Iron release and oxidative DNA damage in splenic toxicity of aniline

Xiaohong Wu, Subburaj Kannan, V-M Ramanujam, M Khan

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Mechanisms by which aniline produces selective toxicity to the spleen are not well understood. Previously, studies showed that aniline exposure induces lipid peroxidation and protein oxidation in the spleen. The present study was aimed to determine the release of free iron and oxidative DNA damage in the spleen following aniline exposure. To achieve this, male SD rats were orally administered 1 mmol/kg/d aniline for 7 d, while controls received the vehicle only. Total splenic iron content showed a significant increase of 200% in the aniline-treated rats, whereas free iron (low-molecular-weight chelatable iron) showed a marked increase of 375% in comparison to controls. Oxidative DNA damage, measured in terms of 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, showed a remarkable increase of 83% in the aniline-treated rats. These results suggest an association between release of free iron and oxidative DNA damage, which could lead to mutagenic and/or carcinogenic responses in the spleen. Copyright

Original languageEnglish (US)
Pages (from-to)657-666
Number of pages10
JournalJournal of Toxicology and Environmental Health - Part A
Volume68
Issue number8
DOIs
StatePublished - Apr 23 2005

Fingerprint

Aniline
DNA Damage
Toxicity
DNA
Iron
toxicity
iron
damage
Spleen
Rats
Lipids
Lipid Peroxidation
lipid
aniline
oxidation
Molecular Weight
Molecular weight
Association reactions
protein
Proteins

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Public Health, Environmental and Occupational Health
  • Pollution
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Iron release and oxidative DNA damage in splenic toxicity of aniline. / Wu, Xiaohong; Kannan, Subburaj; Ramanujam, V-M; Khan, M.

In: Journal of Toxicology and Environmental Health - Part A, Vol. 68, No. 8, 23.04.2005, p. 657-666.

Research output: Contribution to journalArticle

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