Oxidation of cardiac myoglobin in vivo by sodium nitrite or hydroxylamine

John W. Nichols, Lavern J. Weber

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

A non-vascularized fish heart model was used to assess the oxidation of cardiac myoglobin in vivo by compounds known to cause methemoglobinemia. Buffalo sculpin (Enophrys bison) were cannulated from the afferent branchial artery to permit repeated blood sampling and injected intraperitoneally with sodium nitrite, hydroxylamine or aniline. Methemoglobin was formed by sublethal levels of sodium nitrite or hydroxylamine. For hydroxylamine, the time to peak effect was less than 1 h. For sodium nitrite, the onset was less rapid and the effect more prolonged. Aniline had no effect on hemoglobin at any concentration tested. Cardiac myoglobin, assayed at the time of peak effect on hemoglobin, was oxidized in a dosedependent manner by sodium nitrite or hydroxylamine. At high doses of sodium nitrite (50 and 100 mg/kg), the oxidation of myoglobin exceeded that of hemoglobin. The reverse was true of hydroxylamine at all concentrations tested. This study suggests the possibility that cardiac myoglobin is oxidized in occupational or other exposures to sodium nitrite, hydroxylamine and related compounds.

Original languageEnglish (US)
Pages (from-to)484-488
Number of pages5
JournalArchives of Toxicology
Volume63
Issue number6
DOIs
StatePublished - Nov 1989

Keywords

  • Aniline
  • Heart
  • Hydroxylamine
  • Myoglobin
  • Sodium nitrite

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