Premium
Description and evaluation of a short‐term reproduction test with the fathead minnow ( Pimephales promelas )
Author(s) -
Ankley Gerald T.,
Jensen Kathleen M.,
Kahl Michael D.,
Korte Joseph J.,
Makynen Elizabeth A.
Publication year - 2001
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.5620200616
Subject(s) - minnow , vitellogenin , pimephales promelas , methyltestosterone , biology , methoxychlor , xenoestrogen , reproduction , testosterone (patch) , endocrinology , medicine , endocrine disruptor , estrogen , toxicology , reproductive toxicity , no observed adverse effect level , aquatic toxicology , endocrine system , toxicity , hormone , estrogen receptor , pesticide , ecology , fish <actinopterygii> , fishery , genetics , cancer , body weight , breast cancer
Due to the time and expense associated with full life‐cycle testing, most current toxicity tests with fish do not explicitly consider reproductive output as an endpoint but, rather, focus on early life‐stage survival and development. However, some classes of chemicals could adversely impact reproduction at concentrations below those that affect development. Further, estimates of the effects of toxic compounds on reproductive output can be critical to the ecological risk assessment process. In this manuscript, we describe a short‐term reproduction test with the fathead minnow ( Pimephales promelas ) and evaluate the test using two model reproductive toxicants, methoxychlor (an estrogenic compound) and methyltestosterone (an androgenic chemical). The test is initiated with reproductively mature animals and is comprised of a pre‐exposure phase of 14 to 21 d, followed by a chemical exposure of up to 21 d. During and at completion of the test, several endpoints related to reproductive fitness and endocrine function are assessed. Both chemicals evaluated in our study caused a significant decrease in fecundity of the fish at nominal concentrations of 5.0 μg/L (methoxychlor) and 0.2 mg/L (methyltestosterone). Methoxychlor decreased plasma concentrations of one or more steroids (testosterone, 11‐ketotestosterone, β‐estradiol) in both sexes and caused a significant induction of plasma vitellogenin in males, a response consistent with activation of the estrogen receptor by the pesticide (or its metabolites). Methyltestosterone decreased plasma concentrations of sex steroids and adversely affected gonadal status (as evaluated by relative weight and histopathology) in both sexes. The androgenic nature of methyltestosterone was clearly expressed as masculinization of exposed females via formation of nuptial tubercles, structures normally present only in reproductively active males. The chemical also caused a significant induction of plasma vitellogenin in both males and females; this unexpected estrogenic response was most likely due to aromatization of the androgen to a form capable of binding to the estrogen receptor. These studies demonstrate the utility of this short‐term assay for identifying chemicals that exert reproductive toxicity through alterations in endocrine systems controlled by estrogens and androgens.