title: [Induction of nitrosative stress in mitochondria of rats hearts in experimental ischemia-reperfusion of the brain and its correction by ecdysterone].
abstract: On the model of focal ischemia-reperfusion of the brain investigated the induction of nitrosative stress in mitochondria of rats hearts and possible mechanisms of protective action of ecdysterone. It is shown that focal ischemia-reperfusion of the brain induced in myocardial mitochondria the activation of constitutive and inducible de novo synthesis of NO by oxidation of L-arginine and not oxidative synthesis of NO through the recovery of oxidized stable metabolites of NO. Strong evidence of induction of nitrosative stress in heart mitochondria by focal ischemia-reperfusion of the brain, was a significant increase in mitochondrial pool of nitrate- and nitrite-anions and pools of nitrosothiols, that is proof of the formation and decay of peroxynitrite--a key marker of nitrosative stress. Also was observed increase in heart mitochondria by focal ischemia-reperfusion of the brain, content key regulator of de novo synthesis of NO-hydrogen sulfide and activity of inducible arginase II and, as a result, the pool of carbamide, which is also a regulator of the synthesis of NO. Previous introduction for animals herbal extract Serratsula coronata, enriched ecdysterone, reduces induction nitrosative stress in mitochondria of rats hearts under conditions of focal ischemia-reperfusion of the brain.
authors.forename: R R
authors.initials: RR
authors.lastname: Sharipov
authors.forename: A V
authors.initials: AV
authors.lastname: Kotsiuruba
authors.forename: B S
authors.initials: BS
authors.lastname: Kop"iak
authors.forename: V F
authors.initials: VF
authors.lastname: Sahach
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000737:chemistry / Q000494:pharmacology*; D001119:Arginase / Q000235:genetics / Q000378:metabolism; D001120:Arginine / Q000378:metabolism; D019659:Asteraceae / Q000737:chemistry; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D004441:Ecdysterone / Q000737:chemistry / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D030421:Peroxynitrous Acid / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology
chemical_list: D000975:Antioxidants; D010936:Plant Extracts; D030421:Peroxynitrous Acid; D009569:Nitric Oxide; D004441:Ecdysterone; D001120:Arginine; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; C113162:Arg2 protein, rat; D001119:Arginase