Lack of a heritable reproductive defect in the offspring of male rainbow trout exposed to the environmental estrogen 17α-ethynylestradiol

Kim H Brown; Irvin R Schultz; James J Nagler

doi:10.1016/j.aquatox.2008.10.009

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Lack of a heritable reproductive defect in the offspring of male rainbow trout exposed to the environmental estrogen 17α-ethynylestradiol

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Lack of a heritable reproductive defect in the offspring of male rainbow trout exposed to the environmental estrogen 17α-ethynylestradiol

Kim H Brown, Irvin R Schultz and James J Nagler

Aquatic toxicology, Vol.91(1), pp.71-74

2009

DOI: https://doi.org/10.1016/j.aquatox.2008.10.009

Handle:

https://hdl.handle.net/2376/106162

PMCID: PMC2628308

PMID: 19036459

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https://doi.org/10.1016/j.aquatox.2008.10.009View

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Abstract

Environmental estrogens

Reproduction

Heritability

Progeny survival

17α-ethynylestradiol

Rainbow trout

Endocrine disruptors, including environmental estrogens, have been shown to induce heritable effects through both genetic and epigenetic mechanisms in mammals. Despite this information and the wealth of knowledge regarding the significant reproductive impacts endocrine disruptors impose on fishes, no studies have reported whether the observed effects are heritable. Without this information it is difficult to establish the long-term consequences for exposed populations. To determine potential consequences of long-term effects we must consider the possibility that induced reproductive defects in fishes may be heritable. Using rainbow trout ( Oncorhynchus mykiss) as a model this study aims to determine whether a specific reproductive defect observed in 17α-ethynylestradiol exposed male parents, diminished progeny survival, is heritable in the unexposed surviving F1 males. Semen was collected from anesthetized males of the F1 generation upon sexual maturation at two time-points, one year old precocious males and two years old males. In vitro fertilization was used to produce an F2 generation. F2 embryos were then analyzed for survival at 19 days post-fertilization (eye pigmentation) and the different treatment groups statistically compared to the controls. Analysis indicated that F2 offspring survival from F1 males propagated from both exposed and unexposed parents survive normally and no heritable effect was observed in males from the F1 generation for this specific reproductive defect. These results provide scope for the recovery of fish populations exposed to environmental estrogens should the contaminant be removed.

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Title: Lack of a heritable reproductive defect in the offspring of male rainbow trout exposed to the environmental estrogen 17α-ethynylestradiol
Creators: Kim H Brown - Department of Biological Sciences and Center for Reproductive Biology, University of Idaho, Life Science Building Room 252, PO Box 443051, Moscow, ID 83844-3051, USA
Irvin R Schultz - Battelle PNNL-Marine Science Laboratory, 1529 West Sequim Bay Road, Sequim, WA 98382, USA
James J Nagler - Department of Biological Sciences and Center for Reproductive Biology, University of Idaho, Life Science Building Room 252, PO Box 443051, Moscow, ID 83844-3051, USA
Publication Details: Aquatic toxicology, Vol.91(1), pp.71-74
Academic Unit: UNKNOWN
Publisher: Elsevier B.V
Identifiers: 99900546852901842
Language: English
Resource Type: Journal article