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Metabolic androgenization of female Daphnia magna by the xenoestrogen 4‐nonylphenol
Author(s) -
Baldwin William S.,
Graham Stephen E.,
Shea Damian,
LeBlanc Gerald A.
Publication year - 1997
Publication title -
environmental toxicology and chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.1
H-Index - 171
eISSN - 1552-8618
pISSN - 0730-7268
DOI - 10.1002/etc.5620160920
Subject(s) - nonylphenol , xenoestrogen , daphnia magna , testosterone (patch) , biology , metabolism , reproductive toxicity , toxicity , endocrinology , xenobiotic , medicine , toxicology , chemistry , environmental chemistry , biochemistry , estrogen receptor , cancer , breast cancer , genetics , enzyme
Vrtebrates and invertebrates metabolize testosterone to a variety of less‐polar derivatives that elicit varying degrees of androgenicity as well as polar elimination products. We have developed a model, using the cladoceran Daphnia magna , with which the ability of xenobiotics to alter steroid hormone metabolism can be assessed and possible physiologic consequences evaluated during a 3‐week assay. This model was used to assess the effects of the xenoestrogen 4‐nonylphenol on steroid‐metabolic processes. Exposure of daphnids to 100 μg/L 4‐nonylphenol for 48 h caused a significant increase in the accumulation of radioactivity derived from [ 14 C]testosterone provided to the exposure media. More definitive analyses demonstrated that both 25 and 100 μg/L 4‐nonylphenol disrupted components of the testosterone metabolic pathway that would lead to a decrease in the metabolic elimination of testosterone and an increase in the accumulation of androgenic derivatives. Exposure of daphnids to 100 μg/L 4‐nonylphenol significantly decreased fecundity of the organisms while having no effect on survival of the parental organisms. Comparison of metabolic and reproductive effects of 4‐nonylphenol revealed that 71 μg/L, the reproductive chronic value, would reduce the metabolic elimination of testosterone by approximately 50%. This relationship is consistent with that which we have reported for other toxicants and identifies a mechanism, in addition to estrogenicity, that may contribute to the reproductive toxicity of this compound.