发育毒性

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  • developmental toxicity
发育毒性发育毒性
  1. Al(NO3)3对大鼠胚胎的发育毒性研究

    Developmental toxicity of Al ( NO_3 ) _3 on rat embryos

  2. 邻苯二甲酸二丁酯宫内和哺乳期染毒对F1代雄性大鼠的生殖发育毒性

    Reproductive and developmental toxicity of F_1 male rats treated with DBP in utero and during lactation

  3. 甲磺酸胺银杏内酯B的大鼠胚胎-胎仔发育毒性实验研究

    Experimental studies on toxicity of dimethylaminoethyl ginkgolide B mesylate to the development of rat embryos-fetus

  4. 本文应用大鼠全胚胎培养方法检测了二硫化碳(CS2)的发育毒性。孕鼠于妊娠7、8两天经呼吸道吸入浓度为100mg/m~3的CS2,每天染毒4小时。

    The whole embryo culture method was used in testing the development toxicity of carbon disulphide .

  5. 结论结果表明BPA可能对小鼠具有生殖和发育毒性。

    Conclusion The results showed that BPA could induce reproductive and developmental toxicities in mice .

  6. 结论:MT对DPH诱发的动物发育毒性具有明显的拮抗作用。

    CONCLUSIONS : The antioxidant MT exhibited an excellent antagonism to the teratogenesis induced by DPH .

  7. 邻苯二甲酸二丁酯(DBP)广泛存在于环境中,具有一定的生殖发育毒性。

    Dibutyl phthalate ( DBP ) has been found as a ubiquitous environmental pollutant with reproductive and developmental toxicity .

  8. 目的研究双酚A(BPA)对小鼠的生殖和发育毒性。

    Objective To study the effects of bisphenol A ( BPA ) on reproductive and developmental toxicities in mice .

  9. AlCl3致胚胎发育毒性的体外实验研究

    Experimental Study on Developmental Toxicity of AlCl_3 to Rats ' Embryo in Vitro

  10. 结论:FA和VB12联合干预对酒精的发育毒性具有预防控制作用。

    Conclusion : FA and VB12 have significant combined protective effect on preventing the developmental toxicity of alcohol .

  11. 关于酒精对人类胎儿的发育毒性最初报道于1968年,孕妇饮酒会导致胎儿酒精综合症(FAS)。

    The developmental toxicity associated with ethanol was first reported in human fetuses in 1968 . Ethanol exposure during pregnancy can cause fetal alcohol syndrome ( FAS ) .

  12. 因此,目前PBDEs的神经发育毒性越来越受到人们的关注。

    Therefore , recently the developmental neurotoxic effects of PBDEs get more and more attention from people .

  13. 目前认为,DBP的生殖发育毒性的一个重要的机制是其内分泌干扰作用。

    The current view is that the reproductive and developmental toxicity of DBP has an important mechanism that is the interference effect of internal incretion .

  14. 结论氟有潜在的致畸性和胚胎毒性,胚胎组织GSH活性和卵黄囊细胞膜脂流动性降低可能在氟致胚胎发育毒性中起重要作用。

    Conclusions Fluoride could result in embryonic growth retardation and potential teratogenic toxicity . These effects might be due in part to decrease in GSH activity and membrane lipid fluidity .

  15. 目的研究经口混合染毒双酚A(BPA)和壬基酚(NP)对小鼠的生殖和发育毒性。

    Objective To study the effects of oral exposure to mixture of bisphenol A ( BPA ) and nonylphenol ( NP ) on reproductive and developmental toxicities in mice .

  16. 利用传统致畸试验方法对植物活力素(PME)进行了部分的生殖与发育毒性实验。

    The authors studied some of the reproductive and developmental toxicity on Plant Mineral Elements ( PME ) by Teratogenicity Test .

  17. 目的评价普洱熟茶对雄性和雌性SD大鼠潜在的亚慢性和繁殖发育毒性作用。

    Objectives : The present study was aimed at evaluating potential subchronic toxicity and reproductive and developmental toxicity of Pu-erh black tea ( PBT ) to male and female Sprague Dawley ( SD ) rats . 3 .

  18. 目的为研究全反式视黄酸(atRA)的发育毒性及其可能的作用机制,本研究采用植入后体外全胚胎培养方法研究atRA对小鼠胚胎生长发育的影响。

    Objective To investigate the developmental toxicity of all-trans retinoic acid ( atRA ) and its possible mechanism , the post-implantation whole embryo culture ( WEC ) was used .

  19. 目的:研究叶酸(FA)和维生素B12(VB12)联合抗酒精发育毒性的效果。

    Objective : To investigate the combined preventive effect of folic acid ( FA ) and vitamin B12 ( VB12 ) on the developmental toxicity of alcohol .

  20. 应用全胚胎培养方法研究CrCl3对大、小鼠胚胎的发育毒性研究

    Use of whole embryo culture technique for evaluating the developmental toxicity of CrCl_3 in mouse and rat embryos

  21. Rai&VanRyzin巢式模型在发育毒性研究中的应用

    Application of Rai & Van Ryzin nested model in the study of developmental toxicology

  22. 结论MT在体内铅的转运、代谢乃至解毒方面具有一定作用,MT的缺乏可使铅引起的脑组织脂质过氧化反应增强,进一步加重铅的神经发育毒性。

    Conclusions MT may play some roles in aspects of transportation , metabolism and detoxification . Shortage of MT in brain might enhance the lipid peroxidation induced by lead , which will further enhance the neurotoxicity in the development of brain .

  23. 结论吡哆素L-2-吡咯烷酮-5-羧酸酯在本实验条件对SD大鼠无致畸性,无作用剂量为400mg/kg,发育毒性的无作用剂量小于400mg/kg。

    Conclusion Under the presented experimental conditions , metadoxine has no teratogentic effects on SD rats and the no effect dose is 400 mg / kg . And the no effect dose for the developmental toxicity is less than 400mg / kg .

  24. 以上结果为PFOS早期发育毒性机制的进一步研究提供了一定的理论依据,同时对健康安全风险评价具有重要意义。

    This finding provides the theoretical basis for the further study of the mechanism for PFOS early developmental toxicity . and brings great significance to the health and safety risk assessment .

  25. 结论:按Flint评价标准,醋酸铅是脑细胞分化的特异抑制剂,它的脑细胞发育毒性与抑制细胞的增殖和分化有关。

    Conclusion : According to the standard of Flint , PbAc can be a specific inhibitor of brain cell differentiation , its brain cell developmental toxicity is related to the inhibition of cell proliferation and differentiation .

  26. 目的:探讨苯妥英(DPH)神经发育毒性与胚胎脑组织中自由基产生和氧化应激反应的关系。

    AIM : To explore the relationship between the developmental neurotoxicity ( DNT ) induced by prenatal phenytoin ( DPH ) exposure and free radicals and oxidative stress initiated in the embryonic brain .

  27. 提示,咖啡因孕期摄入可引起胚胎发育毒性及成年代谢综合征易感性增加,是IUGR最确切和危险的诱因之一。

    All the proofs implicate that caffeine ingestion during pregnancy could induce embryo developmental toxicity and increase the susceptibility of adult metabolic syndrome . It is also considered as one of the most definite and dangerous inducement of IUGR .

  28. 目的:确定原肠胚前期胚胎对发育毒性药物敏感的时间点,并建立评价Cyc诱导胚胎发育异常机制的分子生物学指标。

    AIM : To seek a sensitive time point for pre-gastrulation embryos exposed to developmental toxic agents , and to establish a molecular biomarker to evaluate the mechanism of cyclophosphamide-induced embryonic abnormalities in vivo .

  29. 本实验结果与整体动物实验结果基本一致,表明V2O5对大鼠的发育毒性敏感,而对小鼠不敏感,存在明显的种属差异。

    This result consists with results in vivo . In comparison with effect of V 2O 5 on rat embryo cultured , indicated rat is more sensitive than mouse to developmental toxicity of vanadium .

  30. 以上结果提示PFOS具有多种肝脏早期发育毒性,低剂量下PFOS暴露,效应miRNA能够调节肝脏脂肪酸代谢相关靶基因的表达,进而调控脂肪酸代谢过程。

    These results suggest that PFOS has a variety of early liver developmental toxicities . the significantly changed miRNA can regulate the expression of target genes involed in liver fatty acid metabolism at low dose of PFOS ( 3.2mg/kg Food ) .