@article{davis_murr_best_fraites_zorrilla_narotsky_stoker_goldman_cooper_2011, title={The effects of prenatal exposure to atrazine on pubertal and postnatal reproductive indices in the female rat}, volume={32}, number={1}, journal={Reproductive Toxicology (Elmsford, N.Y.)}, author={Davis, L. K. and Murr, A. S. and Best, D. S. and Fraites, M. J. P. and Zorrilla, L. M. and Narotsky, M. G. and Stoker, T. E. and Goldman, J. M. and Cooper, R. L.}, year={2011}, pages={43–51} }
 @misc{cooper_laws_das_narotsky_goldman_tyrey_stoker_2007, title={Atrazine and reproductive function: Mode and mechanism of action studies}, volume={80}, number={2}, journal={Birth Defects Research. Part B, Developmental and Reproductive Toxicology}, author={Cooper, R. L. and Laws, S. C. and Das, P. C. and Narotsky, M. G. and Goldman, J. M. and Tyrey, E. L. and Stoker, T. E.}, year={2007}, pages={98–112} }
 @article{gray_wilson_stoker_lambright_furr_noriega_howdeshell_ankley_guillette_2006, title={Adverse effects of environmental antiandrogens and androgens on reproductive development in mammals}, volume={29}, ISSN={["1365-2605"]}, DOI={10.1111/j.1365-2605.2005.00636.x}, abstractNote={Within the last decade, several classes of chemicals have been shown in laboratory studies to disrupt reproductive development by acting as androgen receptor (AR) antagonists and/or inhibitors of fetal Leydig cell testosterone production. Some phthalate esters alter gubernacular differentiation by reducing insulin-like 3 (insl3) mRNA levels. We have found that AR antagonists and inhibitors of fetal testis hormone production generally induce cumulative, apparently dose-additive adverse effects when administered in mixtures. New research has also revealed the presence of androgens in the environment. Effluents from pulp and paper mills display androgenic activity of sufficient potency to masculinize and/or sex-reverse female fish. Effluent from beef cattle concentrated animal feedlot operations from the United States also displays androgenic activity in vitro, due, in part, to the presence of a steroid used to promote growth in beef cattle. In summary, we are only beginning to identify the classes of chemicals that have the potential to alter the androgen signalling pathway in utero. This review will (i) present information on the classes of environmental chemicals that display antiandrogenic and androgenic activities in vitro and in vivo, and (ii) provide an insight into how exposure to mixtures these chemicals might behave in utero.}, number={1}, journal={INTERNATIONAL JOURNAL OF ANDROLOGY}, author={Gray, LE and Wilson, VS and Stoker, T and Lambright, C and Furr, J and Noriega, N and Howdeshell, K and Ankley, GT and Guillette, L}, year={2006}, month={Feb}, pages={96–104} }
 @article{stoker_robinette_cooper_1999, title={Maternal exposure to atrazine during lactation suppresses suckling-induced prolactin release and results in prostatitis in the adult offspring}, volume={52}, ISSN={["1096-0929"]}, DOI={10.1093/toxsci/52.1.68}, abstractNote={The availability of prolactin (PRL) to the neonatal brain is known to affect the development of the tuberoinfundibular (TIDA) neurons and, as a consequence, lead to alterations in subsequent PRL regulation. Without early lactational exposure to PRL (derived from the dam's milk), TIDA neuronal growth is impaired and elevated PRL levels are present in the prepubertal male. These observations, combined with the finding that alterations in PRL secretion (i.e., hyperprolactinemia) in the adult male rat have been implicated in the development of prostatitis, led us to hypothesize that early lactational exposure to agents that suppress suckling-induced PRL release would lead to a disruption in TIDA development, altered PRL regulation, and subsequent prostatitis in the male offspring. To test this hypothesis, suckling-induced PRL release was measured in Wistar dams treated twice daily with the herbicide atrazine (ATR, by gavage, on PND 1-4 at 0, 6.25, 12.5, 25, and 50 mg/kg body weight), or twice daily with the dopamine receptor agonist bromocriptine (BROM, sc, at 0.052, 0.104, 0.208, and 0.417 mg/kg); BROM is known to suppress PRL release. Similarly, atrazine has also been reported to suppress PRL in adult females. Serum PRL was measured on PND 3 using a serial sampling technique and indwelling cardiac catheters. A significant rise in serum PRL release was noted in all control females within 10 min of the initiation of suckling. Fifty-mg/kg ATR inhibited suckling-induced PRL release in all females, whereas 25 and 12.5 mg/kg ATR inhibited this measure in some dams and had no discernible effect in others. The 6.25 mg/kg dose of ATR was without effect. BROM, used here as a positive control, also inhibited suckling-induced PRL release at doses of 0.104 to 0.417 mg/kg, with no effect at 0.052 mg/kg. To examine the effect of postnatal ATR and BROM on the incidence and severity of inflammation (INF) of the lateral prostate of the offspring, adult males were examined at 90 and 120 days. While no effect was noted at 90 days of age, at 120 days, both the incidence and severity of prostate inflammation was increased in those offspring of ATR-treated dams (25 and 50 mg/kg). The 12.5 mg/kg ATR and the two highest doses of BROM increased the incidence, but not the severity, of prostatitis. Combined treatment of ovine prolactin (oPRL) and 25 or 50 mg/kg ATR on PND 1-4 reduced the incidence of inflammation observed at 120 days, indicating that this increase in INF, seen after ATR alone, resulted from the suppression of PRL in the dam. To determine whether or not there is a critical period for these effects, dams were dosed with 25 and 50 mg/kg on PND 6-9 and PND 11-14. Inflammation was increased in those offspring from dams treated on PND 6-9, but this increase was not significant. Dosing on PND 11-14 was without effect. These data demonstrate that ATR suppresses suckling-induced PRL release and that this suppression results in lateral prostate inflammation in the offspring. The critical period for this effect is PND 1-9.}, number={1}, journal={TOXICOLOGICAL SCIENCES}, author={Stoker, TE and Robinette, CL and Cooper, RL}, year={1999}, month={Nov}, pages={68–79} }
 @article{stoker_robinette_cooper_1999, title={Perinatal exposure to estrogenic compounds and the subsequent effects on the prostate of the adult rat: evaluation of inflammation in the ventral and lateral lobes}, volume={13}, number={6}, journal={Reproductive Toxicology (Elmsford, N.Y.)}, author={Stoker, T. E. and Robinette, C. L. and Cooper, R. L.}, year={1999}, pages={463–472} }