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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

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

María V Niklison-Chirou1, Fernando Dupuy, Liliana B Pena

  • 1Departamento de Bioquímica de la Nutrición, Instituto Superior de Investigaciones Biológicas (Consejo Nacional de Investigaciones Científicas y Técnicas-Universidad Nacional de Tucumán), Instituto de Química Biológica Dr. Bernabe Bloj, Chacabuco 461, San Miguel de Tucumán 4000, Argentina.

The International Journal of Biochemistry & Cell Biology
|November 17, 2009
PubMed

Insights

The antimicrobial peptide microcin J25 causes mitochondrial damage through oxidative stress. However, adding L-arginine may shift its effects towards beneficial anti-oxidative activity, mitigating damage.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Mitochondrial Biology

Background:

  • Antimicrobial peptides (AMPs) are crucial in innate immunity.
  • Microcin J25 (MccJ25) is an AMP known to induce reactive oxygen species (ROS).
  • Mitochondrial dysfunction is implicated in various pathologies.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which MccJ25 induces mitochondrial damage.
  • To investigate the role of oxidative stress in MccJ25-mediated apoptosis.
  • To explore the potential protective effects of L-arginine against MccJ25 toxicity.

Main Methods:

  • Mitochondrial isolation from rat hearts.
  • Measurement of reactive oxygen species (ROS) production.
  • Assessment of protein carbonylation and lipid oxidation.
  • Analysis of mitochondrial enzyme activity (Complex III, superoxide dismutase, catalase).
  • In silico modeling of MccJ25-heme c1 interaction.
  • Nitric oxide (NO) production assays.

Main Results:

  • MccJ25 induces mitochondrial protein carbonylation and lipid oxidation, leading to cytochrome c release and inhibition of respiratory Complex III.
  • Oxidative burst caused by MccJ25 contributes to mitochondrial dysfunction and apoptosis.
  • L-arginine supplementation promotes nitric oxide overproduction, counteracting MccJ25's pro-oxidative effects and inhibiting oxygen consumption.
  • MccJ25's pro-oxidative and apoptotic effects are dependent on arginine availability and nitric oxide synthase activity.

Conclusions:

  • MccJ25 induces mitochondrial damage via oxidative stress, targeting mitochondrial proteins and lipids.
  • L-arginine can modulate MccJ25's activity, favoring anti-oxidative and potentially therapeutic outcomes.
  • The balance between oxidative stress and nitric oxide production dictates MccJ25's cellular effects.

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