Page 644 - The Toxicology of Fishes

624 The Toxicology of Fishes

fact, large historical effective population sizes and no evidence of recent population bottlenecks were
found for 15 mummichog populations resident to sites along the Atlantic coast of the United States,
including New Bedford Harbor (Adams et al., 2006).
A review of the published literature suggests that the effect of environmental pollutants on genetic
diversity is mixed (van Straalen and Timmermans, 2002). Some researchers suggest more rigorous
experimental designs are required to establish relationships between genetic alterations and environmen-
tal contamination (Belfiore and Anderson, 1998; Theodorakis, 2003). Hebert and Luiker (1996) con-
cluded that no studies in feral fish have demonstrated conclusively that contaminant exposures have
produced selection pressure “strong enough to purge populations of their diversity.” Clearly additional
research is needed before we can use a population genetics approach to properly evaluate costs associated
contaminant exposure or toxicity.

Studies Involving Variation in Specific Genes
Population genetic approaches typically involve identification of variation in genes unrelated to adapta-
tion or other responses to contaminant exposure. Genomic variation at specific loci would be useful to
identify variation in genes that are involved in chemical adaptation. Candidate genes for adaptation in
New Bedford Harbor mummichog include those believed to be associated with toxicological responses
to DLCs (e.g., AhR signal transduction pathway). In New Bedford Harbor mummichog, AhR1 is highly
polymorphic in loci of the ligand-binding regions (Hahn et al., 2004). The adaptive implications of these
genetic changes were investigated using in vitro transcription and translation systems; however, simple
and clear differences between tolerant and sensitive mummichog populations were not revealed (Hahn
et al., 2004). Regions of AhR1 vary between New Bedford Harbor and reference fish, but these variants
do not differ in binding capacity, affinity for TCDD, or ability to support TCDD-dependent transactivation
(Hahn et al., 2004). Ongoing studies are investigating genetic variation and their functional implications
in other regions of the AhR1 (i.e., regulatory region) (S. Cohen, pers. commun.) and other proteins of
the AhR signaling pathway (i.e., AhR2, AhRR) (M. Hahn, pers. commun.).
In addition to those genes associated with toxicological responses to pollutants, other genetic loci may
be subject to selective pressures and adaptive responses in animals surviving highly degraded environ-
ments; for example, the major histocompatibility complex (MHC) is a component of the vertebrate
adaptive immune system. Genetic variation in MHC loci appears to vary in association with specific
diseases (Coltman et al., 1999). Major differences have been observed between amino acid substitution
patterns at the MHC antigen-binding locus of New Bedford Harbor and reference-site mummichog
(Figure 13.17) (Cohen, 2002; Cohen and Nacci, 2002). New Bedford Harbor mummichog and reference-
site mummichog also exhibit increased prevalence and rare types of parasite infestation (Cohen et al.,
2006). In addition, New Bedford Harbor mummichog and their progeny survive laboratory challenges
to Vibrio harveyii better than reference fish (D. Nacci, unpublished data). Whether variation in MHC
represents an adaptation to parasitic or microbial challenge in New Bedford Harbor fish has not been
determined. Additional questions concern the role that chemical stress and habitat degradation may play
in host–parasite exposures, host–parasite cycles, and variation in MHC; for example, reduced parasite
loads in mummichog from Piles Creek in New Jersey, relative to a reference site, were interpreted as a
sign of a disturbed ecosystem (Hudson et al., 2006; Schmalz et al., 2002).

Evolutionary and Ecological Impacts of Resistance
Aquatic environments modified by intense human industrial and agricultural activities are typically
characterized by physical disruption (e.g., channelization), loss of habitat, excessive nutrient and sediment
enrichment, and elevated levels of diverse contaminants. Because any these factors can contribute to
alterations in community structure and function, it is difficult to evaluate the relative contribution of any
single stressor to changes observed at degraded sites; however, demonstration and characterization of
toxicity resistance may allow identification of relationships between: (1) specific biochemical and
molecular responses (biomarkers) of toxicity and resistance, (2) survival of tolerant species, and (3) loss
of sensitive species. Thus, toxicity resistance to specific contaminants in specific species inhabiting these