Endogenous Metabolite; synthetic form of the thyroid hormone thyroxine (T4)

人血清和羊水中的常见成分是硫酸甲状腺素（T4S）。它主要由外周甲状腺素产生，并在胎儿 I 型 5-单碘化活性较低或被碘酸盐等药物抑制时积聚[1]。

硫酸甲状腺素 (T4S) 在胎羊血清、胆汁、胎便、羊水和尿囊液中含量很高。妊娠十八 (19) 周和十五 (15) 周时女性羊水中的 T4S 浓度（分别为 25.5 ng/dL 和 14.3 ng/dL）。甲状腺功能亢进症患者在摄入1克碘酸一天后，血浆T4S显着升高[1]。前列腺素在体内被大量硫酸化；如果阻止 I 型心肌作用，T4S 的胆汁排泄就会增加 [2]。危重病期间心肌 D1 的心肌作用下降似乎在血清 T4S 水平升高中发挥了作用，该水平明显高于健康受试者。函数[3]。

最近，我们在胎羊血清、胎粪、胆汁、羊水和尿囊液中发现了大量的硫酸甲状腺素（T4S）。然而，人们对甲状腺素在人体内的硫酸盐结合知之甚少。在这项研究中，我们采用了一种新颖、灵敏的T4S RIA来解决这个问题。兔抗血清具有很强的特异性；T4、T3、rT3和3,3'-T2的交叉反应性小于0.002%。其他类似物的交叉反应小于0.0001%。只有rT3S和T3S交叉反应显著（分别为9.9%和2.0%）。甲状腺功能正常者的平均血清T4S浓度（ng/dL）为8.6，甲状腺功能亢进者为14.4，甲状腺功能减退者为5.0，妊娠期为5.9，非甲状腺疾病患者为4.5。妊娠18-19周的女性羊水中T4S浓度（25.5 ng/dL）高于妊娠14-15周的女性（14.3 ng/dL）。甲状腺功能亢进症患者在摄入1克ipodate后1天，血清T4S显著升高。这些数据表明，T4S是人类血清和羊水中的正常成分，主要来源于T4外周，当胎儿I型5'-单脱碘活性低或被药物（如ipodate）抑制时会积聚[1]。

A total of 64 blood samples and 65 liver biopsies were obtained within minutes after death from 79 intensive care patients, randomized for intensive or conventional insulin treatment. Serum T4S and the activities of hepatic D1 and 3,3'-diiodothyronine (T2)-SULT and estrogen-SULT were determined. Results: No differences in T4S or hepatic SULT activities were found between patients treated with intensive or with conventional insulin therapy. T4S levels were significantly elevated compared with healthy references. Furthermore, hepatic D1, but not SULT activity, showed a strong correlation with serum T4S (R = -0.53; P < 0.001) and T4S/T4 ratio (R = -0.62; P < 0.001). Cause of death was significantly correlated with hepatic T2- and estrogen-SULT activities (P < 0.01), with SULT activities being highest in the patients who died of severe brain damage and lowest in the patients who died of a cardiovascular collapse. A longer period of intensive care was associated with higher levels of T4S (P = 0.005), and high levels of bilirubin were associated with low T2-SULT (P = 0.04) activities and high levels of T4S (P < 0.001). Conclusion: Serum T4S levels were clearly elevated compared with healthy references, and the decreased deiodination by liver D1 during critical illness appears to play a role in this increase in serum T4S levels.[3]

[1]. Identification of thyroxine-sulfate (T4S) in human serum and amniotic fluid by a novel T4S radioimmunoassay. Thyroid. 1992 Summer;2(2):101-5.

[2]. Effects of propylthiouracil on the biliary clearance of thyroxine (T4) in rats: decreased excretion of 3,5,3'-triiodothyronine glucuronide and increased excretion of 3,3',5'-triiodothyronine glucuronide and T4 sulfate. Endocrinology. 1989 Oct;125(4):2175-86.

[3]. Increased thyroxine sulfate levels in critically ill patients as a result of a decreased hepatic type Ideiodinase activity. J Clin Endocrinol Metab. 2005 Dec;90(12):6460-5.

The liver metabolizes T4 by deiodination and conjugation to T4 glucuronide (T4G), but little information exists about the formation of T4 sulfate (T4S) in vivo. We have examined the excretion of T4G, T4S, T3 and rT3 glucuronide (T3G and rT3G) in bile, collected under pentobarbital anesthesia 0-8 h or 17-18 h after iv [125I]T4 injection to control and 6-propyl-2-thiouracil (PTU)-treated rats. Radioactivity in bile, plasma, feces, and urine was analyzed by Sephadex LH-20 chromatography and HPLC. PTU induced a 2-fold increase in the biliary excretion of total radioactivity (26.6% vs. 15.0% dose between 0-8 h; 2.0% vs. 1.0% dose between 17-18 h). Biliary metabolites, 17-18 h after T4 injection, in control vs. PTU rats amounted to (percent dose): T4G, 0.44 vs. 0.75; T3G, 0.19 vs. 0.07; rT3G, 0.02 vs. 0.15; and T4S, 0.06 vs. 0.32. Similar results were obtained for control rats when bile was collected between 7-8 h after iv T4. The excretion rate of T3G was lower and that of rT3G higher when bile was continuously collected for 8 h immediately after T4 administration, probably due to prolonged experimental stress. However, regardless of the period of bile collection, PTU induced a more than 24-fold decrease in the T3G/rT3G ratio and a 5-fold increase in T4S excretion. In the animals killed 18 h after T4 injection, PTU treatment increased plasma T4 retention by 50%, reduced urinary I- excretion by 74%, and increased fecal radioactivity by 47%. No conjugates were detected in feces, and the distribution of fecal T4:T3:rT3 was 70:18:2 in control and 68:7:6 in PTU-treated rats. The results indicate that 1) the glucuronidative clearance of T4 is not affected by PTU; 2) the T3G/rT3G ratio in bile is a sensitive indicator of type I deiodinase inhibition; 3) T4 undergoes significant sulfation in rats in vivo, and 4) biliary excretion of T4S is enhanced if its type I deiodination is inhibited.[2]

C15H11I4NO7S

856.93

856.644

C, 21.02; H, 1.29; I, 59.24; N, 1.63; O, 13.07; S, 3.74

77074-49-8

L-Thyroxine;51-48-9;L-Thyroxine sodium salt pentahydrate;6106-07-6

131742

White to off-white solid powder

5.814

144.53

3

8

7

28

625

1

C1=C(C=C(C(=C1I)OC2=CC(=C(C(=C2)I)OS(=O)(=O)O)I)I)C[C@@H](C(=O)O)N

QYXIJUZWSSQICT-LBPRGKRZSA-N

InChI=1S/C15H11I4NO7S/c16-8-1-6(3-12(20)15(21)22)2-9(17)13(8)26-7-4-10(18)14(11(19)5-7)27-28(23,24)25/h1-2,4-5,12H,3,20H2,(H,21,22)(H,23,24,25)/t12-/m0/s1

(2S)-2-amino-3-[4-(3,5-diiodo-4-sulfooxyphenoxy)-3,5-diiodophenyl]propanoic acid

T4 Sulfate; Thyroxine sulphate; L-Tyrosine,O-[3,5-diiodo-4-(sulfooxy)phenyl]-3,5-diiodo-; Thyroxine-4-sulfate; T4 Sulfate; Thyroxine 4'-O-Sulfate; (2S)-2-amino-3-[4-(3,5-diiodo-4-sulfooxyphenoxy)-3,5-diiodophenyl]propanoic acid; Thyroxine sulfate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~140 mg/mL (~163.37 mM)

配方 1 中的溶解度: ≥ 5.75 mg/mL (6.71 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 57.5 mg/mL澄清的DMSO储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: 5.75 mg/mL (6.71 mM) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
例如，若需制备1 mL的工作液，可将 100 μL 57.5 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

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配方 3 中的溶解度: ≥ 2.58 mg/mL (3.01 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。