The freshwater zooplankton, Daphnia magna alternates between asexual and sexual reproductive strategies.Asexual reproduction allows these animals to rapidly exploit abundant resources and favorable environmental conditions, while sexual reproduction produces developmentally-arrested eggs that can withstand extreme environmental conditions.While asexual reproduction is widely studied in ecotoxicological studies, sexual reproduction has been largely ignored and the extent to which xenobiotics can interfere with this process is not known.I hypothesized that certain environmental toxicants can interfere with sexual reproduction in Daphnia magna by disrupting the endocrine regulation of this process.This hypothesis was tested by: 1) demonstrating that multiple aspects of daphnid sexual reproduction could be affected by chemical exposure, 2) elucidating the endocrine processes responsible for regulating an early component of the sexual reproductive phase, and 3) evaluating the susceptibility of this process to disruption by environmental chemicals.Several components of daphnid sexual reproduction were shown to be affected by chemical exposure.The development of secondary sex characteristics in female (abdominal process) and male daphnids (elongated first antennae) was characterized and used as endpoints in chemical exposures.Juvenile female daphnids exposed to the estrogen, diethylstilbesterol and to the juvenile hormone mimic, methoprene showed increased development of the abdominal process when compared to untreated animals.Exposure of juvenile male daphnids to the androgen, androstenedione stimulated the growth of the first antennae.An assay was developed that utilized small daphnid populations to assess the effects of xenobiotic exposure on male and resting egg production.The juvenile hormone mimic, methoprene, was found to stimulate male production in daphnids as well as shift the reproductive output from neonatal production to the production of resting eggs.Further studies focused on elucidating the mechanism by which methoprene increased male production.The crustacean terpenoid hormone, methyl farnesoate, was found to program eggs in the ovaries to develop into males during neonatal development.This effect only occurred when eggs were exposed during a specific period of ovarian maturation just prior to their release into the brood chamber.Methoprene, a known juvenile hormone agonist in insects, stimulated male production in a similar fashion.Other chemicals with differing mechanisms of action did not alter sex ratios in exposed populations using the same experimental design employed with methoprene.Pyriproxyfen, another juvenile hormone mimic, however, did alter sex ratios in both population and individual exposures with a greater potency than methoprene or methyl farnesoate.Binary mixture studies with these insecticides and methyl farnesoate more closely conformed to a concentration addition model than an independent joint action model suggesting that these three chemicals all exert their effects on sex determination via the same target.These results support a mechanism of action of methyl farnesoate disruption for the insecticide methoprene and suggest that increased male production is a unique effect of exposure to chemicals with the ability to mimic methyl farnesoate.This research demonstrates that sexual reproduction in daphnids can be altered by xenobiotic exposure which more fully incorporates the complete life cycle of daphnids into toxicity studies.The characterization of the role of methyl farnesoate in daphnid sex determination improves the basic understanding of crustacean endocrinology and the function of methyl farnesoate in these animals.A model for methyl farnesoate disruption can be generated from this work that allows us to better predict and detect chemicals that act as endocrine disruptors in crustaceans.
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