Centanni M, Sapone A, Taglienti A, Andreoli M
Department of Experimental Medicine, University La Sapienza, Rome, Italy.
Endocrinology. 1991 Oct;129(4):2175-9. doi: 10.1210/endo-129-4-2175.
In mouse thymocytes, a stereospecific saturable energy-dependent and ouabain-inhibitable system facilitates T3, but not T4, entry. We studied here the effect of sodium depletion on cellular uptake of thyroid hormones by mouse thymocytes. Time-course experiments indicated that extracellular sodium depletion reduced [125I]T3 uptake at each time studied. At equilibrium, the removal of extracellular sodium and its substitution with isoosmotic choline decreased saturable [125I]T3 uptake by 60 +/- 10%; this effect was dose dependent. The substitution of sodium with lithium, instead of choline, had no effect on the uptake process. [125I]T4 uptake was lower than that of [125I]T3 and not affected by sodium depletion. The half-maximal effect of sodium deprivation on [125I]T3 uptake was reached at an extracellular sodium concentration of about 40 mM. The variation of external pH influenced T3 accumulation by thymocytes. [125I]T3 progressively decreased from acid to alkaline pH under normal and sodium-depleted conditions; however, the sodium-dependent fraction was more than doubled at physiological pH compared to that at more acidic and more alkaline pH. The sodium ionophore monensin decreased T3 uptake by 51% at a concentration of 20 microM. These results indicated the existence of a sodium-related mechanism of T3 uptake into mouse thymocytes that does not operate for T4 uptake.
在小鼠胸腺细胞中，一个立体特异性的、可饱和的、能量依赖且哇巴因可抑制的系统促进三碘甲状腺原氨酸（T3）而非四碘甲状腺原氨酸（T4）的进入。我们在此研究了钠缺乏对小鼠胸腺细胞摄取甲状腺激素的影响。时间进程实验表明，在每个研究时间点，细胞外钠缺乏均降低了[125I]T3的摄取。在平衡状态下，去除细胞外钠并用等渗胆碱替代，可使可饱和的[125I]T3摄取降低60±10%；这种效应呈剂量依赖性。用锂替代钠而非胆碱，对摄取过程无影响。[125I]T4的摄取低于[125I]T3，且不受钠缺乏的影响。钠缺乏对[125I]T3摄取的半数最大效应在细胞外钠浓度约为40 mM时达到。外部pH值的变化影响胸腺细胞对T3的积累。在正常和钠缺乏条件下，[125I]T3从酸性pH到碱性pH逐渐降低；然而，与更酸性和更碱性pH相比，在生理pH下钠依赖性部分增加了一倍多。钠离子载体莫能菌素在浓度为20 μM时可使T3摄取降低51%。这些结果表明，存在一种与钠相关的T3进入小鼠胸腺细胞的机制，而该机制对T4摄取不起作用。
