A catalyst of peroxynitrite decomposition inhibits murine experimental autoimmune encephalomyelitis

Anne H. Cross, Manuel San, Michael K. Stern, Richard M. Keeling, Daniela Salvemini, Thomas P. Misko

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37 Scopus citations


Peroxynitrite (PN), the product of nitric oxide (NO) reacted with superoxide, is generated at sites of inflammation. Nitrotyrosine (NT), a marker of PN formation, is abundant in lesions of acute experimental autoimmune encephalomyelitis (EAE), and in active multiple sclerosis (MS) plaques. To determine whether PN plays a role in EAE pathogenesis, mice induced to develop EAE were treated with a catalyst specific for the decomposition of PN. Because this catalyst has no effect upon NO, using it allowed differentiation of PN-mediated effects from NO-mediated effects. Mice receiving the PN decomposition catalyst displayed less severe clinical disease, and less inflammation and demyelination than control mice. Encephalitogenic T cells could be recovered from catalyst-treated mice, indicating that the PN decomposition catalyst blocked the pathogenic action of PN at the effector stage of EAE, but was not directly toxic to encephalitogenic T cells. PN plays an important role distinct from that of NO in the pathogenesis of EAE, a major model for MS. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)21-28
Number of pages8
JournalJournal of Neuroimmunology
Issue number1
StatePublished - Jul 10 2000


  • Experimental autoimmune encephalomyelitis
  • Multiple sclerosis
  • Nitric oxide
  • Peroxynitrite
  • Superoxide


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