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PARENT SESSION
MP7 Bioassays for specific hazards
3:00 PM to 6:30 PM, Monday, 07 May 2001
Session Chair: H.T. Ratte
Room 7

(134) Combined chemical and bioassay methods for screening of polycyclic aromatic hydrocarbons in environmental samples.

Machala, Miroslav1, Vondracek, Jan1,2, Blaha, Ludek1,3, Upham, Brad4, Caslavsky, Josef5, Ciganek, Miroslav1, Neca, Jiri1, 1 2 3 4 5

ABSTRACT- Polycyclic aromatic hydrocarbons (PAHs), as well as their their oxygenated and nitrated derivatives, and azaarenes are ubiquitous environmental pollutants. However, contrary to persistent polyhalogenated aromatic hydrocarbons, a relatively high metabolic rate of PAHs complicates assessment of their realistic toxic potencies in both established and novel in vitro assays. In this study, PAHs were extracted from different types of environmental samples, fractioned by LC, and determined by HPLC/DAD, HPLC/MS, GC/MS and MALDI-TOF. Bioassays for the dioxin-like activity, estrogenicity, mutagenicity, and inhibition of gap junctional intercellular communication (GJIC) were used to screen for major adverse effects of contaminants present both in crude extracts and individual fractions in vitro. The last bioassay was used to study processess related to promotion of carcinogenesis.The present study aimed to determine, quantitatively or semi-quantitatively, toxic potencies of individual PAHs and their derivatives to induce dioxin-like activity, estrogenicity and inhibition of GJIC. The toxic equivalency factors were fitted against prototypical inducers of specific effects, including 2,3,7,8-TCDD, 17-estradiol and fluoranthene, and they were used to calculate the toxic equivalents of PAHs in environmental samples. While specific receptor-mediated estrogenicity did not appear to be an important mode of action of PAHs, a number of tested PAHs, as well as their complex environmental mixtures, showed strong dioxin-like activity and inhibition of GJIC potencies, suggesting a significant contribution of PAHs to these modes of toxicity. [Supported by the grant No. NAZV/QC-0194.]

Key words: pahs, dioxin-like toxicity, estrogenicity, gap-junctional intercellular communication