A fish bioassay to evaluate the toxicity associated with the ingestion of benzo[a]pyrene-contaminated benthic prey.

A bioassay was developed to assess the toxic effects of ingested prey contaminated by polycyclic aromatic hydrocarbons (PAHs) using the teleost Fundulus heteroclitus as a predator and the polychaete Nereis virens as a benthic vector. Ten groups of nine male adult Fundulus were exposed for 21 d to 10 different diets of Nereis contaminated with benzo[a]pyrene (BaP) by spiking dead Nereis with BaP (spiked Nereis [SN] diets, 0-26 microg of BaP per gram dry wt) or by exposing living Nereis to a diet, to sediments, or to both contaminated with BaP (exposed Nereis [EN] diets, 0-16 microg/g dry wt). Another group was exposed to commercial fish food, used as reference diet. Condition and prevalence of histopathological changes were not affected. Exposure to the SN diets containing at least 3.5 microg of BaP per gram dry weight caused an induction of ethoxyresorufin-O-deethylase activity in the intestine but not in the liver. In contrast, fish exposed to the highest doses (> or = 13.4 microg of BaP per gram dry wt) had increased cellular proliferation rate in the liver but not in the intestine. Quantifiable levels of free BaP tetrol-like metabolites were detected in the bile of fish exposed to diets containing more than 6.8 microg/g dry weight of BaP, and exhibited a dose-response relationship in fish exposed to SN diets. For a similar dose of BaP, EN and SN diets had similar effects. Thus, the BaP metabolic products that could have been produced in Nereis apparently did not contribute to the biomarkers responses. This bioassay can be applied to a variety of prey contaminated naturally or experimentally with PAHs. The present study supports the use of intestinal biomarkers, in addition to hepatic biomarkers, in environmental monitoring to assess the impact of dietary exposure to PAHs.

Shifting patterns in genetic control at the embryo-alevin boundary in brook charr.

Maternal inputs to offspring early in development are initially high but the process of development suggests that ontogenetic shifts in the importance of maternal genetic variation relative to other sources should occur. We investigated additive genetic variance and covariance for direct (animal), sire, and maternal effects on embryonic length (EL), yolk sac volume (YSV), and alevin (after yolk sac resorption) length (AL) for 460 embryonic and 460 alevin brook charr (Salvelinus fontinalis) in 23 half-sib families (12 sires, 23 dams). There were no additive genetic effects of sires or individual animals on their own phenotype using sire-dam and maternal-animal models for YSV or EL (h(a)2 < 0.05). However, at the alevin stage we detected low but significant heritability for AL (h(a)2 = 0.14 +/- 0.11). Conversely, maternal genetic effects were high for both embryonic traits (h(EL)2 = 0.61 +/- 0.05; h(YSU)2 = 0.57 +/- 0.06) but faded rapidly for postresorption length (h(AL)2 = 0.18 +/- 0.04). Maternal effects in the sire-dam model corresponded highly with those in the animal-dam model. We did not detect significant genetic covariance between progeny and dams for preresorption traits or between sires and dams for any trait. However, following resorption of the yolk sac, the genetic value of dams for AL was negatively correlated with that of individual progeny (r(m,a) = -0.38 +/- 0.13), suggesting trade-offs and/or stabilizing selection between maternal and animal genetic trait value. This finding was supported by models of dam fecundity on offspring length and dam weight in phenotypic space. Heritability estimates using simple regression of embryo phenotype on adult parental phenotype produced upwardly biased estimates of genetic variance (h2 > 1.0). We propose that development through the embryo-alevin boundary may be a major point in salmonids for ontogenetic changes in the genetic architecture of embryo size from maternal genetic effects to those of the individual organism, and that maternal-offspring conflicts in resource allocation related to size may be partially indicated by negative genetic covariance.