Melatonin prevents increases in neural nitric oxide and cyclic GMP production after transient brain ischemia and reperfusion in the Mongolian gerbil (Meriones Unguiculatus)

Juan M. Guerrero, Russel J Reiter, Genaro G. Ortiz, Marta I. Pablos, Ewa Sewerynek, Jih Ing Chuang

Research output: Contribution to journalArticle

96 Citations (Scopus)

Abstract

While nitric oxide (NO) has been implicated as a mediator of glutamate excitotoxicity after cerebral ischemia/reperfusion, melatonin has been reported to inhibit brain NO production by suppressing nitric oxide synthase. The purpose of the present studies was to determine the effect of exogenous melatonin administration on NO-induced changes during brain ischemia/reperfusion. Indicators of cerebral cortical and cerebellar NO production [nitrite/nitrate levels and cyclic guanosine monophosphate(cGMP)] were used to estimate neural changes after transient bilateral carotid artery ligation followed by reperfusion in adult Mongolian gerbils (Meriones unguiculatus). Results show for the first time that melatonin prevents the increases in NO and cGMP production after transient ischemia/reperfusion in frontal cerebral cortex and cerebellum of Mongolian gerbils. The inhibitory effect of melatonin on NO production and its ability to scavenge free radicals and the peroxynitrite anion may be responsible for the protective effect of melatonin on neuronal structures during transient ischemia followed by reperfusion.

Original languageEnglish (US)
Pages (from-to)24-31
Number of pages8
JournalJournal of Pineal Research
Volume23
Issue number1
StatePublished - 1997

Fingerprint

Gerbillinae
Cyclic GMP
Melatonin
Brain Ischemia
Reperfusion
Nitric Oxide
Ischemia
Peroxynitrous Acid
Frontal Lobe
Nitrites
Carotid Arteries
Nitric Oxide Synthase
Cerebral Cortex
Nitrates
Cerebellum
Free Radicals
Anions
Ligation
Glutamic Acid
Brain

Keywords

  • Brain ischemia/reperfusion
  • Melatonin as an antioxidant
  • Neurotoxicity
  • Nitric oxide

ASJC Scopus subject areas

  • Endocrinology

Cite this

Melatonin prevents increases in neural nitric oxide and cyclic GMP production after transient brain ischemia and reperfusion in the Mongolian gerbil (Meriones Unguiculatus). / Guerrero, Juan M.; Reiter, Russel J; Ortiz, Genaro G.; Pablos, Marta I.; Sewerynek, Ewa; Chuang, Jih Ing.

In: Journal of Pineal Research, Vol. 23, No. 1, 1997, p. 24-31.

Research output: Contribution to journalArticle

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AU - Pablos, Marta I.

AU - Sewerynek, Ewa

AU - Chuang, Jih Ing

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N2 - While nitric oxide (NO) has been implicated as a mediator of glutamate excitotoxicity after cerebral ischemia/reperfusion, melatonin has been reported to inhibit brain NO production by suppressing nitric oxide synthase. The purpose of the present studies was to determine the effect of exogenous melatonin administration on NO-induced changes during brain ischemia/reperfusion. Indicators of cerebral cortical and cerebellar NO production [nitrite/nitrate levels and cyclic guanosine monophosphate(cGMP)] were used to estimate neural changes after transient bilateral carotid artery ligation followed by reperfusion in adult Mongolian gerbils (Meriones unguiculatus). Results show for the first time that melatonin prevents the increases in NO and cGMP production after transient ischemia/reperfusion in frontal cerebral cortex and cerebellum of Mongolian gerbils. The inhibitory effect of melatonin on NO production and its ability to scavenge free radicals and the peroxynitrite anion may be responsible for the protective effect of melatonin on neuronal structures during transient ischemia followed by reperfusion.

AB - While nitric oxide (NO) has been implicated as a mediator of glutamate excitotoxicity after cerebral ischemia/reperfusion, melatonin has been reported to inhibit brain NO production by suppressing nitric oxide synthase. The purpose of the present studies was to determine the effect of exogenous melatonin administration on NO-induced changes during brain ischemia/reperfusion. Indicators of cerebral cortical and cerebellar NO production [nitrite/nitrate levels and cyclic guanosine monophosphate(cGMP)] were used to estimate neural changes after transient bilateral carotid artery ligation followed by reperfusion in adult Mongolian gerbils (Meriones unguiculatus). Results show for the first time that melatonin prevents the increases in NO and cGMP production after transient ischemia/reperfusion in frontal cerebral cortex and cerebellum of Mongolian gerbils. The inhibitory effect of melatonin on NO production and its ability to scavenge free radicals and the peroxynitrite anion may be responsible for the protective effect of melatonin on neuronal structures during transient ischemia followed by reperfusion.

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