Ayyappan S, Philip Sachu, Bharathy N, Ramesh V, Kumar C Naveen, Swathi S, Kumar A Arun
Department of Biochemistry, Vivekananda Dental College for Women, Trichengodu, Namakkal, Tamil Nadu, India.
Departments of Biochemistry, Sri Lakshmi Narayana Institute of Medical Sciences, Affiliated to Bharath University, Puducherry, Tamil Nadu, India.
J Pharm Bioallied Sci. 2015 Apr;7(Suppl 1):S16-21. doi: 10.4103/0975-7406.155766.
Neonatal jaundice refers to yellow coloration of the skin and the sclera (whites of the eyes) of newborn babies that result from the accumulation of bilirubin in the skin and mucous membranes. Because bilirubin is potentially toxic to the central nervous system. Genetic disorders of bilirubin conjugation, particularly the common Gilbert's syndrome, can also contribute to neonatal hyperbilirubinemia.
The aim of this study was to evaluate the lipid per-oxidation and antioxidant enzyme activities in patients with neonatal jaundice before and after phototherapy.
The study includes 50 neonatal jaundice patients with average age 2-15 days. All patients of neonatal jaundice receiving phototherapy except feeding, cleaning. Subjects selected were from the patients attending Pediatrics Department. Plasma malondialdehyde (MDA), erythrocyte glutathione peroxidase (GPX), superoxide dismutase and catalase (CAT) to monitor the bilirubin level.
The results show increased levels of bilirubin compared with controls (P < 0.001) shows the level of plasma MDA in control, before and after phototherapy. Represents the level of GPX was significantly increased in after the phototherapy group when compared with before phototherapy and control SPSS soft ware: (P < 0.001). Shows the reduced glutathione (GSH) level in plasma was significantly decreased in the after phototherapy group when compared with before phototherapy and control (P < 0.001). And finally with ascorbic acid and CAT.
It is evident from the study that increased oxidative stress in neonatal jaundice babies leads to decrease in the levels of antioxidants like GSH and ascorbic acid and disturb their metabolism, that weaken their ability to fight the growing stress. Intense oxidative stress and decreased antioxidants may contribute to neural cell death and alter the erythrocytomembrane structure processing in neonatal jaundice.
新生儿黄疸是指新生儿皮肤和巩膜(眼白)发黄,这是由于胆红素在皮肤和黏膜中积聚所致。由于胆红素对中枢神经系统具有潜在毒性。胆红素结合的遗传疾病,尤其是常见的吉尔伯特综合征,也可导致新生儿高胆红素血症。
本研究旨在评估光疗前后新生儿黄疸患者的脂质过氧化和抗氧化酶活性。
该研究纳入50例平均年龄为2至15天的新生儿黄疸患者。所有接受光疗的新生儿黄疸患者,除喂养、清洁外。所选受试者来自儿科就诊患者。检测血浆丙二醛(MDA)、红细胞谷胱甘肽过氧化物酶(GPX)、超氧化物歧化酶和过氧化氢酶(CAT)以监测胆红素水平。
结果显示,与对照组相比胆红素水平升高(P < 0.001),显示了对照组、光疗前后血浆MDA水平。与光疗前和对照组相比,光疗后组中GPX水平显著升高(P < 0.001)。与光疗前和对照组相比,光疗后组血浆中还原型谷胱甘肽(GSH)水平显著降低(P < 0.001)。最后是抗坏血酸和CAT。
从研究中可以明显看出,新生儿黄疸婴儿氧化应激增加导致GSH和抗坏血酸等抗氧化剂水平降低,并扰乱其代谢,削弱了它们抵抗不断增加的应激的能力。强烈的氧化应激和抗氧化剂减少可能导致神经细胞死亡,并改变新生儿黄疸中红细胞膜结构的处理。