Document Detail


The impact of vitamin C supplementation in pregnancy and in vitro upon fetal membrane strength and remodeling.
MedLine Citation:
PMID:  20581351     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Generation of reactive oxygen species (ROS) has been suggested as a mechanism of fetal membrane (FM) weakening leading to rupture, particularly with preterm premature rupture of the fetal membranes (PROM). In vitro, FM incubation with tumor necrosis factor (TNF) mimics physiological FM weakening, concomitant with generation of ROS and collagen remodeling. Proinflammatory cytokines are also postulated to have a role in the development of the FM physiological weak zone where rupture normally initiates in-term gestations. We hypothesized that antioxidant treatment may block ROS development and resultant FM weakening. Two studies examining antioxidant effects upon FM strength were conducted, one in vivo and the other in vitro. Fetal membrane of patients enrolled in a multicenter placebo-controlled trial to determine the effect of vitamin C (1 g/day) and vitamin E (400 IU/day) upon complications of pre-eclampsia were examined for FM biomechanical properties and biochemical remodeling at birth. Separately, biomechanics and biochemical markers of remodeling were determined in FM fragments incubated with TNF with or without vitamin C preincubation. Supplemental dietary vitamin C in combination with vitamin E did not modify rupture strength, work to rupture, or matrix metalloproteinase-9 (MMP9; protein or activity) either within or outside the term FM physiological weak zone. In vitro, TNF decreased FM rupture strength by 50% while increasing MMP9 protein. Vitamin C did not inhibit these TNF-induced effects. Vitamin C alone had a weakening effect on FM in vitro. We speculate that vitamin C supplementation during pregnancy will not be useful in the prevention of preterm PROM.
Authors:
Brian M Mercer; Adli Abdelrahim; Robert M Moore; Jillian Novak; Deepak Kumar; Joseph M Mansour; Marina Perez-Fournier; Cynthia J Milluzzi; John J Moore
Publication Detail:
Type:  Comparative Study; Controlled Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Reproductive sciences (Thousand Oaks, Calif.)     Volume:  17     ISSN:  1933-7205     ISO Abbreviation:  Reprod Sci     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-06-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101291249     Medline TA:  Reprod Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  685-95     Citation Subset:  IM    
Affiliation:
From the Department of Reproductive Biology, Case Western Reserve University, Cleveland, OH 44109, USA. bmm12@case.edu
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MeSH Terms
Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
HD40544-01/HD/NICHD NIH HHS; HD48476/HD/NICHD NIH HHS; M01 RR000080-45/RR/NCRR NIH HHS; M01 RR00080/RR/NCRR NIH HHS; R01 HD048476-05/HD/NICHD NIH HHS; U10 HD040544-09/HD/NICHD NIH HHS; UL1 RR024989/RR/NCRR NIH HHS; UL1 RR024989-04/RR/NCRR NIH HHS

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