Oxidative stress plays a pivotal role in the pathogenesis of neurological disorders. Free radical generation appears to be the mode of lead toxicity. We evaluated the effects of blood lead levels on oxidative stress parameters in children suffering from neurological disorders. Thirty children (aged 3-12 years) with neurological disorders (cerebral palsy [n = 12], seizures [n = 11], and encephalopathy [n = 7]) were recruited in the study group. Sixty healthy children (aged 3-12 years) from similar socio-economic environments and not suffering from any chronic disease were taken as the controls. Blood lead levels and oxidant/antioxidant status were determined. Mean blood lead level was significantly higher while delta-aminolevulinic acid dehydratase (delta-ALAD) activity, a biomarker for lead exposure, was significantly lower in the study group as compared to the control group (P < 0.05 for each). Malondialdehyde (MDA) levels, an end-product of lipid peroxidation, were significantly higher while the antioxidant glutathione (GSH) levels were significantly lower in the study group as compared to the control group (P < 0.05 for each). Activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were significantly higher in the study group than those of the control group (P < 0.05 for each). There were significant negative correlations of blood lead levels with delta-ALAD (r = -0.35; P < 0.05) and GSH (r = -0.31; P < 0.05), and positive correlations with MDA (r = 0.37; P < 0.05), SOD (r = 0.53; P < 0.05), and CAT (r = 0.31; P < 0.05). In turn, delta-ALAD had significant negative correlations with MDA (r = -0.29; P < 0.05), SOD (r = -0.28; P < 0.05) and CAT (r = -0.34; P < 0.05), but positive correlation with GSH (r = 0.32; P < 0.05). Although a causal pathway can not be determined from the present study, our findings indicate lead-induced oxidative stress in blood of children with neurological disorders. Lead-induced oxidative stress as an underlying mechanism for neurological diseases in children warranted further investigation.

中文翻译：

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与儿童血铅水平相关的氧化应激和神经系统疾病。

氧化应激在神经系统疾病的发病机理中起着关键作用。自由基的产生似乎是铅毒性的方式。我们评估了血铅水平对患有神经系统疾病的儿童的氧化应激参数的影响。在研究组中招募了30名神经系统疾病（脑瘫[n = 12]，癫痫发作[n = 11]和脑病[n = 7]）的儿童（年龄3-12岁）。以60名健康儿童（3-12岁）为背景，他们来自相似的社会经济环境，没有任何慢性疾病。测定血铅水平和氧化剂/抗氧化剂状态。平均血铅水平显着升高，而δ-氨基乙酰丙酸脱水酶（delta-ALAD）活性是铅暴露的生物标志物，与对照组相比，研究组的血脂水平显着降低（每个P <0.05）。与对照组相比，研究组的脂质过氧化的最终产物丙二醛（MDA）水平明显较高，而抗氧化剂谷胱甘肽（GSH）水平则显着较低（每个P <0.05）。研究组中的抗氧化酶超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性显着高于对照组（每个P <0.05）。血铅水平与delta-ALAD（r = -0.35; P <0.05）和GSH（r = -0.31; P <0.05）呈显着负相关，与MDA呈正相关（r = 0.37; P <0.05） ，SOD（r = 0.53; P <0.05）和CAT（r = 0.31; P <0.05）。反过来，delta-ALAD与MDA呈显着负相关（r = -0.29; P <0.05），SOD（r = -0.28; P <0.05）和CAT（r = -0.34; P <0.05），与GSH正相关（r = -0.34; P <0.05） r = 0.32； P <0.05）。尽管目前的研究无法确定因果关系的途径，但我们的发现表明，神经系统疾病的儿童血液中铅诱导的氧化应激。铅诱导的氧化应激作为儿童神经系统疾病的潜在机制值得进一步研究。