Evaluation of reactive oxygen species in term low birth babies
DOI:
https://doi.org/10.7439/ijbar.v9i10.4920Keywords:
Malondialdehyde, foetal growthAbstract
Background: Oxidative stress has been implicated as one of the major cause in the pathophysiology of decreased or impaired foetal weight in normal term low birth weight babies. Either increased generation of reactive oxygen species (ROS) or decreased antioxidant levels can be measured to substantiate this finding in view of the increased incidence of term babies with low birth weight.
Aim: The aim of this study is to evaluate the role of reactive oxygen species by measuring the serum malondialdehyde levels in term low weight babies with that of controls with normal weight.
Materials and methods : The study group consisted of 72 term low weight babies weighing 2500 gms of both sexes and 70 controls with >2500 gms of both sexes were included in the study. In the study group babies with birth weight of 2000 g was grouped as group 1a and with weight of >2000 2500g as group 1b. Serum malondialdehyde (MDA) an end product of lipid peroxidation (a measure of free radical damage) were measured using calorimetric thiobarbituric acid method in both study group and control group and were compared with their birth weight and ponderal index. Data was collected and analysed by suitable statistical methods.
Results : The mean MDA levels estimated in the study group was significantly higher (MDA levels 28.5250 +3.0 nmol/L) than in the control group (19.3693+1.60). As the birth weight increased the MDA levels decreased (P 0.01). The mean MDA levels in group 1a (20 among 72) was 32.205 +2.49 nmol/ml and group 1b (52 among 72) was 27.1096+1.72 with p value of 0.01 which was statistically significant.
Conclusion : Our results indicate that in the term low birth weight babies the MDA levels were significantly increased which concludes that ROS species plays a major role in etiopathogenesis of low birth weight babies.
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References
Lin and Santolaya- forgas J. Current concepts of fetal growth restriction: part I. Causes, classification, and pathophysiology. Obstet Gynecol. 1998; 92(6):1044-55.
Jansson, Yu V. The year in neonatology. Med. J. Aust., 1980; 1(5): 198-203.
Heinter Burow, Gaziano JM, Halta A, Zarling EJ. Effects of antioxidant supplementation on lipid peroxidation in healthy and diseased volunteers. Nutr. Cancer 19: 207-212.
Inder TE, Sanderson K, Graham P. Lipid peroxidation as a measure of oxygen free radical damage in the very low birth weight infant. Arch Dis Child Fetal Neonatal Ed. 1994; 70(2):F107-11.
Silver KM, Goldfarb A, Sen CK. Antioxidant supplementation and the control of oxygen toxicity. Amsterdam, Elsevier science publishers B.V., 1994; 163-190.
Pitkanen OM, Hallman M, Andersson SM. Correlation of free oxygen radical induced lipid peroxidation with outcome in low birth weight infants. J Pediatr. 1990; 116(5):760-4.
Nadiger. Estimation of malondialdehyde. Indian Journal of Clinical Biochemistry 1986; 1:133.
Matsubasa T. et al. Oxidative stress in very low birth weight infants as measured by Urinary 8 OHDG. Free Radic Res 2002; 36: 189-93.
Fraco et, Orr WC, Sohal RC. Relationship between antioxidants, peroxidants in undernourished children. Ann. NY Acad. Sci. 1992; 663: 74-84.
Sies H. Oxidative stress. Introductory remarks. Oxidative stress. Orlando Academic press 1-11.
Ghosh S, Hooja V, Miltal SK, Verma RK. Biosocial determinants of birth weights. Indian Paediatrics 1979; 14:107
Lehinger, Bouris A, Chance B. the mitochondrial generation of hydrogen peroxide. General properties and effects of hyper basic O2. Biochem J 1973; 134: 707-716.
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