摘要
用放血法制备大鼠失血性贫血模型；向腹腔内注射铁－氨三乙酸络合物制备铁过剩模型；以元处置大鼠作为对照。向隔离十二指肠段注射￣（５９）ＦｅＣｌ＿３，ｌｈ后测定单位重量十二指肠、肝、脾每分钟脉冲数，同时用放射自显影法显示十二指肠上皮细胞￣（５９）Ｆｅ分布。结果表明：与对照组相比，贫血组大鼠十二指肠吸收铁增加，向肝、脾的铁转运也明显增加。而铁过剩组大鼠进入十二指肠上皮细胞的铁明显减少。免疫组织化学显示肠上皮细胞基底侧有转铁蛋白受体分布。作者认为：十二指肠上皮细胞基底侧存在转铁蛋白及其受体介导的主动非血红素铁运转机制。铁缺乏时这一机制被激活，铁从小肠上皮细胞进入体内增加，上皮细胞内铁减少，促进铁从肠腔进入上皮细胞；铁过剩时，从肠上皮细胞进入体内的铁减少，肠上皮细胞内铁含量增加，减少铁吸收。
ron-deficient animal model was produced by phlebotomy . Iron-over-load was
made by intraperitoneal ferric nitrilotriacetate injection.Non-treted rats were used as
controls.59FeCl3 was injected into the isolatedduodenal segment from the three groups of rats.
One hour later,count perminutes(cpm) was checked on normal saline washed isolated
duodenum,plasma,liver,and spleen .Radioautography and immunohistochemistry werealso
used on the duodenal sections.The iron absorption inereased in iron-deficient,decreased in
iron-overloaded rats. The cpm of plasma, liver andspleen was also more in anemic,less in
iron-overlodrded rats comparingwith controls.Immunohistochemistry showed the basal side
distribution oftransferrin receptor.We suggest that there is a transferrin receptor medi-ated
non-heme iron transportation mechanism in the basal side of the duo-denal absorptive
cell.Under iron deficient conditions,the mechanism isactivated to transport more iron into the
body, promote the entrance ofiron into the absorptive cell.In the iron overloaded rats,reduction
of ac-tivity decreased the entrance of iron into the body and the iron uptake ofduodenal cells.
出处
《营养学报》
CAS
CSCD
北大核心
1995年第4期377-382,共6页
Acta Nutrimenta Sinica
基金
国家自然科学基金
国家教委及日本日中永和协会基金
