Mechanisms of adaptation and fitness costs associated with adaptation to a chemically contaminated environment

Chronic, sublethal exposure to environmental contaminants can lead to physiological and genetic changes at the level of both individuals and populations. This research took as a case study of such phenomena a population of Atlantic killifish (Fundulus heteroclitus) that inhabits a site on the Elizabeth River (VA) with a decades-long history of contamination. Three specific hypotheses were tested in the experiments carried out as part of this research: (1) the ability of the Elizabeth River population of killifish to survive in their polluted environment is due at least in part to genetic adaptations; (2) there are costs (fitness trade-offs) associated with the genetic changes that have occurred in this population; (3) the ability of the Elizabeth River killifish to survive in their highly contaminated environment is associated with changes in the expression and/or activity of xenobiotic metabolism enzymes, changes in parameters associated with antioxidant defenses, or changes in other parameters identifiable through differential display of hepatic mRNA. These hypotheses were tested by using wildcaught killifish from the Elizabeth River and reference sites, as well as their laboratory-raised offspring. Laboratory-raised descendants of Elizabeth River killifish were markedly more resistant to the toxicity of Elizabeth River sediments than were reference site killifish, but also more susceptible to other stressors including low oxygen conditions and photo-enhanced toxicity, confirming the first two hypotheses. Exposure to Elizabeth River sediments caused increases in many of the antioxidant defenses tested in laboratory-raised fish from both populations, and the Elizabeth River killifish showed elevated constitutive levels of several antioxidant defenses in the absence of any chemical exposure. Wildcaught Elizabeth River killifish and their embryonic and larval offspring showed a lack of inducibility of cytochrome P4501A mRNA, protein, and activity, but this lack of inducibility was lost in adults of the first generation of laboratory-raised Elizabeth River killifish, and in all life stages of later generations raised in the laboratory. The hypothesis that the altered expression of cytochrome P4501A was related to the ability to resist the toxicity of the Elizabeth River sediments was not supported by our experiments. Finally, differential display revealed altered expression of multiple hepatic mRNAs in the Elizabeth River killifish (wildcaught and laboratory-raised).