Brain lipid peroxidation and antioxidant status after acute methacrylonitrile intoxication

Drug Chem Toxicol. 2005;28(2):187-95. doi: 10.1081/dct-52536.

Abstract

The status of brain antioxidant enzymes and glutathione in methacrylonitrile (MeAN)-intoxicated Wistar rats was correlated with the levels of lipid peroxidation products. Optimum changes were observed 30 min and 60 min after oral administration of MeAN at dosages of 50 mg/kg body weight per day (0.25 LD50) and 100 mg/kg body weight per day (0.5 LD50). An increase in lipid peroxidation products, decrease in the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), and decrease in reduced glutathione (GSH) were observed. These studies suggest that the membrane lipid peroxidation observed in MeAN intoxication is related, in part, to a compromised antioxidant defense system.

MeSH terms

  • Administration, Oral
  • Animals
  • Brain* / drug effects
  • Brain* / enzymology
  • Brain* / metabolism
  • Catalase / metabolism
  • Dose-Response Relationship, Drug
  • Glutathione
  • Glutathione Peroxidase / metabolism
  • Glutathione Transferase / metabolism
  • Lipid Peroxidation / drug effects*
  • Lipid Peroxides / metabolism
  • Male
  • Methacrylates / toxicity*
  • Nitriles / toxicity*
  • Rats
  • Rats, Wistar
  • Superoxide Dismutase / metabolism
  • Time Factors
  • Toxicity Tests, Acute*

Substances

  • Lipid Peroxides
  • Methacrylates
  • Nitriles
  • methacrylonitrile
  • Catalase
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Glutathione Transferase
  • Glutathione