Reproduction impairment following paternal genotoxin exposure in brown trout (Salmo trutta) and Arctic charr (Salvelinus alpinus)

International audience This work describes some consequences of paternal germ cell DNA damage on the reproduction success in two fish species. Male brown trout (n = 31) and male Arctic charr (n = 28) were exposed to the model genotoxicant MMS at the end of spermatogenesis to generate a significant D...

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Bibliographic Details
Published in:Aquatic Toxicology
Main Authors: Devaux, Alain, Fiat, Luc, Gillet, Christian, Bony, Sylvie
Other Authors: Équipe 5 - Impacts des Polluants sur les Écosystèmes, Laboratoire d'Ecologie des Hydrosystèmes Naturels et Anthropisés (LEHNA), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-École Nationale des Travaux Publics de l'État (ENTPE)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-École Nationale des Travaux Publics de l'État (ENTPE)-Centre National de la Recherche Scientifique (CNRS), Centre Alpin de Recherche sur les Réseaux Trophiques et Ecosystèmes Limniques (CARRTEL), Institut National de la Recherche Agronomique (INRA)-Université Savoie Mont Blanc (USMB Université de Savoie Université de Chambéry )
Format: Article in Journal/Newspaper
Language:English
Published: HAL CCSD 2011
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Online Access:https://hal.science/halsde-00578879
https://doi.org/10.1016/j.aquatox.2010.11.017
Description
Summary:International audience This work describes some consequences of paternal germ cell DNA damage on the reproduction success in two fish species. Male brown trout (n = 31) and male Arctic charr (n = 28) were exposed to the model genotoxicant MMS at the end of spermatogenesis to generate a significant DNA damage level in mature spermatozoa (28% and 25% tail DNA in trout and charr sperm, respectively, evaluated through the comet assay). Sperm from each MMS exposed and control fish was then used to fertilize in vitro an aliquot of a single pool of eggs collected from 4 unexposed females for each species. Each batch of fertilized eggs was monitored individually in the hatchery to follow embryonic and larval abnormalities during the fry development. Paternal exposure did not influence fertilization rate or survival rate at hatching in either species. However, MMS paternal treatment resulted in a large array of morphological abnormalities during embryonic and larval development. At the eyed stage, malformations exhibited a 8 fold increase in trout and a 2 fold increase in charr for larvae stemming from MMS treated males as compared with controls. At the end of yolk sac resorption, an increase in the gross morphological abnormality incidence was found in trout larvae originating from MMS exposed males (2.10% vs. 0.93% in control, p < 0.05). When looking more in detail at bony structures after Alizarin red S staining, a 20% incidence of skeletal defects was recorded at the swimming stage. A positive correlation was found between the paternal sperm DNA damage level and the skeletal abnormality incidence of its progeny. During the next 2 months of development, mortality in trout originating from DNA damaged sperm was 3 times higher than in control. After one year, no effect of paternal treatment was found on growth traits (length and weight) but the gross morphological abnormality incidence was still very high in the treated group (27% malformation incidence vs. 0.5% in control). These results demonstrate ecologically ...