Abstract | OBJECTIVES: 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. METHODS: RESULTS: 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). CONCLUSION: 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.
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Authors | Nuria González-Cinca, Pablo Pérez de la Ossa, José Carreras, Fernando Climent |
Journal | Hormone research
(Horm Res)
Vol. 62
Issue 4
Pg. 191-6
( 2004)
ISSN: 0301-0163 [Print] Switzerland |
PMID | 15375329
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright (c) 2004 S. Karger AG, Basel. |
Chemical References |
- RNA, Messenger
- Triiodothyronine
- 2,3-Diphosphoglycerate
- Phosphoglycerate Mutase
- Bisphosphoglycerate Mutase
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Topics |
- 2,3-Diphosphoglycerate
(blood, metabolism)
- Animals
- Bisphosphoglycerate Mutase
(blood, genetics, metabolism)
- Erythroblasts
(metabolism)
- Hyperthyroidism
(blood, chemically induced, metabolism)
- Hypoxia
(blood, metabolism)
- Male
- Phosphoglycerate Mutase
(blood, genetics, metabolism)
- RNA, Messenger
(blood, metabolism)
- Rabbits
- Reticulocytes
(metabolism)
- Triiodothyronine
(pharmacology)
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