小鼠缺铜对腹腔巨噬细胞产生肿瘤坏死因子和白介素的影响

本实验采用ＡＩＮ－７６￣（ＴＭ）缺铜纯饲料，分别给断奶一周的小鼠喂饲缺铜纯饲料６、７和１０周，结果观察到小鼠经过７周喂养后肝Ｃｕ水平下降；喂养１０周后出现肝细胞色素Ｃ氧化酶（ＣＣＯ）和血清铜蓝蛋白（Ｃｐ）活性下降，而肝Ｃｕ水平回升，缺铜对小鼠静止的腹腔巨噬细胞产生的肿瘤坏死因子－α（ＴＮＦ－α）和白细胞介素６（ＩＬ－６）活性没有改变。而喂饲３周龄刚断奶的Ｂａｌｂ／Ｃ雄性小鼠６周后，小鼠呈现严重的缺铜状态，表现为胸腺萎缩、肝脏肿大以及血清Ｃｐ活性降低，肝Ｃｕ水平、ＣＣＯ和Ｃｕ、Ｚｎ－ＳＯＤ活性明显下降等，并且由缺铜小鼠激活的腹腔巨噬细胞产生的ＴＮＦ－α、ＩＬ－１和ＩＬ－６水平明显低于正常组小鼠。

THE BIOCHEMICAL AND IMMUNOLOGICAL CHANGES DURING EXPERIMENTAL COPPER DEFICIENCY IN MICE

evere Cu deficiency(CuD)was established in 3wk old mice eating Cu deficient dict for 6 weeks.The CuD syroup micc had a reduced thymus weight and an increased livcr weight.All of thc serum Ccruplasmin(Cp)activity,live Cu,cytuchrome oxidase(CCO)and Cu,Zn-SOD activities dccreased.The production of TNF-α,IL-1 and IL-6 from activated peritoneal macrophages of CuD mice was significantly reduced.In the pilot study,4 wk old mice were fed with Cu deficient diet for 6,7 and 10 wks respcctively. After 7 wks on the diet,CuD group had lower liver Cu.After 10 wks on the diet,liver CCO and Cp levels significantly decreased,but liver Cu level rebounded.The TNF-α from un activated peritoneal macrophages of both groups was undetectable;whereas the IL-6 was detectable at low levels,but there wasn't any significant difference betwreen them(P>0.05).