Effects of the synthetic estrogen ethinylestradiol on early life stages of mink frongs and green frogs in the wild and in situ. Park, B., J. & Kidd, K., A. Environmental Toxicology and Chemistry, 24(8):2027-2036, 2005. ![Effects of the synthetic estrogen ethinylestradiol on early life stages of mink frongs and green frogs in the wild and in situ [pdf]](https://bibbase.org/img/filetypes/pdf.svg "pdf")
Paper abstract bibtex Estrogenic contaminants are known to disrupt growth and development in amphibians. Field-based research is needed to elucidate their potential impacts on wild populations. Hatch success, larval growth and development rates, and gonad development were examined in native amphibians exposed to low ng/L concentrations of 17-ethinylestradiol (EE2) in a whole-lake addition experiment at the Experimental Lakes Area, northwestern Ontario, Canada. Egg masses were reared in situ in the EE2-amended lake and in two reference lakes in 2001 and 2002. Hatching success was reduced significantly in green frogs (Rana clamitans) but not in mink frogs (Rana septentrionalis) exposed to EE2. Ethinylestradiol had no consistent effect on mass or development stage of hatchlings in the early larval stages of the caging study. Ethinylestradiol had no effect on sex ratios of either species in situ, and no intersex gonads were observed in exposed or reference green frog tadpoles or in reference mink frog tadpoles. However, 5.6% (total n 18) and 12.5% (total n 56) of EE2-exposed mink frog tadpoles were intersex in the 2001 and 2002 caging studies, respectively. Wild mink frog tadpoles also were examined, and EE2 had no effect on sex ratios. No intersex gonads were observed in reference lake tadpoles or in tadpoles from the experimental lake prior to EE2 additions; however, 2.4, 0, and 28.6% of wild EE2-exposed first-year tadpoles had intersex gonads (2001, 2002, and 2003, respectively). These results indicate that exposure to EE2 in the wild and in situ at concentrations comparable to those detected in effluents and, occasionally, in surface waters can impact gonad development and hatch success in native amphibians.
@article{
title = {Effects of the synthetic estrogen ethinylestradiol on early life stages of mink frongs and green frogs in the wild and in situ},
type = {article},
year = {2005},
keywords = {CONTAMINANTS,ELA,ENDOCRINE DISRUPTION,Ethinylestradiol,FROGS,L114,L224,L260,L442,Whole-lake manipulation,estrogen},
pages = {2027-2036},
volume = {24},
id = {4309d4e4-6719-359b-8ee0-588c1833423b},
created = {2019-07-12T15:07:55.876Z},
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last_modified = {2019-07-22T19:58:57.263Z},
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abstract = {Estrogenic contaminants are known to disrupt growth and development in amphibians. Field-based research is needed to elucidate their potential impacts on wild populations. Hatch success, larval growth and development rates, and gonad development were examined in native amphibians exposed to low ng/L concentrations of 17-ethinylestradiol (EE2) in a whole-lake addition experiment at the Experimental Lakes Area, northwestern Ontario, Canada. Egg masses were reared in situ in the EE2-amended lake and in two reference lakes in 2001 and 2002. Hatching success was reduced significantly in green frogs (Rana clamitans) but not in mink frogs (Rana septentrionalis) exposed to EE2. Ethinylestradiol had no consistent effect on mass or development stage of hatchlings in the early larval stages of the caging study. Ethinylestradiol had no effect on sex ratios of either species in situ, and no intersex gonads were observed in exposed or reference green frog tadpoles or in reference mink frog tadpoles. However, 5.6% (total n 18) and 12.5% (total n 56) of EE2-exposed mink frog tadpoles were intersex in the 2001 and 2002 caging studies, respectively. Wild mink frog tadpoles also were examined, and EE2 had no effect on sex ratios. No intersex gonads were observed in reference lake tadpoles or in tadpoles from the experimental lake prior to EE2 additions; however, 2.4, 0, and 28.6% of wild EE2-exposed first-year tadpoles had intersex gonads (2001, 2002, and 2003, respectively). These results indicate that exposure to EE2 in the wild and in situ at concentrations comparable to those detected in effluents and, occasionally, in surface waters can impact gonad development and hatch success in native amphibians.},
bibtype = {article},
author = {Park, B. J. and Kidd, K. A.},
journal = {Environmental Toxicology and Chemistry},
number = {8}
}
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Field-based research is needed to elucidate their potential impacts on wild populations. Hatch success, larval growth and development rates, and gonad development were examined in native amphibians exposed to low ng/L concentrations of 17-ethinylestradiol (EE2) in a whole-lake addition experiment at the Experimental Lakes Area, northwestern Ontario, Canada. Egg masses were reared in situ in the EE2-amended lake and in two reference lakes in 2001 and 2002. Hatching success was reduced significantly in green frogs (Rana clamitans) but not in mink frogs (Rana septentrionalis) exposed to EE2. Ethinylestradiol had no consistent effect on mass or development stage of hatchlings in the early larval stages of the caging study. Ethinylestradiol had no effect on sex ratios of either species in situ, and no intersex gonads were observed in exposed or reference green frog tadpoles or in reference mink frog tadpoles. However, 5.6% (total n 18) and 12.5% (total n 56) of EE2-exposed mink frog tadpoles were intersex in the 2001 and 2002 caging studies, respectively. Wild mink frog tadpoles also were examined, and EE2 had no effect on sex ratios. No intersex gonads were observed in reference lake tadpoles or in tadpoles from the experimental lake prior to EE2 additions; however, 2.4, 0, and 28.6% of wild EE2-exposed first-year tadpoles had intersex gonads (2001, 2002, and 2003, respectively). These results indicate that exposure to EE2 in the wild and in situ at concentrations comparable to those detected in effluents and, occasionally, in surface waters can impact gonad development and hatch success in native amphibians.","bibtype":"article","author":"Park, B. J. and Kidd, K. 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