Abstract
We attempted to determine if fish that survive toxicant exposure are competitively disadvantaged relative to unexposed cohorts. Coho salmon embryos (27 days old) were subjected to a single, short term (3 h) dose of waterborne n-methyl-n′-nitrosoguanidine (MNNG) (1 μg/ml), were allowed to hatch, and the surviving fish were reared in freshwater hatchery facilities for 6 months. At smoltification, most of the fish (>20 000) were released from the hatchery and allowed to migrate to their natural saltwater feeding grounds; however, a small number (200) were placed in saltwater net pens for one year. In a parallel experiment, 27-day-old embryos were similarly exposed to MNNG ranging from 1–25 μg/ml, but 250 of these fish were retained in freshwater for 10 months and never exposed to saltwater. From the groups that were allowed to migrate, 0·7–0·9% of the fish returned to the hatchery as sexually precocious males (jacks); 4·6–4·7% as sexually mature adults. The return rate, sex ratio, length, weight and pathological condition of treated fish were not statistically different from those of untreated fish. Similarly, no difference between treated and control groups was noted when the mortality rate, growth rate and pathological condition of fish in saltwater net pens were compared. By contrast, fish retained in freshwater showed a dose-dependent decrease in size. In addition, 10–65% of the treated fish (versus 0% of the control fish) developed peripheral nerve neoplasms (neurofibromas). Tumor-bearing fish were the same size as control fish, but tumor-free fish were significantly smaller than control fish. The results of the complete life cycle study revealed no competitive disadvantages arising from toxicant exposure; however, the results of the interrupted life cycle study revealed measurable adverse effects. The data suggest that an unexplained factor related either to saltwater entry, saltwater residence or parr reversion exerted a modifying effect on the consequences of MNNG exposure. Physiological changes associated with smoltification, parr reversion and dietary differences are discussed as possible explanations for the observed differences in body size and tumor prevalence.
Published Version
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