Journal
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Volume 302, Issue 4, Pages R468-R477Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00538.2011
Keywords
nitric oxide; S-nitrosothiols; anoxia/reoxygenation; cytoprotection; nitric oxide synthase
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Funding
- Research Council of Norway
- Danish Natural Science Research Council
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Sandvik GK, Nilsson GE, Jensen FB. Dramatic increase of nitrite levels in hearts of anoxia-exposed crucian carp supporting a role in cardioprotection. Am J Physiol Regul Integr Comp Physiol 302: R468-R477, 2012. First published November 30, 2011; doi:10.1152/ajpregu.00538.2011.-Nitrite (NO2-) functions as an important nitric oxide (NO) donor under hypoxic conditions. Both nitrite and NO have been found to protect the mammalian heart and other tissues against ischemia (anoxia)-reoxygenation injury by interacting with mitochondrial electron transport complexes and limiting the generation of reactive oxygen species upon reoxygenation. The crucian carp naturally survives extended periods without oxygen in an active state, which has made it a model for studying how evolution has solved the problems of anoxic survival. We investigated the role of nitrite and NO in the anoxia tolerance of this fish by measuring NO metabolites in normoxic, anoxic, and reoxygenated crucian carp. We also cloned and sequenced crucian carp NO synthase variants and quantified their mRNA levels in several tissues in normoxia and anoxia. Despite falling levels of blood plasma nitrite, the crucian carp showed massive increases in nitrite, S-nitrosothiols (SNO), and iron-nitrosyl (FeNO) compounds in anoxic heart tissue. NO2- levels were maintained in anoxic brain, liver, and gill tissues, whereas SNO and FeNO increased in a tissue-specific manner. Reoxygenation reestablished normoxic values. We conclude that NO2- is shifted into the tissues where it acts as NO donor during anoxia, inducing cytoprotection under anoxia/reoxygenation. This can be especially important in the crucian carp heart, which maintains output in anoxia. NO2- is currently tested as a therapeutic drug against reperfusion damage of ischemic hearts, and the present study provides evolutionary precedent for such an approach.
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