Document Detail


Ascorbate prevents placental oxidative stress and enhances birth weight in hypoxic pregnancy in rats.
MedLine Citation:
PMID:  22289909     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study isolated the effects of maternal hypoxia independent of changes in maternal nutrition on maternal circulatory and placental molecular indices of oxidative stress and determined whether maternal antioxidant treatment conferred protection. Pregnant rats were subjected to normoxic pregnancy or 13% O2 chronic hypoxia for most of gestation with and without maternal treatment with vitamin C in the drinking water. Maternal hypoxia with and without vitamin C did not affect maternal food or water intake and led to a significant increase in maternal and fetal haematocrit. At gestational day 20, maternal plasma urate and L-cysteine concentrations, and placental levels of 4-hydroxynonenal and heat shock protein 70 were increased while placental heat shock protein 90 levels were decreased in hypoxic pregnancy. The induction of maternal circulatory and placental molecular indices of oxidative stress in hypoxic pregnancies was prevented by maternal treatment with vitamin C. Maternal hypoxia during pregnancy with or without vitamin C increased placental weight, but not total or compartmental volumes. Maternal treatment with vitamin C increased birth weight in both hypoxic and normoxic pregnancies. The data show that maternal hypoxia independent of maternal undernutrition promotes maternal and placental indices of oxidative stress, effects that can be prevented by maternal treatment with vitamin C in hypoxic pregnancy. While vitamin C may not be the ideal candidate of choice for therapy in pregnant women, and taking into consideration differences in ascorbic acid metabolism between rats and humans, the data do underlie that antioxidant treatment may provide a useful intervention to improve placental function and protect fetal growth in pregnancy complicated by fetal hypoxia.
Authors:
H G Richter; E J Camm; B N Modi; F Naeem; C M Cross; T Cindrova-Davies; O Spasic-Boskovic; C Dunster; I S Mudway; F J Kelly; G J Burton; L Poston; D A Giussani
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-01-30
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-16     Completed Date:  2012-07-10     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1377-87     Citation Subset:  IM    
Affiliation:
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Anoxia / metabolism*,  physiopathology
Antioxidants / pharmacology*
Ascorbic Acid / blood,  pharmacology*
Birth Weight / drug effects*
Catalase / metabolism
Cysteine / blood
Disease Models, Animal
Female
Hematocrit
Oxidative Stress / drug effects*
Placenta / drug effects*,  metabolism
Pregnancy
Pregnancy Complications / metabolism,  physiopathology,  prevention & control
Rats
Rats, Wistar
Superoxide Dismutase / metabolism
Uric Acid / blood
Grant Support
ID/Acronym/Agency:
//Biotechnology and Biological Sciences Research Council; //British Heart Foundation
Chemical
Reg. No./Substance:
0/Antioxidants; 50-81-7/Ascorbic Acid; 52-90-4/Cysteine; 69-93-2/Uric Acid; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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