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Reactive oxygen species-independent apoptotic pathway by gold nanoparticles in Candida albicans

Minju Seong1, Dong Gun Lee1

  • 1School of Life Sciences, KNU Creative BioResearch Group (BK21 Plus Program), College of Natural Sciences, Kyungpook National University, Daehak-ro 80, Buk-gu, Daegu 41566, Republic of Korea.

Microbiological Research
|February 21, 2018
PubMed

Insights

Gold nanoparticles (AuNPs) trigger programmed cell death in Candida albicans. This study reveals AuNPs induce DNA damage and mitochondrial dysfunction, leading to apoptosis independently of reactive oxygen species (ROS).

Area of Science:

  • Mycology
  • Nanotechnology
  • Cell Biology

Background:

  • Candida albicans is a major human fungal pathogen causing diverse infections.
  • Gold nanoparticles (AuNPs) show potential as antimicrobial agents.
  • Understanding AuNP-induced cell death mechanisms in C. albicans is crucial.

Purpose of the Study:

  • To investigate the intracellular mechanisms by which AuNPs induce cell death in C. albicans.
  • To determine if reactive oxygen species (ROS) play a role in AuNP-mediated apoptosis.

Main Methods:

  • Propidium iodide influx assay to assess membrane permeability.
  • Analysis of DNA damage (condensation, fragmentation).
  • Assessment of mitochondrial dysfunction (mass, Ca2+ concentration, membrane potential).
  • Measurement of intracellular and mitochondrial ROS levels.
  • Evaluation of apoptotic markers (cytochrome c release, metacaspase activation, phosphatidylserine externalization).
  • Inhibition studies using N-acetylcysteine (ROS scavenger).

Main Results:

  • AuNPs did not affect C. albicans membrane permeability.
  • AuNPs induced DNA damage, including nuclear condensation and fragmentation.
  • AuNPs caused mitochondrial dysfunction.
  • Intracellular and mitochondrial ROS levels were maintained, not overproduced.
  • Apoptosis was triggered via cytochrome c release and metacaspase activation.
  • N-acetylcysteine did not inhibit the AuNP-induced apoptotic pathway.

Conclusions:

  • AuNPs induce apoptosis in C. albicans through DNA damage and mitochondrial dysfunction.
  • The apoptotic pathway activated by AuNPs is independent of reactive oxygen species (ROS) signaling.
Keywords:
Candida albicansGenomic DNA interactionsGold nanoparticlesMitochondrial dysfunctionROS-independent apoptosis

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