镉镍单独及联合作用对小鼠胚胎肢芽细胞蛋白聚糖合成的影响

The change of proteoglycan biosynthesis of mouse embryo limb bud cell induced by single and combined cadmium and nickel

为探讨镉和镍的发育毒性机制及二者的联合作用特点，应用小鼠胚胎肢芽细胞微团培养和３５ＳＯ４掺入合成方法观察了氯化镉、氯化镍单独及联合作用对胚胎肢芽细胞蛋白聚糖合成情况的影响。结果表明，低剂量氯化镉（０．２μｇ／ｍｌ）可促进蛋白聚糖的合成，高剂量氯化镉（≥０．４μｇ／ｍｌ）可明显抑制蛋白聚糖的合成；氯化镍（１１．０～３３．０μｇ／ｍｌ）对蛋白聚糖的合成有明显的抑制作用，氯化镉和氯化镍联合染毒对胚胎肢芽细胞蛋白聚糖的合成抑制有加强作用。提示，蛋白聚糖合成紊乱可能是镉和镍引起肢体发育异常的机制之一。

o investigate the machanism of developmental toxicity of CdCl 2 and NiCl 2 and their combined action, mouse embryo limb bud cell micromass culture and test of 35SO 4 incorporation were carried out to observe the effects of CdCl 2 and NiCl 2 on the proteoglycan biosynthesis. The results showed that CdCl 2 at dosage of 0.2μg/ml could promote the proteoglycan biosynthesis, while CdCl 2 at dosage of 0.4μg/ml or higher levels significantly inhibited the proteoglycan biosynthesis; and NiCl 2 at dosage of 11.0～33.0μg/ml significantly reduced the proteoglycan biosynthesis of mouse embryo limb bud cell also. The two metals in combination could affect the proteoglycan biosynthesis of mouse embryo limb bud cell in potentiation or addition. It is suggested that the proteoglycan biosynthesis disturbance is one of the machanisms of limb defects of CdCl 2 and NiCl 2. moreover, CdCl 2 and NiCl 2 in combination exhibited their effects on the proteoglycan biosynthesis in a synergi way.\ \