Abstract:
:In this study, biphenyl-2,2',6,6'-tetracarbaldehyde, an initial byproduct formed from the ozonation of pyrene, and biphenyl-2,2',6,6'-tetracarboxylic acid, a subsequent pyrene ozonation byproduct, were evaluated using two toxicology assays to compare the toxicity of ozonation byproducts with that of the parent compound. The first assay measured the potential for the compounds to block gap junctional intercellular communication (GJIC) using the scrape loading/dye transfer technique in normal WB-344 rat liver epithelial cells. The second assay evaluated the ability of the compounds to affect neutrophil function by measuring the production of superoxide in a human cell line (HL-60). Pyrene significantly blocked intercellular communication (f = 0.2-0.5) at 40 microM and complete inhibition of communication (f < 0.2) occurred at 50 microM. Gap junctional intercellular communication in cells exposed to biphenyl-2,2',6,6'-tetracarbaldehyde reached f < 0.5 at a concentration of 15 microM. At concentrations greater than 20 microM, biphenyl-2,2',6,6'-tetracarbaldehyde was cytotoxic and the inhibition of GJIC was caused by cell death. Biphenyl-2,2',6,6'-tetracarboxylic acid was neither cytotoxic nor inhibitory to GJIC at the concentrations tested (10-500 microM). Exposure to biphenyl-2,2',6,6'-tetracarbaldehyde resulted in a concentration-dependent decrease in phorbol 12-myristate 13-acetate-stimulated O2- production. Neither exposure to pyrene nor biphenyl-2,2',6,6'-tetracarboxylic acid caused a significant toxic effect on neutrophil function.
journal_name
Environ Toxicol Chemjournal_title
Environmental toxicology and chemistryauthors
Luster-Teasley SL,Ganey PE,DiOrio M,Ward JS 3rd,Maleczka RE Jr,Trosko JE,Masten SJdoi
10.1897/04-679.1subject
Has Abstractpub_date
2005-03-01 00:00:00pages
733-40issue
3eissn
0730-7268issn
1552-8618journal_volume
24pub_type
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