作者
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
发表日期
2010/2/1
期刊
The international journal of biochemistry & cell biology
卷号
42
期号
2
页码范围
273-281
出版商
Pergamon
简介
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 …
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MV Niklison-Chirou, F Dupuy, LB Pena, SM Gallego… - The International Journal of Biochemistry & Cell …, 2010