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(P727) Impact of Chromium and Zinc on the Biological Activity of Aromatic Hydrocarbons.
Sorrentino, Claudio*,1, Chambers, Chris2, Courtenay, Simon3, Wirgin, Isaac1, 1 Nelson Institute of Environmental Medicine, NYU School of Medicine, Tuxedo, NY, U.S.A.2 Coastal Ecology Branch, NMFS - Howard Marine Sciences Laboratory, Highlands, NJ, U.S.A.3 Canadian Department of Fisheries and Oceans, Gulf Fisheries Centre, Moncton, New Brunswick, CANADA
ABSTRACT- The expression of cytochrome P4501A1 (CYP1A1) is widely used as a biomarker of exposure to aromatic hydrocarbons (AHs) and early biological effects. In adult Atlantic tomcod (Microgadus tomcod), co-administration of cadmium, nickel, chromium, and arsenic inhibits hepatic CYP1A1 mRNA expression induced by a single i.p. injection of an AH. This study was designed to determine whether zinc and chromium alter AH-induced toxicity in tomcod early life-stages and to correlate the phenotypic alterations, if any, to changes in the expression of AH receptor (AhR) pathway genes. Hudson River (HR) and Miramichi River (MR) tomcod embryos were exposed from day 15 post-fertilization to 1 ppm waterborne PCB77 or benzo[a]pyrene (B[a]P), in the presence or absence of graded doses of ZnCl2 (1 and 10 ppm) or K2CrO4 (1, 10, and 100 ppm). HR embryos hatched earlier (~1 wk) than those from the MR. B[a]P-induced toxicity was markedly different between populations, with the MR embryos being more sensitive (84% mortality in MR vs 9% in HR). In the MR population, B[a]P-induced mortality was gradually inhibited by K2CrO4 and to a lesser extent by ZnCl 2 (max. inhib. 33%). Exposure to either of the AHs decreased the hatching time in both populations by approximately 10 days. ZnCl 2 enhanced B[a]P-induced decrease in hatching time, whereas K2CrO 4 had a limited inhibitory effect. These alterations correlated, at least in part, with changes in the transcription of genes involved in the AhR pathway as measured by slot-blot and RT-PCR on RNA extracted from individual 1-day-old larvae.
Key words: aromatic hydrocarbons, metals, gene expression, early life stage toxicity
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