Decreased glutamine synthetase, increased citrulline–nitric oxide cycle activities, and oxidative stress in different regions of brain in epilepsy rat model

Abstract

To understand their role in epilepsy, the nitric oxide synthetase (NOS), argininosuccinate synthetase (AS), argininosuccinate lyase (AL), glutamine synthetase (GS), and arginase activities, along with the concentration of nitrate/nitrite (NOx), thiobarbituric acid reactive substances (TBARS), and total antioxidant status (TAS), were estimated in different regions of brain in rats subjected to experimental epilepsy induced by subcutaneous administration of kainic acid (KA). The short-term (acute) group animals were killed after 2 h and the long term (chronic) group animals were killed after 5 days of single injection of KA (15 mg/kg body weight). After decapitation of rats, the brain regions were separated and in their homogenates, the concentration of NOx, TBARS and TAS and the activities of NOS, AS, AL, arginase and glutamine synthetase were assayed by colorimetric methods. The results of the study demonstrated the increased activity of NOS and formation of NO in acute and chronic groups epilepsy. The activities of AS and AL were increased and indicate the effective recycling of citrulline to arginine. The activity of glutamine synthetase was decreased in acute and chronic groups of epilepsy compared to control group and indicate the modulation of its activity by NO in epilepsy. The activity of arginase was not changed in acute group; however it was decreased in chronic group and may favor increased production of NO in this condition. The concentration TBARS were increased and TAS decreased in acute and chronic groups of epilepsy and supports the oxidative stress in epilepsy.

Restoration Of Glutamine Synthetase Activity, Nitric Oxide Levels And Amelioration Of Oxidative Stress By Propolis In Kainic Acid Mediated Excitotoxicity

“…Epileptic form activity was shown to cause excessive production of ROS/RNS, a factor believed to be involved in the mechanisms leading to neurodegeneration and cell death (Itoh and Watanabe, 2009). The increased production of NO and increased oxidative stress in kainic acid mediated excitotoxicity and epilepsy has been reported earlier (Swamy et al, 2009(Swamy et al, , 2011a.…”

“…It was earlier reported that GS becomes nitrated and inhibited during PTZ induced seizure model at repeated PTZ seizure induction, but there was no decrease in GS protein level (Bidmon et al, 2008). Our earlier studies demonstrated that increased production of NO, increased activity of NOS, decreased activity of GS and increased oxidative stress in KA mediated excitotoxicity (Swamy et al, 2009(Swamy et al, , 2011a. Therefore the present study was conducted to assess the neuroprotective effects of the bee product propolis , by estimating the glutamine synthetase activity, nitric oxide (NO), thiobarbituric acid reactive substances (TBARS) concentration and total antioxidant status (TAS) in cerebral cortex (CC), cerebellum (CB) and brain stem (BS) of rats supplemented with propolis and subjected to KA mediated excitotoxicity.…”

Redox Processes in Neurodegenerative Disease Involving Reactive Oxygen Species

“…Its deficiency may couple OS to neuronal death and degeneration, thus providing the basis for novel treatment. The concentration of TBARS was increased and total AO status was decreased in epilepsy, supporting a role for OS [19]. Treatments designed to prevent lipid peroxidation may be more effective for epilepsy prophylaxis than administration of antiepileptic drugs that mask convulsive seizures while brain injury continues [20].…”

Differences in the System of Nitrogen Synthesis and Content of Metabolites in Antioxidant Systems of Sportsmen of Different Sex

“…Unexpectedly, it is possible to explain the increase of activity of iNOS also and decline of activity of arginase metabolism of arginine, namely for limitation of ureapoiesis, which, due to formation of ureidosuckcynate [7] can inhibit such necessary for work iNOS resynthesis of arginine from a citrulline in the citrulline loop [13].…”

“…By reliable reason of growth of iNOS activity(almost exceptionally due to induction of this enzyme) in the process of contention period for sportsmen and for sportswomen, there can be a simultaneous increase of both pools of inductors (inflammatory cytokinites of TNF, Inf-gamma, Il-1 but other) and generation of activator of induction, -super anion oxide [13]. Activating of this enzyme can have negative consequences for work of heart of sportsmen, promoting the apoptosis of cardiomiocytes [11,14].…”