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本文应用恒河猴,对醋酸铅致甲状腺的毒性作用及其机制进行了实验观察。实验结果表明,染毒后动物血铅和δ-ALAD水平显著改变(P<0.05或<0.01),TSH水平明显高于对照组,而T_3水平低于对照组(P<0.05或<0.01),且呈良好的剂量一反应关系。甲状腺铅含量高剂量组明显高于对照组,低剂量组与对照组接近。血铅水平与甲状腺铅含量之间呈明显正相关(r=0.954,P<0.01).组织病理学检查见高剂量组甲状腺滤泡上皮呈高柱状,数目增多。提示在5～15mg/kg剂量的水平之下,铅可以造成甲状腺功能损害,其损害机制可能是铅在甲状腺内竞争与碘结合蛋白结合,而引起碘不足。
In this paper, rhesus monkeys were used to study the toxic effects of lead acetate on thyroid and its mechanism. The results showed that the level of blood lead and δ-ALAD in the animals significantly changed (P <0.05 or <0.01), the level of TSH was significantly higher than that in the control group, while the level of T_3 was lower than that in the control group (P <0.05 or <0.01) And showed a good dose-response relationship. Thyroid lead content of high-dose group was significantly higher than the control group, low-dose group and the control group close. Blood lead levels and thyroid lead content was positively correlated (r = 0.954, P <0.01) .Histopathological examination showed high-dose thyroid follicular epithelium was tall columnar, the number increased. It is suggested that lead may cause thyroid dysfunction under the level of 5 ~ 15mg / kg. The possible mechanism is that lead may compete with iodine binding protein in the thyroid to cause iodine deficiency.