Neuroprotection by nitric oxide against hydroxyl radical-induced nigral neurotoxicity
Autor: | I Hanbauer, Chuang C. Chiueh, Kochupurackal P. Mohanakumar |
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Rok vydání: | 1998 |
Předmět: |
Male
Lipid Peroxides Radical Dopamine Pharmacology In Vitro Techniques Nitric Oxide Citric Acid Nitric oxide Lipid peroxidation Rats Sprague-Dawley Cellular and Molecular Neuroscience chemistry.chemical_compound medicine Animals Drug Interactions Ferrous Compounds Hydrogen peroxide Ferrous citrate Hydroxyl Radical Neurotoxicity medicine.disease Corpus Striatum Rats Substantia Nigra nervous system chemistry Biochemistry Hydroxyl radical Sodium nitroprusside medicine.drug |
Zdroj: | Journal of chemical neuroanatomy. 14(3-4) |
ISSN: | 0891-0618 |
Popis: | We investigated the effects of nitric oxide on an in vitro and in vivo generation of hydroxyl radicals, and in vivo neurotoxicity caused by intranigral infusion of ferrous citrate in rats. The formation of hydroxyl radicals in vitro, without exogenous hydrogen peroxide, was dose-dependent. Some nitric oxide donors (e.g. sodium nitroprusside) stimulated, while others (nitroglycerin, diethylamine/nitric oxide, nitric oxide in Ringer's solution) suppressed hydroxyl radical generation in vitro. A significant increase in extra-cellular hydroxyl radicals was detected in a brain microdialysis study. Intranigral infusion of ferrous citrate caused long-lasting lipid peroxidation and dopamine depletion in the ipsilateral nigral region and striatum, respectively. Sub-acute dopamine depletion in the striatum was positively correlated with acute lipid peroxidation in substantia nigra. Intranigral administration of nitric oxide did not affect striatal dopamine. Interestingly, nitric oxide in Ringer's protected nigral neurones against the oxidative injury. The results demonstrate that a regional increase in the levels of iron can result in hydroxyl radical generation and lipid peroxidation leading to neurotoxicity. It also demonstrates that exogenous nitric oxide can act as hydroxyl radical scavenger and protect neurones from oxidative injury. |
Databáze: | OpenAIRE |
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