Hypoxanthine transport in the guinea pig and human placenta is a carrier-mediated process that does not involve nucleoside transporters

L. Felipe Barros

doi:10.1016/S0002-9378(94)70086-9

Hypoxanthine transport in the guinea pig and human placenta is a carrier-mediated process that does not involve nucleoside transporters

L. Felipe Barros^*

^*Corresponding author for this work

Universidad de Chile

Research output: Contribution to journal › Article › peer-review

14 Scopus citations

Abstract

OBJECTIVE: The purpose of this study was to characterize the mechanisms involved in the placental clearance of hypoxanthine. STUDY DESIGN: Uptake of isotope-labeled compounds was measured in the in situ perfused guinea pig placenta and in membrane vesicles isolated from the human syncytiotrophoblast. RESULTS: In the guinea pig hypoxanthine uptake (from the fetal circulation) proceeded by a saturable (Michaelis constant ≈90 μmol/L), sodium-dependent mechanism that was inhibited by 19 mmol/L papaverine but not by 10 wmol/L nitrobenzylthioinosine or 10 mmol/L uridine. Uridine uptake was blocked by nitrobenzylthioinosine but not by papaverine or 4 mmol/L hypoxanthine. In human brush-border (maternal-facing) membrane vesicles hypoxanthine influx was sodium independent and best fitted to a saturable (Michaelis constant 290 ± 45 μmol/L) plus a linear component. Saturable influx was blocked by papaverine but not by nitrobenzylthioinosine. Uridine uptake was not affected by 4 mmol/L hypoxanthine. Mediated hypoxanthine uptake by human basal (fetal-facing) membrane vesicles was not detected. CONCLUSION: At both placental blood-tissue interfaces hypoxanthine transport occurs through specific mechanisms that are different from the nucleoside transporters.

Original language	English
Pages (from-to)	111-117
Number of pages	7
Journal	American Journal of Obstetrics and Gynecology
Volume	171
Issue number	1
DOIs	https://doi.org/10.1016/S0002-9378(94)70086-9
State	Published - 1994
Externally published	Yes

Bibliographical note

Funding Information:
From the Departamento de Fisiologia y Biofisica, Facultad de Medicina, Universidad de Chile. Supported by Fondo Nacional de Investigacion Cientifica y Tecnologica (FONDECYT) 1326-91 (Chile) and the Wellcome Trust (U.K.). The author was the recipient of a Faculty of Medicine Fellowship, University of Chile. Received for publication July 8, 1993; revised December 8, 1993; accepted December 28, 1993. Reprint requests: L.F. Barros, MD, PhD, Department of Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom. Copyright © 1994 by Mosby-Year Book, Inc. 0002-9378/94 $3.00 + 0 6/1/54622

ASJC Scopus subject areas

Obstetrics and Gynecology

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10.1016/S0002-9378(94)70086-9

Cite this

@article{c340d8bfdfe84d93bbb1f8ff32f34642,

title = "Hypoxanthine transport in the guinea pig and human placenta is a carrier-mediated process that does not involve nucleoside transporters",

abstract = "OBJECTIVE: The purpose of this study was to characterize the mechanisms involved in the placental clearance of hypoxanthine. STUDY DESIGN: Uptake of isotope-labeled compounds was measured in the in situ perfused guinea pig placenta and in membrane vesicles isolated from the human syncytiotrophoblast. RESULTS: In the guinea pig hypoxanthine uptake (from the fetal circulation) proceeded by a saturable (Michaelis constant ≈90 μmol/L), sodium-dependent mechanism that was inhibited by 19 mmol/L papaverine but not by 10 wmol/L nitrobenzylthioinosine or 10 mmol/L uridine. Uridine uptake was blocked by nitrobenzylthioinosine but not by papaverine or 4 mmol/L hypoxanthine. In human brush-border (maternal-facing) membrane vesicles hypoxanthine influx was sodium independent and best fitted to a saturable (Michaelis constant 290 ± 45 μmol/L) plus a linear component. Saturable influx was blocked by papaverine but not by nitrobenzylthioinosine. Uridine uptake was not affected by 4 mmol/L hypoxanthine. Mediated hypoxanthine uptake by human basal (fetal-facing) membrane vesicles was not detected. CONCLUSION: At both placental blood-tissue interfaces hypoxanthine transport occurs through specific mechanisms that are different from the nucleoside transporters.",

keywords = "Hypoxanthine transport, guinea pig placenta, human placenta, nitrobenzylthioinosine, nucleoside transport",

author = "Barros, {L. Felipe}",

note = "Funding Information: From the Departamento de Fisiologia y Biofisica, Facultad de Medicina, Universidad de Chile. Supported by Fondo Nacional de Investigacion Cientifica y Tecnologica (FONDECYT) 1326-91 (Chile) and the Wellcome Trust (U.K.). The author was the recipient of a Faculty of Medicine Fellowship, University of Chile. Received for publication July 8, 1993; revised December 8, 1993; accepted December 28, 1993. Reprint requests: L.F. Barros, MD, PhD, Department of Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom. Copyright {\textcopyright} 1994 by Mosby-Year Book, Inc. 0002-9378/94 $3.00 + 0 6/1/54622",

year = "1994",

doi = "10.1016/S0002-9378(94)70086-9",

language = "English",

volume = "171",

pages = "111--117",

journal = "American Journal of Obstetrics and Gynecology",

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T1 - Hypoxanthine transport in the guinea pig and human placenta is a carrier-mediated process that does not involve nucleoside transporters

AU - Barros, L. Felipe

N1 - Funding Information: From the Departamento de Fisiologia y Biofisica, Facultad de Medicina, Universidad de Chile. Supported by Fondo Nacional de Investigacion Cientifica y Tecnologica (FONDECYT) 1326-91 (Chile) and the Wellcome Trust (U.K.). The author was the recipient of a Faculty of Medicine Fellowship, University of Chile. Received for publication July 8, 1993; revised December 8, 1993; accepted December 28, 1993. Reprint requests: L.F. Barros, MD, PhD, Department of Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom. Copyright © 1994 by Mosby-Year Book, Inc. 0002-9378/94 $3.00 + 0 6/1/54622

PY - 1994

Y1 - 1994

N2 - OBJECTIVE: The purpose of this study was to characterize the mechanisms involved in the placental clearance of hypoxanthine. STUDY DESIGN: Uptake of isotope-labeled compounds was measured in the in situ perfused guinea pig placenta and in membrane vesicles isolated from the human syncytiotrophoblast. RESULTS: In the guinea pig hypoxanthine uptake (from the fetal circulation) proceeded by a saturable (Michaelis constant ≈90 μmol/L), sodium-dependent mechanism that was inhibited by 19 mmol/L papaverine but not by 10 wmol/L nitrobenzylthioinosine or 10 mmol/L uridine. Uridine uptake was blocked by nitrobenzylthioinosine but not by papaverine or 4 mmol/L hypoxanthine. In human brush-border (maternal-facing) membrane vesicles hypoxanthine influx was sodium independent and best fitted to a saturable (Michaelis constant 290 ± 45 μmol/L) plus a linear component. Saturable influx was blocked by papaverine but not by nitrobenzylthioinosine. Uridine uptake was not affected by 4 mmol/L hypoxanthine. Mediated hypoxanthine uptake by human basal (fetal-facing) membrane vesicles was not detected. CONCLUSION: At both placental blood-tissue interfaces hypoxanthine transport occurs through specific mechanisms that are different from the nucleoside transporters.

AB - OBJECTIVE: The purpose of this study was to characterize the mechanisms involved in the placental clearance of hypoxanthine. STUDY DESIGN: Uptake of isotope-labeled compounds was measured in the in situ perfused guinea pig placenta and in membrane vesicles isolated from the human syncytiotrophoblast. RESULTS: In the guinea pig hypoxanthine uptake (from the fetal circulation) proceeded by a saturable (Michaelis constant ≈90 μmol/L), sodium-dependent mechanism that was inhibited by 19 mmol/L papaverine but not by 10 wmol/L nitrobenzylthioinosine or 10 mmol/L uridine. Uridine uptake was blocked by nitrobenzylthioinosine but not by papaverine or 4 mmol/L hypoxanthine. In human brush-border (maternal-facing) membrane vesicles hypoxanthine influx was sodium independent and best fitted to a saturable (Michaelis constant 290 ± 45 μmol/L) plus a linear component. Saturable influx was blocked by papaverine but not by nitrobenzylthioinosine. Uridine uptake was not affected by 4 mmol/L hypoxanthine. Mediated hypoxanthine uptake by human basal (fetal-facing) membrane vesicles was not detected. CONCLUSION: At both placental blood-tissue interfaces hypoxanthine transport occurs through specific mechanisms that are different from the nucleoside transporters.

KW - Hypoxanthine transport

KW - guinea pig placenta

KW - human placenta

KW - nitrobenzylthioinosine

KW - nucleoside transport

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U2 - 10.1016/S0002-9378(94)70086-9

DO - 10.1016/S0002-9378(94)70086-9

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C2 - 8030685

AN - SCOPUS:0028030341

SN - 0002-9378

VL - 171

SP - 111

EP - 117

JO - American Journal of Obstetrics and Gynecology

JF - American Journal of Obstetrics and Gynecology

IS - 1

ER -

Hypoxanthine transport in the guinea pig and human placenta is a carrier-mediated process that does not involve nucleoside transporters

Abstract

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ASJC Scopus subject areas

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