Oxidative stress varies with the mode of delivery in intrauterine growth retardation: Association with Apgar score

被引:19
作者
Sridhar, M. G. [1 ]
Setia, Sajita
John, Mathew
Bhat, Vishnu
Nandeesha, H.
Sathiyapriya, V.
机构
[1] Jawaharlal Inst Postgrad Med Educ & Res, Dept Biochem, Pondicherry 605006, India
[2] Jawaharlal Inst Postgrad Med Educ & Res, Dept Paediat, Pondicherry 605006, India
关键词
IUGR; oxidative stress; malondialdehyde; protein carbonylation; Apgar score;
D O I
10.1016/j.clinbiochem.2007.01.023
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objective: To assess if oxidative injury in intrauterine growth retarded and healthy newborns is affected by the mode of delivery and whether Apgar score as a marker of neonatal survival is dependent on lipid and protein oxidative injury assessed by measuring malondialdehyde and protein carbonylation. Methods: 30 IUGR newborns, 15 born by normal vaginal delivery and 15 born by elective caesarean section, and 40 healthy control infants, 30 born by normal vaginal delivery and 10 born by elective caesarean section, were studied at birth. Cord blood was collected for determination of malondiadehyde and protein carbonylation. Results: IUGR newborns had significantly elevated NIDA and protein carbonylation than the control group. Apgar scores, both at 1 and 5 min, were significantly lower in the IUGR group. These were assessed by independent sample t test. Using one-way ANOVA we found that MDA and protein carbonyls levels were not statistically different in healthy control group and in IUGR subgroup born by caesarean section however they were significantly different in other groups. Linear regression analysis revealed that Apgar scores both at I min and 5 min were dependent on MDA in IUGR newborns. Apgar score was however not dependent on protein carbonylation in the same group. Conclusion: Apgar score in IUGR newborns is dependent on the extent of oxidative injury and elective caesarean section minimises the same. (c) 2007 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:688 / 691
页数:4
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