N-acetylcysteine protects against fluoride-induced oxidative damage in primary rat hepatocytes

Toxicol In Vitro. 2013 Dec;27(8):2279-82. doi: 10.1016/j.tiv.2013.09.019. Epub 2013 Oct 2.


Fluoride induces the overproduction of free radicals, which might in turn affect various biochemical parameters. Therefore, the aim of this study was to elucidate the role of N-acetylcysteine (NAC) in decreasing fluoride-induced oxidative stress. The fluoride intoxicated (0.002; 0.082; 0.164mmol/l) rat hepatocytes was pre-treated (60min) and simultaneously treated with NAC (1mmol/l). The resulting levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and intracellular reduced glutathione (GSH) were measured along with the total antioxidant status (TAS) to determine whether NAC treatment reduced cell damage and/or the antioxidant state. These results suggest that NAC pre-treatment provides protection against fluoride-induced oxidative stress in hepatocytes.

Keywords: Fluoride; Fluorosis; N-acetylcysteine; Oxidative stress; Rat hepatocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcysteine / pharmacology*
  • Animals
  • Antioxidants / pharmacology*
  • Cells, Cultured
  • Glutathione / metabolism
  • Glutathione Peroxidase / metabolism
  • Glutathione Reductase / metabolism
  • Hepatocytes / drug effects*
  • Hepatocytes / metabolism
  • Oxidative Stress / drug effects
  • Rats
  • Rats, Wistar
  • Sodium Fluoride / toxicity*
  • Superoxide Dismutase / metabolism


  • Antioxidants
  • Sodium Fluoride
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Glutathione Reductase
  • Glutathione
  • Acetylcysteine