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Republication or reproduction of this report or its storage and/or dissemination by electronic means is permitted without the need for formal IUPAC permission on condition that an acknowledgment Endocrine disruptors in the environment (IUPAC Technical Report)Abstract: Many chemical substances of natural or anthropogenic origin are suspected or known to be endocrine disruptors, which can influence the endocrine system of life. This observation has led to increased interest on the part of the public and the media, as well as to a steep rise of research activities in the scientific community. New papers and results are presented so fast that it is impossible to give a complete review of this emerging research field. Therefore, this paper tries to give insight into some topics of the great scope of endocrine disruptors in the environment. To get a general idea of the biochemical and biological background, some parts of the endocrine systems of mammalians and nonmammalians are explained. The sections that follow describe important mechanisms of endocrine disruption such as interactions with hormone receptors. Test strategies for anthropogenic chemicals on various organisms are critically reviewed with respect to their problems and gaps concerning endocrine disruptors. The main emphasis of the paper is on the chemical substances suspected or known to be endocrine disruptors. To get a better comprehension of their behavior in the environment, physicochemical data such as water solubility or K ow , as well as information about their use and/or function are reviewed and compared. The main routes of exposure for most chemicals are shortly described, and data about concentrations in the environment (soil/sediment, water) are detailed.

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We found that MAGED2 mutations caused X-linked polyhydramnios with prematurity and a severe but transient form of antenatal Bartter's syndrome. MAGE-D2 is essential for fetal renal salt reabsorption, amniotic fluid homeostasis, and the maintenance of pregnancy. (Funded by the University of Groningen and others.).

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Partial or full life-cycle tests are needed to assess the potential of endocrine-disrupting compounds (EDCs) to adversely affect development and reproduction of fish. Small fish species such as zebrafish, Danio rerio, are under consideration as model organisms for appropriate test protocols. The present study examines how reproductive effects resulting from exposure of zebrafish to the synthetic estrogen 17alpha-ethinylestradiol (EE2) vary with concentration (0.05 to 10 ng EE2 L(-1), nominal), and with timing/duration of exposure (partial life-cycle, full life-cycle, and two-generation exposure). Partial life-cycle exposure of the parental (F1) generation until completion of gonad differentiation (0-75 d postfertilization, dpf) impaired juvenile growth, time to sexual maturity, adult fecundity (egg production/female/day), and adult fertilization success at 1.1 ng EE2 L(-1) and higher. Lifelong exposure of the F1 generation until 177 dpf resulted in lowest observed effect concentrations (LOECs) for time to sexual maturity, fecundity, and fertilization success identical to those of the developmental test (0-75 dpf), but the slope of the concentration-response curve was steeper. Reproduction of zebrafish was completely inhibited at 9.3 ng EE2 L(-1), and this was essentially irreversible as a 3-mo depuration restored fertilization success to only a very low rate. Accordingly, elevated endogenous vitellogenin (VTG) synthesis and degenerative changes in gonad morphology persisted in depurated zebrafish. Full life-cycle exposure of the filial (F2) generation until 162 dpf impaired growth, delayed onset of spawning and reduced fecundity and fertilization success at 2.0 ng EE2 L(-1). In conclusion, results show that the impact of estrogenic agents on zebrafish sexual development and reproductive functions as well as the reversibility of effects, varies with exposure concentration (reversibility at < or = 1.1 ng EE2 L(-1) and irreversibility at 9.3 ng EE2 L(-1)), and between partial and full life-cycle exposure (exposure to 10 ng EE2 L(-1) during critical period exerted no permanent effect on sexual differentiation, but life-cycle exposure did).

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