Basha Mahaboob P, Begum Shabana, Mir Bilal Ahmed
Department of Zoology, Bangalore University, Bangalore, Karnataka, India.
Maharanis Science College for Women, Bangalore, Karnataka, India.
Toxicol Int. 2013 Sep;20(3):201-7. doi: 10.4103/0971-6580.121666.
Oxidative stress is considered as a possible molecular mechanism involved in lead (Pb(2+)) neurotoxicity. Very few studies have been investigated on the occurrence of oxidative stress in developing animals due to Pb(2+) exposure. Considering the vulnerability of the developing brain to Pb(2+), this study was carried out to investigate the effects of Pb(2+) exposure in brain regions especially on antioxidant enzyme activities along with ameliorative effects of ethylenediaminetetraacetic acid (EDTA) and clinoptilolite.
Three-week old developing Swiss mice Mus musculus were intraperitoneally administered with Pb(2+) acetate in water (w/v) (100 mg/kg body weight/day) for 21 days and control group was given distilled water. Further Pb(2+)-toxicated mice were made into two subgroups and separately supplemented with EDTA and clinoptilolite (100 mg/kg body weight) for 2 weeks.
In Pb(2+)-exposed mice, in addition to increased lipid peroxidation, the activity levels of catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH) found to decrease in all regions of brain indicating, existence of severe oxidative stress due to decreased antioxidant function. Treatment of Pb(2+)-exposed mice with EDTA and clinoptilolite lowered the lipid peroxidation (LPO) levels revealing their antioxidant potential to prevent oxidative stress. Similarly their administration led to recover the level of catalase, SOD, and GPx enzymes affected during Pb(2+) toxicity in different regions of brain.
The protection of brain tissue against Pb(2+)-induced toxicity by clinoptilolite and EDTA in the present experiment might be due to their ability to react faster with peroxyl radicals there by reducing the severity of biochemical variable indicative of oxidative damage. Thus, the results of present study indicate the neuroprotective potential of clinoptilolite and EDTA against Pb(2+) toxicity.
氧化应激被认为是铅(Pb(2+))神经毒性可能涉及的分子机制。关于发育中的动物因暴露于Pb(2+)而发生氧化应激的研究极少。鉴于发育中的大脑对Pb(2+)的易损性,本研究旨在探讨Pb(2+)暴露对脑区的影响,特别是对抗氧化酶活性的影响,以及乙二胺四乙酸(EDTA)和斜发沸石的改善作用。
给3周龄发育中的瑞士小家鼠腹腔注射溶于水(w/v)的醋酸铅(100 mg/kg体重/天),持续21天,对照组给予蒸馏水。进一步将铅中毒小鼠分为两个亚组,分别补充EDTA和斜发沸石(100 mg/kg体重),持续2周。
在暴露于Pb(2+)的小鼠中,除脂质过氧化增加外,过氧化氢酶、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽(GSH)的活性水平在脑的所有区域均降低,表明由于抗氧化功能下降存在严重的氧化应激。用EDTA和斜发沸石处理暴露于Pb(2+)的小鼠可降低脂质过氧化(LPO)水平,显示出它们预防氧化应激的抗氧化潜力。同样,它们的给药导致在Pb(2+)毒性作用期间受影响的脑不同区域的过氧化氢酶、SOD和GPx酶水平恢复。
在本实验中,斜发沸石和EDTA对脑组织免受Pb(2+)诱导的毒性的保护作用可能是由于它们能够更快地与过氧自由基反应,从而降低指示氧化损伤的生化变量的严重程度。因此,本研究结果表明斜发沸石和EDTA对Pb(2+)毒性具有神经保护潜力。