Microcin J25 triggers cytochrome c release through irreversible damage of mitochondrial proteins and lipids

María V. Niklison-Chirou, Fernando Dupuy, Liliana B. Pena, Susana M. Gallego, Maria Laura Barreiro-Arcos, Cesar Avila, Clarisa Torres-Bugeau, Beatriz E. Arcuri, Augusto Bellomio, Carlos Minahk, Roberto D. Morero

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16 Citations (SciVal)


We previously showed that the antimicrobial peptide microcin J25 induced the over-production of reactive oxygen species with the concomitant release of cytochrome c from rat heart mitochondria via the opening of the mitochondrial permeability transition pore. Here, we were able to demonstrate that indeed, as a consequence of the oxidative burst, MccJ25 induces carbonylation of mitochondrial proteins, which may explain the irreversible inhibition of complex III and the partial inhibition of superoxide dismutase and catalase. Moreover, the peptide raised the levels of oxidized membrane lipids, which triggers the release of cytochrome c. From in silico analysis, we hypothesize that microcin would elicit these effects through interaction with heme c1 at mitochondrial complex III. On the other hand, under an excess of l-arginine, MccJ25 caused nitric oxide overproduction with no oxidative damage and a marked inhibition in oxygen consumption. Therefore, a beneficial anti-oxidative activity could be favored by the addition of l-arginine. Conversely, MccJ25 pro-oxidative-apoptotic effect can be unleashed in either an arginine-free medium or by suppressing the nitric oxide synthase activity.

Original languageEnglish
Pages (from-to)273-281
Number of pages9
JournalInternational Journal of Biochemistry and Cell Biology
Issue number2
Publication statusPublished - 1 Feb 2010


  • Cardiolipin
  • Cytochrome c
  • Microcin
  • Mitochondria
  • Reactive oxygen species

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology


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