论文部分内容阅读
目的:探讨妊娠期补锌对染汞孕鼠胚胎发育毒性的保护作用。方法:建立孕鼠动物模型,应用不同剂量的氯化甲基汞(0.01、0.05、2.00mg/kg.d)及5.00mg/kg.d硫酸锌于妊娠6～9天连续灌胃,蒸馏水灌胃为对照组,观察孕鼠及胚胎的汞毒性及硫酸锌的影响。应用ICP-MS法测定各组胎鼠脑组织汞含量;Westernblot法检测各组胎鼠脑bcl-2蛋白表达情况;TUNEL法检测各组胎鼠脑细胞凋亡情况。结果:各组均未发现死胎、吸收胎及畸形胎;0.01、0.05mg/kg.d氯化甲基汞对孕鼠及胎鼠生长发育没有明显的抑制作用;2.00mg/kg.d氯化甲基汞可以明显抑制孕鼠体重增长及胎鼠身长、体重及尾长的增长(P<0.05),但对孕鼠产仔数、胎窝总重及胎盘总重没有明显的影响,0.05mg/kg.d、2.00mg/kg.d氯化甲基汞组胎鼠脑组织汞含量较对照组明显升高(P<0.05),bcl-2蛋白表达明显下降(P<0.05),脑细胞凋亡较对照组明显升高(P<0.05);应用硫酸锌预处理后,氯化甲基汞对孕鼠及胚胎的毒性作用明显降低(P<0.05),胎鼠脑组织汞含量较染汞组明显降低(P<0.05),bcl-2蛋白表达明显升高(P<0.05),胎鼠脑细胞凋亡明显降低(P<0.05)。结论:孕期补锌可以降低氯化甲基汞对孕鼠胚胎的毒性作用,其机制与锌通过升高bcl-2蛋白的表达而抑制细胞凋亡有关。
Objective: To investigate the protective effect of zinc supplementation during pregnancy on the embryotoxicity of pregnant mice with mercury. Methods: Animal models of pregnant rats were established. Methylmercury chloride (0.01,0.05 and 2.00mg / kg.d) and 5.00mg / kg.d. Stomach as control group, to observe the mercury toxicity of pregnant rats and embryos and zinc sulfate. The contents of mercury in fetal rat brain tissue were measured by ICP-MS. The expression of bcl-2 protein in fetal rat brain was detected by Western blot. The apoptosis of fetal rat brain was detected by TUNEL. Results: No stillbirth, aborted fetus and deformed fetus were found in all groups. 0.01, 0.05 mg / kg.d methylmercury chloride did not significantly inhibit the growth of pregnant rats and fetuses; 2.00mg / kg.d chlorinated Methylmercury significantly inhibited body weight gain and body length, body weight and tail length of pregnant rats (P <0.05), but had no significant effect on litter size, total litter size and total placental weight in pregnant rats. 0.05mg / kg.d, 2.00mg / kg.d mercury in methylmercury chloride group fetal brain tissue mercury levels were significantly higher than the control group (P <0.05), bcl-2 protein was significantly decreased (P <0.05), brain cells (P <0.05). After pretreatment with zinc sulfate, the toxic effect of methylmercury chloride on pregnant rats and embryos was significantly decreased (P <0.05), and the content of mercury in fetal rat brain tissue was significantly higher than that of the control group Mercury group was significantly lower (P <0.05), bcl-2 protein expression was significantly increased (P <0.05), fetal rat brain cell apoptosis was significantly reduced (P <0.05). Conclusion: Zinc supplementation during pregnancy can reduce the toxic effect of methylmercury chloride on embryos of pregnant mice, and its mechanism is related to the inhibition of apoptosis by increasing the expression of bcl-2 protein by zinc.