Zalatnai A, Nagy S U, Csaba G
Acta Morphol Acad Sci Hung. 1980;28(1-2):83-94.
Iodide uptake of the thyroid following the joint administration of 1-methyl-2-mercapto-imidazole (MMI) and TSH was studied by autoradiography at various points of time throughout 125 days in pinealectomized and sham-operated rats. In the pinealectomized group iodide uptake decreased. The enhanced TSH effect also decreased by the end of the experiment, suggesting the existence of a mechanism antagonizing the TSH effect. It is assumed that prolonged TSH dominance stimulates the pineal which, in turn, inhibits iodide uptake by the thyroid. This mechanism would thus prevent the TSH dominant state to influence the thyroid. As this prevention occurred also in pinealectomized animals it is postulated that some other as yet unknown structures exert a similar effect. It is suggested that the pineal body acts upon the follicular cells of the thyroid, exerting thus a peripheral inhibitory effect on iodide-uptake.
通过放射自显影术,在125天内的不同时间点,研究了松果体切除和假手术大鼠联合给予1-甲基-2-巯基咪唑(MMI)和促甲状腺激素(TSH)后甲状腺对碘的摄取情况。在松果体切除组中,碘摄取减少。到实验结束时,增强的TSH效应也降低了,这表明存在一种拮抗TSH效应的机制。据推测,长期的TSH优势会刺激松果体,而松果体反过来会抑制甲状腺对碘的摄取。因此,这种机制将阻止TSH优势状态影响甲状腺。由于这种阻止作用在松果体切除的动物中也会发生,因此推测一些其他未知结构也会发挥类似作用。有人认为松果体作用于甲状腺的滤泡细胞,从而对碘摄取产生外周抑制作用。