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

Research output: Contribution to journalArticle

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 languageEnglish (US)
Pages (from-to)95-102
Number of pages8
JournalAmino Acids
Volume24
Issue number1-2
StatePublished - 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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    Saavedra-Molina, A., Ramírez-Emiliano, J., Clemente-Guerrero, M., Pérez-Vázquez, V., Aguilera-Aguirre, L., & González-Hernández, J. C. (2003). Mitochondrial nitric oxide inhibits ATP synthesis effect of free calcium in rat heart. Amino Acids, 24(1-2), 95-102.