The effect of N-acetyl cysteine on oxidative stress and apoptosis in the liver tissue of rats exposed to cadmium

Arch Environ Occup Health. 2021;76(8):518-525. doi: 10.1080/19338244.2021.1887796. Epub 2021 Feb 24.

Abstract

We considered the oxidative damage induced by cadmium (Cd) and apoptosis, and the role of N-acetylcysteine (NAC) in preserving cells against Cd toxicity in the liver of male rats. NAC significantly improved total antioxidant capacity (TAC) and decreased malondialdehyde (MDA) in rats exposed to single and continuous dose of Cd. Single and continuous exposure to Cd caused a significant increase in Bax expression (by 1.5-fold and 3.61-fold, respectively) and significant decrease in expression of Bcl2 compared to control (by 9.14-fold and 2.36-fold, respectively). The expression of Caspase 3 and 8 in rats exposed to Cd was significantly higher than control group (P < 0.05). NAC protects liver tissue against Cd by elevating antioxidants capacity, mitigating oxidative stress, as well as down-regulating of apoptotic factors.

Keywords: Antioxidants; N-acetyl cysteine; apoptosis; cadmium; oxidative stress.

MeSH terms

  • Acetylcysteine / pharmacology*
  • Animals
  • Antioxidants / metabolism
  • Apoptosis / drug effects*
  • Cadmium / toxicity*
  • Caspase 3 / genetics
  • Caspase 8 / genetics
  • Gene Expression / drug effects
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Malondialdehyde / metabolism
  • Oxidative Stress / drug effects*
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Rats
  • bcl-2-Associated X Protein / genetics

Substances

  • Antioxidants
  • Bax protein, rat
  • Bcl2 protein, rat
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • Cadmium
  • Malondialdehyde
  • Casp3 protein, rat
  • Casp8 protein, rat
  • Caspase 3
  • Caspase 8
  • Acetylcysteine