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

Abstract

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.

Transgenerational effects from early developmental exposures to bisphenol A or 17α-ethinylestradiol in medaka, Oryzias latipes

“…Toxicological studies that examined effects of environmental chemicals such as BPA and EE2 have identified several phenotypic abnormalities in fish and other species, with reproductive impairment among the reported phenotypic defects 14 . In a transgenerational study with rainbow trout, studies suggest that EE2 exposure in males caused diminished progeny survival in F1, but did not cause similar effects in F2 embryos 21 . However, no information is available on embryo survival at F3 and F4 generations.…”

“…In contrast, the activity of BPA mediated by estrogen receptors associated with the cell membrane is equal to that of estradiol 20 . Both compounds are present in water at concentrations that are sufficient to affect development, osmoregulation, and reproduction in aquatic organisms 14 21 . Specifically, BPA occurs in the ng/L range in surface waters and up to the mg/L range in groundwater 14 , and once in sediment, does not readily degrade 22 .…”

Can metal stress induce transferable changes in gene transcription in Daphnia magna?

“…Although possibly of major importance to environmental toxicology and risk assessment, studies on transgenerational epigenetic effects in more environmentally relevant species are scarce, e.g. Brown et al(2009). In Daphnia magna, one of the standard species in aquatic toxicology, DNA methylation has recently been detected (Vandegehuchte et al, 2009a).…”

Epigenetics and its implications for ecotoxicology

“…Brown et al (2009) reported reduced embryonic survival in the rainbow trout Oncorhynchus mykiss due to exposure of males to the endocrine disrupting chemical 17a-ethynilestradiol (EE2) during late spermatogenesis. These authors discussed that this was potentially mediated by an epigenetic mode of action.…”