Studies on nitric oxide (No), citrulline-no cycle enzmes, arginase, glutamine synthetase and oxidative status in anoxia (Hypobaric Hypoxia) and reperfusion states in rat brain
Nitric oxide is postulated to be involved in the pathophysiology of neurological disorders due to hypoxia/ anoxia in brain due to increased release of glutamate and activation ofNmethyl- D-aspartate receptors. Reactive oxygen species have been implicated in pathophysiology of many neurological di...
Saved in:
| Main Author: | |
|---|---|
| Format: | Monograph |
| Language: | English |
| Published: |
Pusat Pengajian Sains Perubatan
2012
|
| Subjects: | |
| Online Access: | http://eprints.usm.my/55504/1/DR.%20MUMMEDY%20SWAMY%20-%20e.pdf http://eprints.usm.my/55504/ |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | Nitric oxide is postulated to be involved in the pathophysiology of neurological disorders
due to hypoxia/ anoxia in brain due to increased release of glutamate and activation ofNmethyl-
D-aspartate receptors. Reactive oxygen species have been implicated in
pathophysiology of many neurological disorders and in brain function. To understand
their role in anoxia (hypobaric hypoxia) and reperfusion (reoxygenation), the nitric oxide
synthase, argininosuccinate synthetase, argininosuccinate lyase, glutamine synthetase and
arginase activities along with the concentration of nitrate /nitrite, thiobarbituric acid
reactive substances and total antioxidant status were estimated in cerebral cortex,
cerebellum and brain stem of rats subjected to anoxia and reperfusion. The results of this
study clearly demonstrated the increased production of nitric oxide by increased activity
of nitric oxide synthase. The increased activities of argininosuccinate synthetase and
argininosuccinate lyase suggest the increased and effective recycling of citrulline to
arginine in anoxia, making nitric oxide production more effective and contributing to its
toxic effects. The decreased activity of glutamine synthetase may favor the prolonged
availability of glutamic acid catising excitotoxicity leading to neuronal damage iii anoxia
and reperfusion. The increased formation of thiobarbituric acid reactive substances and
decreased total antioxidant status indicate the presence of oxidative stress in anoxia and
reperfusion. The increased arginase and sustained decrease of GS activity in reperfusion
group likely to be protective. |
|---|