Vitamin E protects against iron-hexachlorobenzene induced porphyria and formation of 8-hydroxydeoxyguanosine in the liver of C57BL/10ScSn mice

Monika É Horváth, Stephen P. Faux, Andrew G. Smith, Anna Blázovics, Marco Van Der Looij, János Fehér, Kevin H. Cheeseman

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The effect of vitamin E treatment on total porphyrin content, lipid peroxidation (LOOH) and 8-hydroxydeoxyguanosine (8-OHdG) was studied in the livers of C57BL/10ScSn mice following hexachlorobenzene (HCB) and iron treatment. HCB was administered i.p. (totalling 300 mg/kg) twice, with 1 week interval. Three days after the first HCB injection iron-dextran was given i.p. (500 mg Fe per kg). Vitamin E was administered weekly (20 mg/kg) by s.c. injection. Both total hepatic porphyrin and LOOH levels were significantly (P<0.001) increased in the HCB-iron treated group as compared with the control group. Mice treated additionally with vitamin E had significant (P<0.001) lower levels as compared with the HCB-iron group. Similarly, the levels of 8-OHdG were significantly (P<0.001) increased above controls after HCB-iron treatment and this increase was reduced after co-treatment with vitamin E (P<0.02). The data support the hypothesis that the mechanism of hepatic porphyrinogenicity of HCB with iron overload is an oxidative free radical process.

Original languageEnglish
Pages (from-to)97-102
Number of pages6
JournalToxicology Letters
Issue number1
Publication statusPublished - May 31 2001



  • 8-Hydroxyguanosine
  • DNA
  • Hexachlorobenzene
  • Liver
  • Porphyria
  • Vitamin E

ASJC Scopus subject areas

  • Toxicology

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