机构地区:[1]上海交通大学医学院附属新华医院 上海市环境与儿童健康重点实验室,200092 [2]上海交通大学医学院细胞生物研究室
出 处:《中华预防医学杂志》2008年第3期160-164,共5页Chinese Journal of Preventive Medicine
摘 要:目的探讨慢性中度铅中毒对幼兔海马组织的影响。方法16只离乳(45d)雄性健康新西兰幼兔,数字表法随机分为空白组和染铅组,每组8只,染铅组喂含5mg·kg^-1·d^-1醋酸铅的饲料,持续6周,建立慢性中度铅中毒幼兔模型。用原子吸收分光光谱仪测定血铅,海马组织经微波消解后,用电感耦合等离子体质谱仪测铅,光学显微镜(简称光镜)和电子显微镜(简称电镜)观察海马的组织结构和超微结构,免疫组织化学法分析海马组织CA1区锥体细胞膜上的N-甲基-D-天冬氨酸受体亚单位1(NR1)、亚单位2A(NR2A)和亚单位2B(NR2B)的蛋白表达。结果染铅组的血铅(μg/L)和海马铅(ng/g)显著升高[染铅组血铅(428.63±9.46)μg/L,空白组血铅(66.38±3.93)μg/L,t血铅=100.08,P〈0.01;染铅组海马铅(44.57±2.03)ng/g,空白组海马铅(21.20±1.53)ng/g,t海马铅=26.05,P〈0.01];海马湿重(g)和海马湿重系数(‰)显著降低[染铅组海马湿重(0.735±0.012)g,空白组海马湿重(0.808±0.010)g,t海马湿重=12.97,P〈0.01;染铅组海马湿重系数(0.458±0.004)‰,空白组海马湿重系数(0.476±0.005)%。,t海马湿重系数=7.87,P〈0.01];CA1区NR1和NR2A阳性表达率降低[染铅组NR1阳性表达率(37.44±2.05)%,空白组NR1阳性表达率(41.81±2.50)%,tNR1=3.82,P〈0.01;染铅组NR2A阳性表达率(21.97±1.08)%,空白组NR2A阳性表达率(25.48±1.30)%,tNR2A=5.89,P〈0.01];光镜和电镜下观察到海马组织神经元和胶质细胞的组织结构和超微结构改变。结论慢性中度铅中毒损伤幼兔的海马组织,海马组织形态和NMDA受体亚单位蛋白表达发生改变。Objective To understand the effects of moderate lead poisoning on the hippocampus tissue of rabbits in juvenile stage. Methods Sixteen 45-day-old male New Zealand rabbits were randomly divided into blank group and lead-exposed group,8 for each group. Rabbits in the lead-exposed group were treated with 5 mg· kg^-1·d^-1 lead acetate in their forage for 6 weeks to establish a moderate lead poisoning animal model. The blood lead levels and the lead contents in the hippocampus were determined by atomic absorption spectrometer and inductively coupled plasma-mass spectrometry respectively. Histopathology and ultra-microstructure in the hippocampus tissue were observed by light microscope and electron microscope. The NR1, NR2A and NR2B protein expressions in the CA1 hippocampal region were analyzed through immunohistochemical method. Results Compared with those of blank group, the blood lead levels of leadexposed group were significant increased, (428. 63 ± 9.46) vs (66. 38 ± 3.93 ) μg/L( t = 100. 08, P 〈 0. 01 ) ; and lead contents of hippocampus was significantly increased, (44. 57 ± 2. 03 )vs(21.20 ± 1.53 )ng/g, (t = 26.05, P 〈 0. 01 ) ; the hippocampus wet weight were significant decreased, (0. 735 ± 0. 012 ) vs (0. 808± 0. 010), ( t = 12. 97, P 〈 0. 01 ) ; the coefficient of hippocampus wet weight, was (0. 458 ± 0. 004 ) vs (0. 476± 0. 005), (t =7.87 ,P 〈0. 01 ). The significant declines in both the positive rate of NR1 and NR2A in the CA1 hippocampal region for NR1 : ( 37.44 ± 2. 05 ) % vs (41.81 ± 2. 50 ) % ( t = 3.82, P 〈 0. 01 ) and for NR2A: 21.97 ± 1.08 vs 25.48 ± 1.30(t =5.89 ,P 〈0.01 ) were also observed. With light microscope and electron microscope, the histopathology and ultra-microstructure of neuron and glial cell in the hippocampus tissue were changed. Conclusion The impairment of hippocampus of rabbits in juvenile stage with chronic moderate lead poisoning were observed, and the histopathology and N-methyl-D
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