Meeting Abstract
Oxidative stress, a central mechanism in the aging process, occurs when the production of damaging reactive oxygen species exceeds the ability of antioxidant defense to neutralize these unstable molecules. While it is known that chronic glucocorticoid exposure can increase oxidative stress levels (Glucocorticoid-induced Oxidative Stress), less is understood about how an acute rise in glucocorticoids affects oxidative stress. Recent work from our laboratory has reported that an increase in oxidative stress follows an acute stress response, but whether this is specifically due to increased glucocorticoids remains unclear. We fed Japanese quail (Coturnix japonica) mealworms injected with either corticosterone (CORT quail), the main avian glucocorticoid, or sesame oil (control quail) to determine if corticosterone was responsible for the rise in oxidative stress during an acute stress response. Forty-five min post-ingestion we collected blood samples to measure total antioxidant capacity (TAC) and reactive oxygen metabolites (ROMs). We found that CORT quail had higher plasma corticosterone concentrations 10min post-ingestion compared to control quail. However, while plasma corticosterone levels returned to baseline by 45min in both CORT and control quail, TAC levels were reduced at this time in the CORT compared to the control quail. Plasma ROMs levels did not differ between treatment groups. Lower TAC levels following corticosterone ingestion suggests that acute increases in corticosterone contribute to oxidative stress during an acute stress response.
