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Embryotoxicity of the alkylphenol degradation product 4-nonylphenol to the crustacean Daphnia magna.

机译:烷基苯酚降解产物4-壬基苯酚对甲壳类水蚤(Daphnia magna)的胚胎毒性。

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摘要

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.
机译:实验室研究表明,某些烷基酚和农药会引起对甲壳类动物的发育毒性。本研究的目的是评估烷基酚降解产物4-壬基酚通过已知的干扰睾丸激素代谢消除的能力而对甲壳类水蚤具有胚胎毒性。母体水蚤直接接触睾丸激素会导致新生儿发育异常,包括早期胚胎发育的部分停滞,壳脊柱异常和首次触角发育。尽管异常情况与贯穿整个睾丸激素浓度-反应曲线所观察到的情况截然不同,但将母体水蚤暴露于4-壬基苯酚的浓度也会产生发育异常。因此,4-壬基苯酚是蚤类中的一种发育性毒物,但其毒性与睾丸激素蓄积增加引起的毒性不一致。进一步的实验表明,睾丸激素对发育中的胚胎具有直接毒性,而母体生物体可以作为这种毒性的载体。相比之下,直接胚胎暴露和母体早期暴露于4-壬基苯酚均不会引起与连续母体和妊娠暴露期间观察到的胚胎毒性相一致的胚胎毒性。因此,在这些暴露水平下4-壬基苯酚不是直接对胚胎有毒,而是由妊娠期间母体的影响介导了毒性。发生发育异常的阈值浓度(约44微克/升)表明,典型的4-壬基苯酚环境浓度不会对发育毒性造成紧急危害。但是,这些影响确实发生在足够低的水平上,以致需要评估其他甲壳类对这种以前未表征的毒性模式的相对敏感性。

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    LeBlanc G A; Mu X; Rider C V;

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