@article{mu_rider_hwang_hoy_leblanc_2005, title={Covert signal disruption: Anti-ecdysteroidal activity of bisphenol a involves cross talk between signaling pathways}, volume={24}, ISSN={["1552-8618"]}, DOI={10.1897/04-063r.1}, abstractNote={Abstract}, number={1}, journal={ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY}, author={Mu, XY and Rider, CV and Hwang, GS and Hoy, H and LeBlanc, GA}, year={2005}, month={Jan}, pages={146–152} }
 @article{mu_leblanc_2004, title={Cross communication between signaling pathways: Juvenoid hormones modulate ecdysteroid activity in a crustacean}, volume={301A}, ISSN={["2471-5646"]}, DOI={10.1002/jez.a.104}, abstractNote={Abstract}, number={10}, journal={JOURNAL OF EXPERIMENTAL ZOOLOGY PART A-ECOLOGICAL AND INTEGRATIVE PHYSIOLOGY}, author={Mu, XY and Leblanc, GA}, year={2004}, month={Oct}, pages={793–801} }
 @article{mu_leblanc_2004, title={Synergistic interaction of endocrine-disrupting chemicals: Model development using an ecdysone receptor antagonist and a hormone synthesis inhibitor}, volume={23}, ISSN={["1552-8618"]}, DOI={10.1897/03-273}, abstractNote={Abstract}, number={4}, journal={ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY}, author={Mu, XY and LeBlanc, GA}, year={2004}, month={Apr}, pages={1085–1091} }
 @article{mu_rider_leblanc_2002, title={Abstracts from the Eleventh International Symposium on Pollutant Responses in Marine Organisms (PRIMO 11) - Endocrine disrupters}, volume={54}, number={3-5}, journal={Marine Environmental Research}, author={Mu, X. Y. and Rider, C. V. and Leblanc, G. A.}, year={2002}, pages={741–754} }
 @article{mu_leblanc_2002, title={Developmental toxicity of testosterone in the crustacean Daphnia magna involves anti-ecdysteroidal activity}, volume={129}, ISSN={["0016-6480"]}, DOI={10.1016/S0016-6480(02)00518-X}, abstractNote={Testosterone has been shown to cause developmental arrest of embryonic daphnids (Daphnia magna). The present study was undertaken to determine whether this toxicity might be due to anti-ecdysteroidal activity associated with testosterone. The effect of testosterone on molt frequency of early instar daphnids was first evaluated to determine whether testosterone interfered with this ecdysteroid-regulated process. Molt frequency was delayed by exposure to testosterone and this effect was mitigated by co-exposure to the ecdysteroid 20-hydroxyecdysone. Testosterone exposure concentrations that interfered with molting also elicited developmental abnormalities among neonatal organisms produced by maternal organisms that were continuously exposed to testosterone or among embryos that were removed from unexposed mothers and exposed directly to the hormone. Embryos were significantly protected against the developmental toxicity of testosterone by co-exposure to 20-hydroxyecdysone. Taken together, these results demonstrated that the embryo toxicity of testosterone to daphnids is due largely to its ability to interfere with ecdysteroid control of development. Experiments next were conducted to determine whether testosterone interfered with ecdysteroidal activity by acting as an ecdysone receptor antagonist or by reducing endogenous ecdysone levels. Testosterone significantly antagonized the action of 20-hydroxyecdysone in an ecdysone-responsive cell line. Testosterone had no discernable effect on endogenous ecdysone levels in daphnids. These results demonstrated that (1). ecdysteroids regulate critical processes in daphnid embryo development, (2). testosterone elicits embryo toxicity to daphnids by interfering with ecdysteroid activity, and (3). ecdysteroid receptor antagonism could be one mechanism by which testosterone elicits these effects.}, number={2}, journal={GENERAL AND COMPARATIVE ENDOCRINOLOGY}, author={Mu, XY and LeBlanc, GA}, year={2002}, month={Nov}, pages={127–133} }
 @article{mu_leblanc_2002, title={Environmental antiecdysteroids alter embryo development in the crustacean Daphnia magna}, volume={292}, ISSN={["0022-104X"]}, DOI={10.1002/jez.10020}, abstractNote={Abstract}, number={3}, journal={JOURNAL OF EXPERIMENTAL ZOOLOGY}, author={Mu, XY and LeBlanc, GA}, year={2002}, month={Feb}, pages={287–292} }
 @article{leblanc_mu_rider_2000, title={Embryotoxicity of the alkylphenol degradation product 4-nonylphenol to the crustacean Daphnia magna}, volume={108}, ISSN={["0091-6765"]}, DOI={10.2307/3434824}, abstractNote={Laboratory studies have suggested that some alkylphenols and pesticides elicit developmental toxicity to crustaceans. The purpose of the present study was to evaluate the possibility that the alkylphenol degradation product 4-nonylphenol is embryotoxic to the crustacean Daphnia magna through its known ability to interfere with the metabolic elimination of testosterone. Direct exposure of maternal daphnids to testosterone caused developmental abnormalities in neonates that consisted of partial arrest of early embryonic development and abnormalities in shell spine and first antennae development. Exposure of maternal daphnids to concentrations of 4-nonylphenol also produced developmental abnormalities though the profile of abnormalities was distinct from that observed throughout the testosterone concentration-response curve. Thus, 4-nonylphenol is a developmental toxicant in daphnids, but its toxicity is not consistent with that elicited by elevated testosterone accumulation. Further experiments demonstrated that testosterone was directly toxic to developing embryos, and the maternal organism can serve as the vector for this toxicity. In contrast, neither direct embryo exposure nor early maternal exposure to 4-nonylphenol elicited embryotoxicity consistent with that observed during continuous maternal and gestational exposure. Thus, 4-nonylphenol is not directly embryotoxic at these exposure levels, but rather toxicity is mediated by maternal influences during gestation. The threshold concentration for the occurrence of developmental abnormalities ( approximately 44 microg/L) indicates that typical environmental concentrations of 4-nonylphenol pose no imminent hazard with respect to developmental toxicity. However, these effects do occur at sufficiently low levels to warrant evaluation of the relative susceptibility of other crustacean species to this previously uncharacterized mode of toxicity.}, number={12}, journal={ENVIRONMENTAL HEALTH PERSPECTIVES}, author={LeBlanc, GA and Mu, XY and Rider, CV}, year={2000}, month={Dec}, pages={1133–1138} }