Cytotoxicity and genotoxicity of copper oxide nanoparticles in human skin keratinocytes cells

Int J Toxicol. 2013 Jul;32(4):296-307. doi: 10.1177/1091581813487563. Epub 2013 May 10.

Abstract

The wide scale use of copper oxide nanoparticles (CuONPs) due to their unique properties and important applications in magnetic, thermal, electrical, sensor devices, and cosmetics makes human beings more prone to the exposure of CuONPs and its potential adverse effects. Exposure to such nanoparticles is mainly through skin and inhalation. Therefore, the aim of the present study was to assess the apoptotic and genotoxic potential of CuONPs (50 nm) in the human skin epidermal (HaCaT) cells and its underlying mechanism of cellular toxicity. Significant decreases in cell viability were observed with CuONPs exposure in a dose- and time-dependent manner and also induced significant reduction in glutathione and induction in lipid peroxidation, catalase, and superoxide dismutase in HaCaT cells. A significant increase in caspase-3 activity was observed with CuONPs exposure in HaCaT cells indicating apoptosis. Apoptosis or necrosis was confirmed with fluorescent staining (acridine orange and propidium iodide). The CuONPs also induced DNA damage that was mediated by oxidative stress. This study investigating the effects of CuONPs in human skin cells has provided valuable insights into the mechanism of potential toxicity induced by CuONPs.

Keywords: DNA damage; apoptosis; copper oxide nanoparticles; human skin cells; oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Caspase 3 / metabolism
  • Catalase / metabolism
  • Cell Line
  • Cell Survival / drug effects
  • Copper / toxicity*
  • DNA Damage / drug effects*
  • Glutathione / metabolism
  • Humans
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism
  • L-Lactate Dehydrogenase / metabolism
  • Lipid Peroxidation / drug effects
  • Nanoparticles / chemistry
  • Nanoparticles / toxicity*
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism
  • Skin / cytology
  • Skin / drug effects*
  • Skin / metabolism
  • Superoxide Dismutase / metabolism

Substances

  • Reactive Oxygen Species
  • Copper
  • L-Lactate Dehydrogenase
  • Catalase
  • Superoxide Dismutase
  • CASP3 protein, human
  • Caspase 3
  • Glutathione
  • cuprous oxide