell stress response mediated by Heat Shock Protein -70 in the adult zebrafish telencephalon and optic tectum. Furthermore, the AKT-GSK3B signaling pathway widely known to mediate neuronal survival and plasticity pathways was significantly disrupted in both brain areas. The Akt-GSK3B pathway is known to contribute to healthy metabolic function in adult neurons. Here, we subjected adult zebrafish to 4 days of unpredictable light exposure for the purpose of investigating the effect of this stressor on lipid peroxidase, as well as the capacity of stressed neurons to repair oxidative damage by measuring catalase, superoxide dismutase, and glutathione peroxidase activity. Preliminary results indicate increases in lipid peroxidase in fish with exposure to altered light cycles, as well as significant changes in protective enzymes meant to address reactive oxygen species production. These results, if confirmed, will illustrate some of the metabolic underpinnings of cognitive dysfunction that occurs as a result of sleep disruption stress