Pavia Júnior M A, Paier B, Noli M I, Hagmüller K, Zaninovich A A
CONICET, Hospital de Clínicas, University of Buenos Aires, Argentina.
J Endocrinol. 1997 Jul;154(1):113-7. doi: 10.1677/joe.0.1540113.
The effect of in vivo administration of cadmium chloride on the pituitary-thyroidal axis was assessed in 200 g body weight Wistar rats. A dose of 2.5 mg/kg body weight was injected i.v. 24 h before the experiments were initiated. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations in cadmium-treated rats were significantly (P < 0.01) decreased, whereas plasma TSH failed to increase in response to low T4 and T3. However, the TSH response to TRH and the pituitary content of TSH in these rats were both normal. Cadmium induced a significant (P < 0.01) decrease in 4-h thyroidal 131I uptake and in thyroid/plasma radioactivity ratio. The in vitro conversion of T4 to T3 in the pituitary was significantly (P < 0.01) blocked by cadmium whereas there was no in vivo effect. Parameters of peripheral T4 kinetics in cadmium-treated rats, such as metabolic clearance rate (P < 0.01), fractional turnover rate (P < 0.01), absolute disposal rate (P < 0.05), urinary clearance (P < 0.05) and faecal clearance (P < 0.05), were all decreased by cadmium. The lack of response of TSH to low plasma T4 and T3 and the normal response to exogenous TRH in this and in other non-thyroidal illness syndromes produced by other pathologies suggest a decreased stimulation of pituitary thyrotrophs by endogenous TRH.
在体重200克的Wistar大鼠中评估了体内注射氯化镉对垂体 - 甲状腺轴的影响。在实验开始前24小时，静脉注射2.5毫克/千克体重的剂量。镉处理大鼠的血浆甲状腺素（T4）和三碘甲状腺原氨酸（T3）浓度显著降低（P < 0.01），而血浆促甲状腺激素（TSH）未能因低T4和T3而增加。然而，这些大鼠中TSH对促甲状腺激素释放激素（TRH）的反应以及垂体中TSH的含量均正常。镉导致4小时甲状腺131I摄取和甲状腺/血浆放射性比值显著降低（P < 0.01）。镉在体外显著阻断了垂体中T4向T3的转化（P < 0.01），而在体内则没有影响。镉处理大鼠外周T4动力学参数，如代谢清除率（P < 0.01）、分数周转率（P < 0.01）、绝对处置率（P < 0.05）、尿清除率（P < 0.05）和粪便清除率（P < 0.05），均因镉而降低。在这种情况以及由其他病理产生的其他非甲状腺疾病综合征中，TSH对低血浆T4和T3缺乏反应而对外源TRH反应正常，这表明内源性TRH对垂体促甲状腺细胞的刺激减少。
