Maternal 3,3'-Diiodothyronine Sulfate Formation from Guinea Pig Placenta Perfused with 3,3',5-Triodothyronine.
Maternal 3,3'-Diiodothyronine Sulfate Formation from Guinea Pig Placenta Perfused with 3,3',5-Triodothyronine.
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豚鼠胎盘灌注3,3‘，5-三碘甲状腺原氨酸形成母体3,3’-二碘甲状腺原氨酸硫酸盐。
DOI：
10.31579/2640-1045/101
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发表时间：
2021-09
期刊：
影响因子：
--
通讯作者：
Chen DB
中科院分区：
文献类型：
--
作者：
Wu SY;Emerson CH;Tjioe E;Chen DB
血清3，3 '，5-三碘甲状腺原氨酸（T3）在近足月胎儿中保持较低水平，以防止生长中的胎儿过度暴露于其在哺乳动物中的活性分解代谢作用。本研究通过在妊娠豚鼠中原位胎盘灌注外环标记的[125 I]-T3来深入了解胎盘在T3代谢、T3及其代谢物的胎儿向母体转移中的作用，妊娠豚鼠在妊娠晚期（足月= 65天）母体血清中硫酸化3，3 '-二碘甲状腺原氨酸（T2 S）水平升高，与人类妊娠相似。在妊娠58 - 65天之间对妊娠豚鼠进行的单程胎盘灌注进行了研究。在两个单独的实验中，在37°C下用外环标记的[125 I]-T3原位灌注豚鼠胎盘的脐动脉。当30分钟后胎盘流出物中达到稳态放射性水平时，在60分钟灌注结束时获得母体血清和脐带流出物用于分析。在胎盘灌注[125 I]-T3后，在母体血清中很容易检测到硫酸化[125 I]-T2 S作为T3的主要代谢产物，这表明胎盘内环脱碘酶和磺基转移酶可能在胎儿T3体内平衡和硫酸化碘甲腺原氨酸代谢产物从胎儿向母体转移中发挥重要作用。胎盘中3型脱碘酶（D3）的表达和甲状腺激素磺基转移酶活性可能在保护胎儿发育器官免受妊娠晚期活性甲状腺激素过度暴露中起重要作用。D3和磺基转移酶的联合活性促进了T2 S向母体循环的胎盘转移。T2 S的母体循环起源于胎儿T3，其作为胎儿甲状腺功能生物标志物的作用值得进一步评价和研究。
Serum 3, 3’,5-triiodothyronine (T3) remains low in near-term fetus to prevent the growing fetus from undue exposure to its active catabolic effect in mammals. The present study was undertaken to gain insight in the role of placenta in T3 metabolism, fetal to maternal transfer of T3, and its metabolites by in situ placenta perfusion with outer-ring labeled [125I]-T3 in pregnant guinea pig, a species showing increased sulfated 3, 3’-diiodothyronine (T2S) levels in maternal serum in late pregnancy (term = 65 days), similarly to humans in pregnancy. One-pass placenta perfusions performed on pregnant guinea pigs were studied between 58 – 65 days of gestation. In two separate experiments, the umbilical artery of the guinea pig placenta was perfused in situ at 37°C with outer-ring labeled [125I]-T3. Maternal sera and umbilical effluents were obtained for analysis at the end of a 60-minute perfusion, when the steady-state levels of radioactivity were reached in the placenta effluent after 30-minute. Sulfated [125I]-T2S was readily detected in the maternal serum as the major metabolite of T3 following the perfusion of placenta with [125I]-T3, suggesting that placental inner-ring deiodinase and sulfotransferase may play an important role in fetal T3 homeostasis and in the fetal to maternal transfer of sulfated iodothyronine metabolites. The expression of type 3 deiodinase (D3) and thyroid hormone sulfotransferase activity in placenta may play an important role to protect developing organs against undue exposure to active thyroid hormone in late gestation in the fetus. The combined activities of D3 and sulfotransferase promoted a placental transfer of T2S into maternal circulation. The maternal circulation of T2S is fetal T3 in origin and its role as a fetal thyroid function biomarker deserves further evaluations and studies.