Naber T H, van den Hamer C J, van den Broek W J, van Tongeren J H
Department of Medicine, University Hospital Nijmegen, The Netherlands.
Biol Trace Elem Res. 1992 Nov;35(2):137-52. doi: 10.1007/BF02783726.
In zinc deficiency, the function of leukocytes is impaired. However, the results of studies on the zinc concentration of blood cells in zinc deficiency are conflicting, probably in part because of technical and analytical problems. The aim of this study was to investigate, under standard conditions, the uptake of 65Zn-labeled zinc by blood cells, taken from zinc-deficient rats and from rats in which an inflammation is induced. In both conditions, the serum zinc concentration is reduced. In clinical practice, this makes it difficult to determine whether the decrease in serum zinc is the result of a real or an apparent zinc deficiency. In stress, like an inflammatory disease, the decrease of zinc reflects an apparent zinc deficiency because of redistribution of serum zinc into the liver and because of decrease in serum albumin concentration. Over 70% of the serum zinc is bound to albumin. Blood cells from zinc-deficient and control rats were isolated using a discontinuous Percoll gradient and incubated under nearly physiological conditions in a 65Zn-containing medium. A significant increase in the in vitro uptake of 65Zn-labeled zinc by the blood cells of zinc-deficient rats was seen: erythrocytes 1.3, mononuclear cells 2.0, and polymorphonuclear cells 2.6 times the control values. During inflammation, no change in 65Zn-labeled zinc uptake by erythrocytes and mononuclear cells was demonstrated after 2 d, although the serum zinc and albumin concentrations were decreased, but a small but significant increase in zinc uptake by polymorphonuclear cells was observed. This study of 65Zn uptake in vitro under standard conditions may prove of value for distinguishing in patients real zinc deficiency from apparent zinc deficiency owing to, e.g., stress, although additional experiments should be performed.
锌缺乏时，白细胞功能受损。然而，关于锌缺乏时血细胞锌浓度的研究结果相互矛盾，这可能部分归因于技术和分析方面的问题。本研究的目的是在标准条件下，研究从缺锌大鼠和诱导炎症的大鼠获取的血细胞对65Zn标记锌的摄取情况。在这两种情况下，血清锌浓度均降低。在临床实践中，这使得难以确定血清锌降低是真正锌缺乏还是表观锌缺乏的结果。在应激状态下，如炎症性疾病，锌的降低反映的是表观锌缺乏，这是由于血清锌重新分布到肝脏以及血清白蛋白浓度降低所致。超过70%的血清锌与白蛋白结合。使用不连续的Percoll梯度分离缺锌大鼠和对照大鼠的血细胞，并在接近生理条件下于含65Zn的培养基中孵育。结果发现，缺锌大鼠血细胞对65Zn标记锌的体外摄取显著增加：红细胞摄取量为对照值的1.3倍，单核细胞为2.0倍，多形核细胞为2.6倍。在炎症期间，尽管血清锌和白蛋白浓度降低，但在2天后红细胞和单核细胞对65Zn标记锌的摄取未见变化，不过观察到多形核细胞的锌摄取有小幅但显著的增加。尽管还应进行额外实验，但在标准条件下对65Zn体外摄取的这项研究可能有助于区分患者是真正的锌缺乏还是因例如应激导致的表观锌缺乏。
