摘要
为确定缺铁非贫血大鼠是否存在脑组织生化异常，我们应用低铁饮食建立了铁缺乏非贫血期大鼠模型，用三电极等离子体原子发射直读光谱仪测定脑组织铁含量，酶组化法测定纹状体单胺氧化酶（ＭＡＯ）活性，高效液相色谱电化学检测器测定大脑皮层及海马中单胺类神经递质及其代谢产物的含量。结果显示，在铁缺乏非贫血期实验组大鼠脑组织铁含量及ＭＡＯ活性均明显降低，大脑皮层去甲肾上腺素及５－羟色胺（５－ＨＴ）含量显著高于对照组，海马中５－ＨＴ的代谢产物５—羟吲哚乙酸显著低于对照组。结果表明，在铁缺乏非贫血期大鼠脑组织已存在单胺类神经递质的代谢异常。
Anirondeficiencynonanemicratmodelwasestablishedbyfeedingwithlow-irondiet(11.9mg/kg)tostudyifthereexistsbiochemicalabnormalityinbraintissues.Ironcontentsofthebrain,activitiesofmonoamineoxidase(MAO)inthecorpusstriatum,andthecontentsofmonoamineneurotransmiteranditsmetaboliteinthecerebralcortexandhippocampusweredeter-minedbyDCP-AEStechnique,enzymehistochemicalmethod,andhighperformanceliquidchro-matographywithelectrochemicaldetection(HPLC-ECD),respectively.ResultsshowedthatironcontentsandactivitiesofMAOinbraintissuesofirondeficiencynonanemicratsreducedsignificant-ly,andcontentsofnorepinephrine(NE)and5-hydroxytryptamine(5-HT)incerebralcortexweresignificantlyhigherthanthoseofcontrols,while5-hydroxydroxytryptamineacid(5-HIAA)metabo-liteof5-HTinthehippocampuswaslowerthanthatofcontrols.Itindicatedthatthereexistedmetabolicabnormalityofmonoamineneurotransmitterinthebraintissuesofirondeficiencynonane-micrats.Also,thisstudylaidabiochemicalbasisforabnormalmentalandbehavioraldevelopmentcausedbyirondeficiency.
出处
《中华预防医学杂志》
CAS
CSCD
北大核心
1996年第6期351-353,共3页
Chinese Journal of Preventive Medicine
