Mitochondrial nitric oxide inhibits ATP synthesis effect of free calcium in rat heart

Alfredo Saavedra-Molina; J. Ramírez-Emiliano; M. Clemente-Guerrero; V. Pérez-Vázquez; L. Aguilera-Aguirre; J. C. González-Hernández

Mitochondrial nitric oxide inhibits ATP synthesis effect of free calcium in rat heart

Alfredo Saavedra-Molina, J. Ramírez-Emiliano, M. Clemente-Guerrero, V. Pérez-Vázquez, L. Aguilera-Aguirre, J. C. González-Hernández

Obstetrics & Gynecology

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

Nitric oxide is a small potentially toxic molecule and a diatomic free radical. We report the interaction of L-arginine, oxygen and calcium with the synthesis of nitric oxide in heart mitochondria. Nitric oxide synthesis is increased in broken rat heart mitochondria compared with intact and permeabilized mitochondria. Intact mitochondria subjected to hypoxia-reoxygenation conditions accumulated nitric oxide that inhibits oxygen consumption and ATP synthesis. ATPase activity is not affected during this augment of nitric oxide. Physiological free calcium concentrations protected mitochondria from the damage caused by the accumulation of nitric oxide. Higher concentrations of the divalent cation increase the damage exerted by nitric oxide.

Original language	English (US)
Pages (from-to)	95-102
Number of pages	8
Journal	Amino Acids
Volume	24
Issue number	1-2
State	Published - Mar 1 2003

Keywords

ATP synthesis
Calcium
Heart
Hypoxia-reoxygenation
Mitochondria
Nitric oxide

ASJC Scopus subject areas

Biochemistry
Clinical Biochemistry
Organic Chemistry

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abstract = "Nitric oxide is a small potentially toxic molecule and a diatomic free radical. We report the interaction of L-arginine, oxygen and calcium with the synthesis of nitric oxide in heart mitochondria. Nitric oxide synthesis is increased in broken rat heart mitochondria compared with intact and permeabilized mitochondria. Intact mitochondria subjected to hypoxia-reoxygenation conditions accumulated nitric oxide that inhibits oxygen consumption and ATP synthesis. ATPase activity is not affected during this augment of nitric oxide. Physiological free calcium concentrations protected mitochondria from the damage caused by the accumulation of nitric oxide. Higher concentrations of the divalent cation increase the damage exerted by nitric oxide.",

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AU - Pérez-Vázquez, V.

AU - Aguilera-Aguirre, L.

AU - González-Hernández, J. C.

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