镁对镍、钴、锌、镉离子致蟾蜍胚胎毒性的影响

Mg^(2+)effects on the Embryotoxicity and Teratogenicity of Ni^(2+),Co^(2+),Zn^(2+),and Cd^(2+)for Frog Embryos in the FETAX Assay

[目的 ]用FETAX设计 ,研究Mg2 + 对Ni2 + 、Co2 + 、Zn2 + 和Cd2 + 致Xenopus胚胎的胚胎毒性与致畸作用的影响。 [方法 ]在 7次检测中 ,分别于含Mg2 + 5个等级浓度 (0、6 2、62、62 0、62 0 0 μmol/L)的FETAX培养液中 ,设空白对照与加入NiCl2 (5 6μmol/L)、CoCl2 (180 0 μmol/L)、ZnCl2 (3 0 0 μmol/L)和CdCl2 (18μmol/L)的 2 5个组 ,每个组内的受精卵均经 5～10 1h孵育。在该检测中限定Mg2 + (62 0 μmol/L)为标准浓度。在该浓度时Ni2 + 、Co2 + 、Zn2 + 和Cd2 + 组胚胎死亡率 <10 % ,畸形率 >95 %。 [结果 ]对照组于标准浓度时平均畸形率为 (5 4± 1 3 ) % ,低于该等级的 62 μmol/L为 (3 2± 7) % ,≤ 6 2μmol/L为 10 0 %。表明Mg2 + 不足与补加可极显著地增强与降低胚胎畸形率及其严重程度与胚胎毒性 (P <0 0 0 0 1,ANO VA分析 )。 [结论 ]对此 ,推测这可能与涉及在两价金属离子转运之间的金属吸收、细胞通道或对关键性分子靶 (即DNA聚合酶 )结合的竞争有关。

The influence of Mg 2+ on the embryotoxicity and teratogenicity of Ni 2+ ,Co 2+ ,Zn 2+ ,and Cd 2+ for Xenopus embryos was studied by an adaptation of the FETAX protocol. In seven experiments,twenty five groups of embryos were grown from 5 to 101 hours post fertilization in FETAX media that contained five graded MgCl 2 concentrations (0,6 2,62,620,or 6 200 μmol/L),with or without added NiCl 2 (56 μmol/L),CoCl 2(1,800 μmol/L),ZnCl 2 (300 μmol/L),or CdCl 2(18 μmol/L). The FETAX assays were performed with the standard Mg 2+ concentration (620 μmol/L). The incidence of malformations in control embryos averaged 5 4±1 3%;the incidence of malformations in the controls increased at low Mg 2+ concentrations (32±7% at 62 μmol/L;100% at ≤6 2 μmol/L). The specified additions of Ni 2+ ,Co 2+ ,Zn 2+ ,or Cd 2+ caused death in <10% of exposed embryos and malformations in >95% when tested under standard conditions (620 μmol Mg 2+ /L)? Mg 2+ deprivation greatly enhanced and Mg 2+ supplementation significantly reduced the incidence and severity of the teratogenic and embryotoxic effects of Ni 2+ ,Co 2+ ,Zn 2+ ,and Cd 2+ ( P <0 000 1 by ANOVA). [Conclusion] The authors propose that Mg 2+ may competer with the other divalent metal ions for a carrier mechanism involved in metal absorption or cellular uptake,or for binding to critical molecular targets( e.g., DNA polymerases) as the main causes of the effects observed.