Assessment of Redox Imbalance in Idiopathic Fetal Growth Restricted Pregnancies
- *Corresponding Author:
- Dr. BD Banerjee
Professor and Lab Incharge
Environmental Biochemistry and Molecular Biology Laboratory
Department of Biochemistry
University College of Medical Sciences and GTB Hospital
University of Delhi, Dilshad Garden, Delhi-110095, India
Tel: 09868835502; 011-22135362(O)
E-mail: [email protected]
Received date: July 18, 2012; Accepted date: September 06, 2012; Published date: September 10, 2012
Citation: Goel G, Banerjee BD, Pathak R, Guleria K, Radhakrishnan G, et al. (2012) Assessment of Redox Imbalance in Idiopathic Fetal Growth Restricted Pregnancies. Reprod Sys Sexual Disorders 1:112. doi:10.4172/2161-038X.1000112
Copyright: © 2012 Goel G, et al. This is an open-access article distributed underthe terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Fetal growth restriction (FGR) is one of the most significant causes of perinatal morbidity and mortality. The known causes are poor maternal nutrition, hypertensive disorders complicating pregnancy, maternal medical disorders (multiple pregnancy, congenital fetal malformations), and lifestyle influences. However, in vast majority of cases, the cause still remains unknown. Recent studies have suggested the role of oxidative stress in the pathophysiology of FGR. The aim of this study was to evaluate non-enzymatic oxidative stress biomarkers in maternal and cord blood of idiopathic FGR cases.
Methods: A total of 100 women subjects aged 18 to 35 years, who fulfilled the recruitment criteria, were enrolled in the study after taking an informed written consent. Non-enzymatic oxidative stress was measured by the quantification of 8-hydroxy-2-deoxy-guanosine (8-OHdG), malondialdehyde (MDA), protein carbonyl, reduced glutathione (GSH) and ferric reducing ability of plasma (FRAP) in maternal and cord blood samples of FGR pregnancies of idiopathic origin and compared with those of normal healthy mother-infant pairs.
Results: The levels of 8-OHdG, MDA and protein carbonyl were significantly higher in the ‘idiopathic’ FGR group as compared to the controls, where as the GSH and FRAP were significantly lower.
Conclusion: Increased oxidative stress has been found significantly associated with the increased risk of developing idiopathic FGR.