Potential effects of exposure to contaminants with estrogenic activity are currently being examined in fish from a lake experimentally treated with the synthetic estrogen, ethynylestradiol (EE2). EE2 was added to Lake 260, a small Precambrian shield lake in the Experimental Lakes Area (ELA) of northwestern Ontario, from late May to October 2001. Concentrations of EE2 in epilimnetic waters ranged between 4.0 and 8.1 ng/L, with a mean (±SD) of 6.0 ± 2.8 ng/L. Male fathead minnows (Pimephales promelas) captured from Lake 260 after EE2 additions began contained 9000-fold higher concentrations of the egg yolk precursor vitellogenin (VTG), than were detected in fish captured from the same lake prior to the EE2 additions, or when compared to fatheads from reference lakes during the same sample period. VTG in females was induced 8- to 80-fold and was sustained beyond the normal window of vitellogenesis in Lake 260. Histological examination of tissues from EE2-exposed male fatheads in Lake 260 showed widespread fibrosis and inhibition of testicular development. Enlargement of liver cells, edema in the interstitium between kidney tubules, and eosinophilic deposits in the kidney tubule lumen were also evident in male fatheads from Lake 260. Further studies will examine the relationships between biochemical and histological alterations and population level effects.

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This study compared parr from three strains of rainbow trout Oncorhynchus mykiss to examine intraspecific variation in metabolic traits, hypoxia tolerance and upper thermal tolerance in this species. At the strain level, variation in absolute aerobic scope (AAS), critical oxygen level (O ), incipient lethal oxygen saturation (ILOS) and critical thermal maximum (CT ) generally exhibited consistent differences among the strains, suggesting the possibility of functional associations among these traits. This possibility was further supported at the individual level by a positive correlation between ILOS and O and a negative correlation between O and AAS. These results indicate that intraspecific differences in hypoxia tolerance among strains of O. mykiss may be primarily determined by differences in the ability to maintain oxygen uptake in hypoxia and that variation in aerobic scope in normoxia probably plays a role in determining the ability of these fish to sustain metabolism aerobically as water oxygen saturation is reduced.

Effects of growth acceleration on eye development have been examined in genetically modified salmonids. Growth hormone (GH) transgenic coho salmon ( Oncorhynchus kisutch (Walbaum, 1792)) show dramatically elevated overall body growth and an absolute increase in eye size, but relative eye growth is shifted from negatively allometric to more isometric. Thus, transgenic fish possess significantly smaller eyes relative to nontransgenic fish of the same size. Ration-restricted limitation of growth in transgenic salmon to that of wild type restores relative eye growth rate, suggesting that effects on eyes are an indirect consequence of modification of growth rate rather than a direct effect of GH overexpression. Heart, spleen, and liver did not show changes in proportion among groups, whereas total brain size showed the same response as eye. Relative eye and brain size were also reduced in a fast-growing domesticated strain of rainbow trout ( Oncorhynchus mykiss (Walbaum, 1792)), suggesting modifications of allometry are a more general effect of growth acceleration. GH mRNA levels from the transgene were elevated in eyes, whereas IGF-I mRNA was not, suggesting this organ may be regulated in a different fashion than other organs. Neural tissues with critical structural requirements for optimal function may be subject to less modification of growth rate than are other organ systems.

Carotenoids are primarily responsible for the characteristic red flesh coloration of salmon. Flesh coloration is an economically and evolutionarily significant trait that varies inter- and intra-specifically, yet the underlying genetic mechanism is unknown. Chinook salmon ( Oncorhynchus tshawytscha ) represents an ideal system to study carotenoid variation as, unlike other salmonids, they exhibit extreme differences in carotenoid utilization due to genetic polymorphisms. Here, we crossed populations of Chinook salmon with fixed differences in flesh coloration (red versus white) for a genome-wide association study to identify loci associated with pigmentation. Here, the beta-carotene oxygenase 2-like ( BCO2-l ) gene was significantly associated with flesh colour, with the most significant single nucleotide polymorphism explaining 66% of the variation in colour. BCO2 gene disruption is linked to carotenoid accumulation in other taxa, therefore we hypothesize that an ancestral mutation partially disrupting BCO2-l activity (i.e. hypomorphic mutation) allowed the deposition and accumulation of carotenoids within Salmonidae. Indeed, we found elevated transcript levels of BCO2-l in white Chinook salmon relative to red. The long-standing mystery of why salmon are red, while no other fishes are, is thus probably explained by a hypomorphic mutation in the proto-salmonid at the time of divergence of red-fleshed salmonid genera (approx. 30 Ma).