Transfer and metabolism of thyrotropin releasing hormone across the perfused human term placenta
Autor: | Nicholas M. Fisk, Rekha Bajoria, E Oteng-Ntim |
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Rok vydání: | 1996 |
Předmět: |
Dipeptidase
endocrine system medicine.medical_specialty Placenta Endocrinology Diabetes and Metabolism Clinical Biochemistry Thyrotropin-releasing hormone Peptide hormone Tritium Biochemistry Iodine Radioisotopes Endocrinology Pregnancy Internal medicine medicine Humans Thyrotropin-Releasing Hormone Fetus biology Biochemistry (medical) Transplacental Biological Transport Metabolism Fetal Blood Phenylmercury Compounds Prolactin Perfusion biology.protein Female hormones hormone substitutes and hormone antagonists |
Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 81:3476-3482 |
ISSN: | 1945-7197 0021-972X |
DOI: | 10.1210/jcem.81.10.8855788 |
Popis: | The transport and uptake of TRH was investigated in the maternal-fetal-placental unit of perfused human term placenta. The degradation of TRH in biological fluid was first determined by incubating [125I]TRH with 100 microL 50% maternal or cord sera with or without pretreatment with 200 microM of p-hydroxymercuriphenyl sulfonic acid (p-HMSA), a proline dipeptidase inhibitor. Transplacental transfer of TRH was then studied by adding 10 microCi of [125I]- or [3H]TRH to the maternal circulation of dually perfused isolated lobule of human term placenta with or without 200 microM p-HMSA. Creatinine was used as an internal marker. The rate of degradation of TRH (P0.001) and inhibition by p-HMSA were significantly higher in maternal than cord sera (P0.05). In the maternal circulation, TRH concentration declined rapidly from 100% at time 0 to 33.5 +/- 1.2% at 120 min. The fetal concentration increased from undetectable levels to a maximum of 1.8 +/- 0.3% at 120 min with a low feto-maternal ratio (0.08 +/- 0.02). Perfusion in the presence of p-HMSA, however, did not significantly change fetal concentration, or the maternal and fetal concentration-time integral levels of TRH. Chromatography of maternal, fetal, and placental homogenates showed that TRH was metabolized by the placenta into small molecular weight fragments predominantly released in the maternal circulation. These results suggest that human placenta acts as an enzymatic barrier to the free passage of TRH. |
Databáze: | OpenAIRE |
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