机构地区:[1]贵州医科大学病理学教研室,贵阳550004 [2]贵州医科大学分子生物学重点实验室、附属医院病理科
出 处:《中华地方病学杂志》2016年第3期178-181,共4页Chinese Journal of Endemiology
基 金:国家自然科学基金(81160335);科技部支撑计划(2013BA105803);贵州省科技厅国际合作项目(黔科合外G字[2011]7014号)
摘 要:目的观察慢性氟中毒大鼠大脑及血清氧化应激水平改变及维生素E(VitaminE,VE)的拮抗作用,探讨慢性氟中毒脑损伤机制。方法健康纯系SD大鼠30只,按体质量采用随机数字表法分为3组,每组10只,雌雄各半。对照组自由饮用自来水,含氟量〈0.5mg/L;染氟组饮水中加入氟化钠,含氟量为50.0mg/L;染氟-VE拮抗组饮水含氟量为50.0mg/L,同时给予VE50.0mg/kg灌胃,每天1次。各组大鼠均给予标准饲料,含氟量6.2mg/kg。实验周期为10个月,处死大鼠,氟离子选择电极法测定骨氟含量;取脑组织和血清,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性、比色法测定谷胱甘肽过氧化物酶(GSH.Px)活性、硫代巴比妥酸荧光法测定丙二醛(MDA)含量以及比色法测定脑组织匀浆中羟自由基(OH-)、过氧化氢(H:02)、超氧阴离子自由基(咙)水平。结果染氟组大鼠骨氟含量明显高于对照组[(211.07±48.52)比(33.40±9.26)mg/kg,P〈0.01]。染氟组大鼠脑组织中SOD及GSH-P)【活性[(20.10±1.98)kU/g、(28.70±19.35)kU/L]均低于对照组[(37.05±3.13)kU/g、(59.63±12.83)kU/L,P均〈0.01],而染氟.VE拮抗组SOD活性[(26.27±1.74)kU/g]高于染氟组(P〈0.01);染氟组大鼠血清SOD及GSH—Px活性[(11.55±1.75)kU/L、(79.50±19.18)U/L]均低于对照组[(20.79±2.43)kU/L、(170.00±14.68)U/L,P均〈0.01],而染氟一VE拮抗组SOD活性[(17.23±0.68)kU/L]高于染氟组(P〈0.01);染氟组大鼠脑组织及血清MDA含量[(8.84±0.69)μmol/L、(1.46±0.11)nmol/L]均高于对照组[(1.27±0.74)μmol/L、(0.834-0.10)nmolL,P均〈0.01],而染氟.VE拮抗组MDA含量[(4.51±1.13)μmol/L、(1.29±0.02)nmol/L]均低于染氟组(P均〈0.01);染氟组Objective To detect the levels of oxidative stress in brain and serum of rats with chronic fluorosis and the antagonistic effects of vitamin E (VitE), and to reveal the role of oxidative stress in brain injury. Methods Thirty healthy SD rats were divided into three groups based on body weight by means of a random number table (10 rats in each group, half male and half female). In the control group, the rats were fed with drinking water containing less than 0.5 mg/L fluoride; in the fluoride group, the rats were fed with high doses of sodium fluoride in drinking water (50.0 mg/L) and the VitE antagonistic group were fed with the same content of fluoride in drinking water as the fluoride group, but adding VitE (50.0 mg/kg) by intragastric administration once a day. All rats were fed with normal diet (6.2 mg/kg). After exposure to fluoride for 10 months, all rats were put to death, dental fluorosis of the rats was examined and the fluoride content in bone was determined by fluoride-ion selective electrode; the activity of superoxide dismutase (SOD) was determined by the xanthine oxidase method and glutathione peroxidase (GSH-Px) by the colorimetric method, the level of malonaldehyde (MDA) by the glucosinolates barbituric acid fluorescence method and the levels o f OH-, H2O2 and O2 in rat serum and/or brain were detected by the i colorimetric method. Results In the rats of the fluoride group, fluoride content in bone was higher as compared to control [bone fluoride: (211.07 ± 48.52) vs. (33.40 ± 9.26) mg/kg, P 〈 0.01]. The activities of SOD and GSH-Px in rat brains of the fluoride group [(20.10 ± 1.98) kU/g, (28.70 ± 19.35) kU/L] were significantly lower than those of controls [(37.05 ± 3.13) kU/g, (59.63 ± 12.83) kU/L, all P 〈 0.01], the activity of SOD in VitE antagonistic group [(26.27 ± 1.74) kU/g] was higher than the fluoride group (P 〈 0.01); the activities of SOD and GSH-Px in rat serum of the fluoride group were significantly decr
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