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首页> 外文期刊>Journal of Clinical and Diagnostic Research >Oxidative Stress in the Development of Genetic Generalised Epilepsy: An Observational Study in Southern Indian Population BC05-BC08
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Oxidative Stress in the Development of Genetic Generalised Epilepsy: An Observational Study in Southern Indian Population BC05-BC08

机译:遗传性癫痫发展中的氧化应激:印度南部人口BC05-BC08的观察研究。

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Introduction: Oxidative stress resulting from excessive generation of Reactive Oxygen Species (ROS) plays a significant role in neurodegeneration associated with seizures/epilepsy.Aim: To evaluate oxidative stress markers and antioxidant enzymes in Genetic Generalised Epilepsy (GGE) and to know the extent of oxidative stress induced by Anti-Epileptic Drugs (AEDs) with the time duration of treatment.Materials and Methods: In this case-control study, 310 GGE patients (male:female=203:107), who were on AED treatment (n=235) and 75 untreated patients (male:female=49:26) along with 310 age and sex matched healthy controls were recruited. Oxidative stress markers such as Nitric Oxide (NO), Malondialdehyde (MDA) and antioxidant enzyme activities namely Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and Catalase (CAT) were measured spectrophotometrically.Results: Significantly higher levels of serum NO, MDA and low levels of plasma Total Antioxidant Capacity (TAC) were found in patients as compared to controls (p5 years compared to other groups (= 1 year and 1-= 5 years) (p=0.02, p=0.01, p=0.001, p=0.01 and p=0.05 respectively). Further, significant increase in the levels of NO, MDA and decreased activities of SOD, CAT were found in treated patients compared to untreated patients (p<0.05) denoting that additional oxidative stress induced by AEDs which results in seizure recurrence and drug intractability.Conclusion: Our study demonstrated that GGE patients have additional oxidative stress due to AEDs and decreased antioxidant enzyme activities causing an imbalance between oxidant and antioxidant status, which might contribute to the pathogenesis of GGE.
机译:简介:过量产生的活性氧(ROS)引起的氧化应激在与癫痫/癫痫相关的神经退行性变中起重要作用。目的:评估遗传性全身癫痫(GGE)中的氧化应激标志物和抗氧化酶,并了解其程度抗癫痫药(AED)诱导的氧化应激随治疗时间的延长。材料与方法:在本病例对照研究中,接受AED治疗的310名GGE患者(男性:女性= 203:107)(n =招募了235名患者)和75名未经治疗的患者(男:女= 49:26)以及310名年龄和性别相匹配的健康对照组。用分光光度法测量了氧化应激标记物,如一氧化氮(NO),丙二醛(MDA)和抗氧化酶活性,即超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GPx)和过氧化氢酶(CAT)。结果:血清NO,MDA含量明显升高与对照组相比,患者的血浆总抗氧化能力(TAC)较低(p5年,其他组(= 1年和1- = 5年))(p = 0.02,p = 0.01,p = 0.001,分别为p = 0.01和p = 0.05)。此外,与未治疗的患者相比,治疗的患者中NO,MDA的水平显着升高,SOD,CAT的活性显着降低(p <0.05),这表明AED诱导了额外的氧化应激结论:我们的研究表明,GGE患者由于AED引起额外的氧化应激,抗氧化酶活性降低,导致氧化和抗氧化状态之间的不平衡,这可能导致癫痫复发和药物难治性。可能会导致GGE的发病。

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