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There is still controversy whether adverse effects by genotoxic anthropogenic pollutants are linked to the decline of fish populations. Further investigations into the relationship between genotoxic stress and detrimental effects on development and reproduction in fish are required. For this end, zebrafish (F0 generation) were exposed in vivo to the alkylating model genotoxin methyl methanesulfonate (MMS) from fertilization to the age of 1 year. F0 fish were mated over 6 months to check for reproductive capacities. F1 fish grew up without exposure in order to allow for regeneration. Mortality of F0 fish depended on MMS concentrations. In MMS-exposed F0 fish, times of first spawning were delayed and fertility was reduced. Using the alkaline comet assay and the micronucleus test, significant genotoxic effects were found in the livers, gills and gonads of either sex in the F0 generation. No detrimental effects on growth were found. In F1 fish with parental exposure, teratogenic effects were increased, and larval survival was reduced. However, fertility capacities of the non-exposed F1 generation had recovered. Development and survival rates further recovered in the F2 generation. Anthropogenic genotoxicants may thus play a considerable role in the decline of wild fish populations.

Since generative tissues are a link between the generations, the detection of genetic damage in testis and ovary of fish is conductive to elucidating the relationship between genotoxicity and impairment of reproduction. In the current study, exposure of zebrafish to methyl methanesulfonate over two weeks caused concentration dependent genotoxic effects in gonads, liver and gills using the alkaline comet assay. Likewise, the micronucleus frequency was elevated in all of these organs. Thus, the comet assay and the micronucleus test proved appropriate for the detection of genotoxicity in primary male and female gonad cells and histological sections of the gonads from zebrafish, respectively.

The estuary of the River Elbe between Hamburg and the North Sea (Germany) is a sink for contaminated sediment and suspended particulate matter (SPM). One major concern is the effect of human activities on the hydrodynamics, particularly the intensive dredging activities in this area that may result in remobilization of sediment-bound pollutants. The aim of this study was to identify pollutants contributing to the toxicological risk associated with re-suspension of sediments in the Elbe Estuary by use of an effect-directed analysis that combines chemical and biological analyses in with specific fractionation techniques. Sediments were collected from sites along the Elbe Estuary and a site from a small harbor basin of the Elbe Estuary that is known to be polluted. The sixteen priority EPA-PAHs were quantified in organic extracts of sediments. In addition, dioxin equivalents of sediments were investigated by use of the 7-ethoxyresorufin O-deethylase assay with RTL-W1 cells and the Ah receptor-mediated luciferase transactivation assay with H4IIE-luc cells. Quantification of the 16 priority PAHs revealed that sediments were moderately contaminated at all of the sites in the Elbe River Estuary (<0.02-0.906 mu g/g dw). Sediments contained relatively small concentrations of dioxin equivalents (Bio-TEQ) with concentrations ranging from 15.5 to 322 pg/g dw, which were significantly correlated with dioxin equivalents calculated based on toxicity reference values and concentrations of PAH. The concentration of Bio-TEQ at the reference site exceeded 200,000 pg/g dw. In a potency balance the 16 PAHs explained between 47 and 118% of the Bio-TEQ in the luciferase assay, which can be explained by the constant input of PAHs bound to SPM from the upper course of the Elbe River into its estuary. Successful identification of a significant portion of dioxin-like activity to priority PAHs in complex environmental samples such as sediments has rarely been reported.