ABSTRACT

EROD Activity ................................................................... 182 8.2.2 Phase II of Biotransformation ........................................................... 183

8.3 Resistance in Fish Populations ..................................................................... 184 8.3.1 Reduced CYP1A Inducibility and Sensitivity to Early Life Stage

Toxicities in Resistant Populations of Atlantic Killifish ................... 187 8.3.2 Reduced CYP1A Expression and Sensitivity to Early Life Stage

Toxicities in Atlantic Tomcod from Hudson River ........................... 188 8.3.3 Downstream Effects of the Refractory CYP1A Phenotype in

Killifish ............................................................................................. 189 8.4 Studies of Mechanisms of Resistance in Fish Populations ........................... 190

8.4.1 Heritability of Resistance Phenotypes .............................................. 190 8.4.2 Open-Ended Approaches to Identify Genes Associated with

Resistance ......................................................................................... 191 8.4.3 AHR Pathway Expression and Resistance........................................ 192 8.4.4 AHR Polymorphisms and Resistance ............................................... 193

8.4.4.1 Selection or Random Genetic Drift at AHR2 in Tomcod? ............................................................................. 195

8.4.5 Do Changes in DNA Methylation Contribute to Resistance? ........... 196 8.4.6 Does Histone Modification Occur in Fish Populations and

Contribute to Resistance? ................................................................. 197

Contamination of the environment with organic compounds is a widespread phenomenon and occurs from both point and diffuse nonpoint sources. Aquatic ecosystems are often the final sink for contaminants from both sources. Acute toxicity of adult organisms from chemical exposures is rarely observed anymore in natural populations. However, more subtle and pernicious toxic outcomes may still be prevalent. Two toxic outcomes in fishes from exposure to these chemicals include neoplasia and early life stage toxicities. Fish populations in North American estuaries, European coastal waters, and tributaries of the Laurentian Great Lakes have suffered epizootics of preneoplastic and neoplastic hepatic and skin lesions presumably due to exposure to these contaminants. These examples include systems that are contaminated with polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polyaromatic hydrocarbons (PAHs) (reviewed in Wirgin and Waldman 1998). Two species with documented elevated prevalences of hepatic tumors include Atlantic tomcod from the PCB-contaminated Hudson River, New York (Dey et al. 1993), and Atlantic killifish from the PAH-contaminated Elizabeth River, Virginia (Vogelbein et al. 1990). Studies with flatfishes in Puget Sound, Washington, have indicated that significant relationships exist between tumor levels and sediment concentrations of PAHs, and less strong associations with PCBs (Myers et al. 2003). Furthermore, increased disease prevalence may be exacerbated by other stressors, such as global warming, overharvest, and invasive species (Lafferty et al. 2004).