PARENT SESSION
SA3 - Molecular/Cellular Toxicology
Chair: Schlenk, Dan1, 1 University of California-Riverside, Riverside, CA
8:00 AM to 12:00 PM - Sunday, 17 November 2002
Room Ballroom H
(025) Metals Modulate Aryl Hydrocarbon-Induced Gene Expression and Early Life Stage Toxicity.
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- Natural populations are constantly exposed to a plethora of anthropogenic and naturally occurring chemicals. Metals and aromatic hydrocarbons (AHs) are ubiquitous contaminants that, to some extent, co-occur in virtually all ecosystems. In Atlantic tomcod (Microgadus tomcod), cadmium, nickel, arsenic, and chromium inhibit the in vivo hepatic expression of CYP1A1 mRNA induced by acute exposure to individual AHs. Our hypothesis is that co-exposure to metals can alter AH-induced gene expression and ultimately result in the modulation of some of the phenotypic effects of exposure to AHs. To test this hypothesis, tomcod embryos were exposed until hatching to water contaminated with 1 ppm PCB77 or benzo[a]pyrene (B[a]P), alone or in combination with graded doses of arsenite (0.1 - 10 ppm), chromium (1 - 100 ppm), or zinc (1 and 10 ppm). Some, but not all, the phenotypic effects of exposure to AHs were modulated by co-exposure to the metals. For example, 1 ppm PCB77 or B[a]P induced a high frequency of malformations, including yolk-sac and cardiac edema, and severely underdeveloped or absent jaw. This effect was not altered by the presence of metals in the water. Conversely, both AHs accelerate time to hatching and the presence of NaAsO2 or K2CrO4 in the water completely inhibited this effect. Remarkably, when ZnCl2 was in the water, the AH-induced shortening of the time to hatch was enhanced. The expression of several genes involved the AhR pathway, or that are controlled by it, correlate to some, but not all, the phenotypic effects observed.
Key words: aromatic hydrocarbons, metals, gene expression, early life stage toxicity