Chow S Y, Yen-Chow Y C, White H S, Woodbury D M
Am J Physiol. 1986 Apr;250(4 Pt 1):E464-9. doi: 10.1152/ajpendo.1986.250.4.E464.
Iodide uptake by primary cultures of turtle thyroid cells decreased linearly with reduction of Na+ concentration in the medium, but changes in medium Cl- concentration did not affect iodide uptake. Ouabain, furosemide, monensin, and perchlorate all decreased 125I-uptake by cultured thyroid cells, whereas amiloride and triamterene did not. Ouabain, monensin, perchlorate, and amiloride depolarized the membrane of cultured cells, whereas furosemide and triamterene had no effect. Ouabain and perchlorate increased intracellular Na+ and Cl- and decreased K+ activities; furosemide and monensin reduced all three ions, but triamterene had no effect. Amiloride decreased intracellular Na+ and increased intracellular Cl- activities, however, its effect on K+ activity could not be determined because of interference by this compound of the K+ ion exchanger. All the agents, except furosemide, inhibited Na+-K+-ATPase activity. These experiments demonstrate that 1) Na+-I- cotransport is responsible for most iodide accumulation in thyroid cells; 2) Na+-I- cotransport system is linked to the Na+-K+ pump; 3) active iodide transport does not always correlate with Na+-K+-ATPase activity; 4) a perchlorate-sensitive iodide transport system is present in thyroid cells; 5) transport processes, not involved in active iodide transport (Na+-Cl- cotransport and Na+-H+ counter transport), are also present in cultured thyroid cells.
乌龟甲状腺细胞原代培养物对碘化物的摄取随着培养基中Na⁺浓度的降低而呈线性下降,但培养基中Cl⁻浓度的变化不影响碘化物的摄取。哇巴因、呋塞米、莫能菌素和高氯酸盐均降低培养的甲状腺细胞对¹²⁵I的摄取,而氨氯地平和氨苯蝶啶则无此作用。哇巴因、莫能菌素、高氯酸盐和氨氯地平使培养细胞的膜去极化,而呋塞米和氨苯蝶啶则无影响。哇巴因和高氯酸盐增加细胞内Na⁺和Cl⁻并降低K⁺活性;呋塞米和莫能菌素降低这三种离子的活性,但氨苯蝶啶无作用。氨氯地平降低细胞内Na⁺并增加细胞内Cl⁻活性,然而,由于该化合物对K⁺离子交换器的干扰,无法确定其对K⁺活性的影响。除呋塞米外,所有试剂均抑制Na⁺-K⁺-ATP酶活性。这些实验表明:1)Na⁺-I⁻共转运是甲状腺细胞中大多数碘化物积累的原因;2)Na⁺-I⁻共转运系统与Na⁺-K⁺泵相连;3)活性碘化物转运并不总是与Na⁺-K⁺-ATP酶活性相关;4)甲状腺细胞中存在对高氯酸盐敏感的碘化物转运系统;5)培养的甲状腺细胞中也存在不参与活性碘化物转运的转运过程(Na⁺-Cl⁻共转运和Na⁺-H⁺逆向转运)。