Hydrogen peroxide release by mitochondria from normal and hypoxic lungs

W. J. Russell, Robert Jackson

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Ischemia/reperfusion mechanisms contribute to lung injury after transplantation, pulmonary embolism, and resolution of atelectasis. Alveolar tissue becomes hypoxic and deprived of substrate only when both ventilation and perfusion are interrupted, a situation modeled in vivo by complete, unilateral lung collapse. Because previously hypoxic mitochondria may be an important intracellular source of superoxide and hydrogen peroxide (H2O2) during reperfusion and re-oxygenation, the authors, in this study, investigated whether mitochondrial H2O2 release changed as a result of lung hypoxia/hypoperfusion resulting from collapse. Mitochondria were isolated from hypoxic (previously collapsed) right or contralateral left rabbits' lungs and from control rabbits' lungs. Mitochondrial H2O2 release, a marker of superoxide production, was measured fluorometrically after incubation with or without 1 mmol/L cyanide and 0.1 mmol/L nicotinamide adenine dinucleotide. Mitochondrial recovery was determined by assaying succinate dehydrogenase activity in mitochondrial preparations and lung homogenates. Lung succinate dehydrogenase activity and mitochondrial recovery were comparable among groups. Calculated lung mitochondrial content did not change (control subjects: left 7.9 ± 0.5, right 13.8 ± 1.7; hypoxic: left 10.3 ± 1.3, right 10.5 ± 2.4, all mg mitochondrial protein/lung). Mitochondria released hydrogen peroxide at approximately 5.6 nmol/h/mg pro in buffer alone and 14.8 nmol/h/mg pro in buffer with cyanide and nicotinamide adenine dinucleotide. However, lung collapse and resulting hypoxia caused no change in mitochondrial number or capacity to release H2O2 in vitro. Based on these findings, it is suggested that other sources of reactive oxygen metabolites, including xanthine oxidase and activated neutrophils, contribute to the oxidant injury observed in this model.

Original languageEnglish
Pages (from-to)239-243
Number of pages5
JournalAmerican Journal of the Medical Sciences
Volume308
Issue number4
StatePublished - Jan 1 1994
Externally publishedYes

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Hydrogen Peroxide
Mitochondria
Lung
Pulmonary Atelectasis
Succinate Dehydrogenase
Cyanides
Superoxides
NAD
Reperfusion
Buffers
Rabbits
Xanthine Oxidase
Mitochondrial Proteins
Lung Injury
Pulmonary Embolism
Oxidants
Ventilation
Neutrophils
Ischemia
Perfusion

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Hydrogen peroxide release by mitochondria from normal and hypoxic lungs. / Russell, W. J.; Jackson, Robert.

In: American Journal of the Medical Sciences, Vol. 308, No. 4, 01.01.1994, p. 239-243.

Research output: Contribution to journalArticle

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