The activation of rat peritoneal macrophages by 2,3,7,8-tetrachlorodibenzo-p-dioxin

N. Z. Alsharif, S. J. Stohs

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Abstract

The toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD] and its bioisosteres involves binding to a specific TCDD [Ah] receptor, interaction of this complex with chromatin, and the ultimate production of a pleiotropic response. We have hypothesized that TCDD toxicity also involves the production of oxidative stress [OS], and phagocytic cell activation may be a source of reactive oxygen species [ROS] following TCDD exposure. Evidence is provided for the activation of peritoneal exudate cells [PEC] following exposure of rats to TCDD. Increases of 2.5- and 3-fold in ROS production by PEC were observed 24 hrs following treatment of female Sprague-Dawley rats with a single dose of 50 μg TCDD/kg, utilizing the iodonitrotetrazolium and cytochrome c [cyt-c] reduction assays, respectively. However, no increases in ROS production by isolated PEC were observed following in vitro incubation with 5, 25, 50, 100, 125 and 10,000 ng TCDD/ml of the assay medium using the nitroblue tetrazolium and cyt-c reduction assays. Phorbol myristate acetate was utilized as a positive control and resulted in a 3.5-fold increase in ROS production after a 15 min incubation with 3 × 106 PEC/ml at 37° C. PEC activation may contribute to OS following TCDD exposure, and the process may be receptor mediated.

Original languageEnglish (US)
Pages (from-to)899-904
Number of pages6
JournalChemosphere
Volume25
Issue number7-10
DOIs
StatePublished - Jan 1 1992

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All Science Journal Classification (ASJC) codes

  • Environmental Engineering
  • Environmental Chemistry
  • Chemistry(all)
  • Pollution
  • Health, Toxicology and Mutagenesis

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