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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Gold Nanoparticle Synthesis
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Cationic gold nanoparticles elicit mitochondrial dysfunction: a multi-omics study.

Audrey Gallud1, Katharina Klöditz1, Jimmy Ytterberg2

  • 1Nanosafety & Nanomedicine Laboratory, Division of Molecular Toxicology, Institute of Environmental Medicine, Karolinska Institutet, 171 77, Stockholm, Sweden.

Scientific Reports
|March 15, 2019
PubMed
Summary
This summary is machine-generated.

Cationic gold nanoparticles (Au-NPs) cause cell death by disrupting mitochondria, triggering autophagy. Non-cationic Au-NPs showed no significant toxicity in this nanosafety study.

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Area of Science:

  • Nanosafety
  • Systems Biology
  • Toxicology

Background:

  • Systems biology approaches are vital for understanding nanoparticle (NP) toxicity.
  • Assessing biological responses to engineered nanomaterials is crucial for safety.

Purpose of the Study:

  • To investigate the impact of different gold nanoparticle (Au-NP) surface functionalizations on cellular responses.
  • To elucidate the mechanisms underlying Au-NP-induced cytotoxicity.

Main Methods:

  • Combined transcriptomics and proteomics analysis of human monocytic cells exposed to functionalized Au-NPs.
  • Cytotoxicity screening, in vivo lethality assays in Caenorhabditis elegans.
  • Mitochondrial function assays, cellular localization studies, and autophagy monitoring.

Main Results:

  • Ammonium-terminated Au-NPs exhibited significant cytotoxicity in vitro and in vivo, unlike carboxylated or PEG-ylated Au-NPs.
  • Proteomics and transcriptomics identified mitochondrial dysfunction as a key effect of cationic Au-NPs.
  • Cationic Au-NPs localized in mitochondria, induced autophagy, and cell death was exacerbated by autophagy inhibition.

Conclusions:

  • Cationic Au-NPs induce rapid cell death through mitochondria-dependent pathways.
  • Surface chemistry of Au-NPs critically determines their toxicological profile.
  • Systems biology provides a powerful framework for nanosafety assessment.