González-Cinca Nuria, Pérez de la Ossa Pablo, Carreras José, Climent Fernando
Unitat de Bioquímica, Departament de Ciéncies Fisiològiques I, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Universitat de Barcelona, Barcelona, Spain.
Horm Res. 2004;62(4):191-6. doi: 10.1159/000080897. Epub 2004 Sep 16.
The effects of triiodothyronine (T(3)) and hypoxia on 2,3-bisphosphoglycerate (2,3-BPG) studied in vitro are unclear. To clarify these effects we selected a more physiologic approach: the in vivo study in rabbits. We also present the changes produced by T(3) and hypoxia on phosphoglycerate mutase (PGAM), which requires 2,3-BPG as a cofactor, and 2,3-BPG synthase (BPGS), the enzyme responsible for 2,3-BPG synthesis in erythroblasts and reticulocytes.
Hyperthyroidism was induced by daily T(3) injection (250 microg/kg), hypoxia by a mixture of 90% nitrogen and 10% oxygen and hypothyroidism by propylthiouracil (PTU) added to drinking water.
Both T(3) administration and hypoxic conditions increased 2,3-BPG levels and BPGS mRNA levels and activity in erythroblasts but not in reticulocytes. Unlike BPGS, both PGAM mRNA levels and activity were increased in erythroblasts and reticulocytes under hyperthyrodism and hypoxia. The antihormone PTU produced opposite effects to T(3).
The results presented here suggest that both hyperthyroidism and hypoxia modulate in vivo red cell 2,3-BPG content by changes in the expression of BPGS. Similarly, the changes in PGAM activity are also explained by changes in its expression.
三碘甲状腺原氨酸（T3）和缺氧对2,3-二磷酸甘油酸（2,3-BPG）的体外研究结果尚不清楚。为了阐明这些影响，我们选择了一种更符合生理的方法：对兔子进行体内研究。我们还展示了T3和缺氧对磷酸甘油酸变位酶（PGAM）和2,3-BPG合酶（BPGS）产生的变化，PGAM需要2,3-BPG作为辅因子，而BPGS是负责在成红细胞和网织红细胞中合成2,3-BPG的酶。
通过每日注射T3（250μg/kg）诱导甲状腺功能亢进，通过90%氮气和10%氧气的混合物诱导缺氧，并通过在饮用水中添加丙硫氧嘧啶（PTU）诱导甲状腺功能减退。
给予T3和缺氧条件均增加了成红细胞中2,3-BPG水平、BPGS mRNA水平和活性，但网织红细胞中未增加。与BPGS不同，在甲状腺功能亢进和缺氧情况下，成红细胞和网织红细胞中的PGAM mRNA水平和活性均增加。抗激素PTU产生了与T3相反的作用。
此处呈现的结果表明，甲状腺功能亢进和缺氧均通过改变BPGS的表达来调节体内红细胞2,3-BPG含量。同样，PGAM活性的变化也可以通过其表达的变化来解释。
