The early protective effects of L-arginine and Ng-nitro-L-arginine methyl ester after experimental acute spinal cord injury. A light and electron microscopic study

Yüceer, Nurullah; Attar, Ayhan; Sargon, Mustafa F.; Egemen, Nihat; Türker, R. K.; Demirel, E.

doi:10.1054/jocn.1999.0210

Cited by 9 publications

(10 citation statements)

References 32 publications

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“…For example, the production of nitric oxide was recently identified as a major contributor to neural cell death after SCI (81,114). Although no posttreatment studies exist, pretreatment with N G -nitro-L-arginine methyl ester (L-NAME) has demonstrated some morphological improvements (153). Another promising intervention is activation of A1 adenosine receptors either by adenosine or a selective receptor agonist in a site-specific manner.…”

Section: ) Reduction Of Edema and Free Radical Productionmentioning

confidence: 99%

Recent Advances in Pathophysiology and Treatment of Spinal Cord Injury

Hulsebosch

2002

Advances in Physiology Education

301

219

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Thirty years ago, patients with spinal cord injury (SCI) and their families were told "nothing can be done" to improve function. Since the SCI patient population is reaching normal life expectancy through better health care, it has become an obviously worthwhile enterprise to devote considerable research effort to SCI. Targets for intervention in SCI toward improved function have been identified using basic research approaches and can be simplified into a list: (1) reduction of edema and free-radical production, (2) rescue of neural tissue at risk of dying in secondary processes such as abnormally high extracellular glutamate concentrations, (3) control of inflammation, (4) rescue of neuronal/glial populations at risk of continued apoptosis, (5) repair of demyelination and conduction deficits, (6) promotion of neurite growth through improved extracellular environment, (7) cell replacement therapies, (8) efforts to bridge the gap with transplantation approaches, (9) efforts to retrain and relearn motor tasks, (10) restoration of lost function by electrical stimulation, and (11) relief of chronic pain syndromes. Currently, over 70 clinical trials are in progress worldwide. Consequently, in this millennium, unlike in the last, no SCI patient will have to hear "nothing can be done."

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Section: ) Reduction Of Edema and Free Radical Productionmentioning

confidence: 99%

Recent Advances in Pathophysiology and Treatment of Spinal Cord Injury

Hulsebosch

2002

Advances in Physiology Education

301

219

View full text Add to dashboard Cite

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“…Synthesis of GSH is closely related to the cell redox state represented by NAD(P)H/NAD(P) ratio that is dependent on glucose-6-phosphate dehydrogenase activity. GSH depletion could contribute to neuronal apoptosis in HD through oxidative stress and mitochondrial dysfunction (24).…”

Section: Discussionmentioning

confidence: 99%

Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats

Vasiljevic

Jovanovic

Čolić

et al. 2004

Jugoslav Med Biohem

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The aetiology of neuronal death in neurodegenerative diseases, including Huntington's disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington's disease. The other group of animals were pretreated with 7nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi-and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington's disease.

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“…Zapa`eno je izrazito smanjenje produkcije NOa, kako u strijatumu, mestu direktne aplikacije neurotoksina, tako i u kori prednjeg mozga obostrano u eksperimentalnim grupama `ivotinja koje su pored 1-NAME primile i odgovaraju}u dozu HK (Slike 1 i 2). Prema mi{ljenju mnogih autora, neselektivni NOS inhibitor L-NAME, vr{i supresiju akumulacije nitrita i smanjuje o{te}enje neurona posredovano NMDA-receptorima (21,22). U daljem istra`ivanju kori{}en je 7-NI, nakon ~ije aplikacije je odmah u strijatum data i HK.…”

Section: Diskusijaunclassified

Nitric oxide synthase inhibitors prevents quinolinic acid-induced neurotoxicity: the role of nitric oxide and glucose-6-phosphate dehydrogenase in cell death

Maksimovic

Jovanovic

Colic

et al. 2002

Jugoslav Med Biohem

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In the present study we employed Nw-nitro-L-arginine methyl ester, non-specific potent nitric oxide synthase inhibitor and a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, reportedly to investigate the possible involvement of nitric oxide in quinolinic acid-induced striatal toxicity in the rat. Quinolinic acid was administered unilaterally into striatum of adult Wistar rats in the single dose of 150 nmol/L. The other two group of animals were pretreated with Nw-nitro-L-arginine methyl ester and 7-nitroindazole respectively. Control groups of animals were treated with 0,154 mmol/L saline solution likewise. Nitrite levels was decreased in the ipsi- and contralateral striatum and forebrain cortex in the group treated with nitric oxide synthase inhibitors and neurotoxin compared to quinolinic acid-treated animals. In the same structures, activity of glucose-6-phosphate dehydrogenase was also decreased, compared to quinolinic acid-treated animals. These results indicate that application of the nitric oxide synthase inhibitors, supressed nitrite accumulation and glucose-6-phosphate dehydrogenase activity and attenuated quinolinic acid-induced neuronal damage in the striatum and forebrain cortex.

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The early protective effects of L-arginine and Ng-nitro-L-arginine methyl ester after experimental acute spinal cord injury. A light and electron microscopic study

Cited by 9 publications

References 32 publications

Recent Advances in Pathophysiology and Treatment of Spinal Cord Injury

Recent Advances in Pathophysiology and Treatment of Spinal Cord Injury

Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats

Nitric oxide synthase inhibitors prevents quinolinic acid-induced neurotoxicity: the role of nitric oxide and glucose-6-phosphate dehydrogenase in cell death

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