| Popis: |
Stimulation of glutamate receptors induces neuronal nitric oxide (NO) release, which in turn modulates glutamate transmission. The present study evaluated the effects of acute, chronic or combined stress on NO production via the accumulation of nitrite, the stable metabolite of NO, in the prefrontal cortex and hippocampus of male Wistar rats. Given that glutathione (GSH) plays a critical role in protecting cells from oxidative stress, as well as maintaining the thiol redox state, GSH levels in cytosolic fractions of both brain structures were examined. A significant increase in nitrite levels was obtained after 3 weeks of chronic isolation stress, followed by combined stresses (chronic + acute stress). Moreover, GSH levels were significantly decreased after chronic and both combined stresses in both brain structures. Our data support the idea that GSH might represent an important buffer of NO toxicity in the brain, indicating that compromised redox buffering controlled by GSH makes neuronal cells susceptible to endogenous physiological flux of NO. Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry; Belgrade (Serbia); 24-28 September 2012 |
