Interleukin 1-induced depression of iron and zinc: role of granulocytes and lactoferrin.
Interleukin 1-induced depression of iron and zinc: role of granulocytes and lactoferrin.
复制标题
白介素 1 诱导的铁和锌抑制：粒细胞和乳铁蛋白的作用。
DOI：
10.1152/ajpendo.1987.252.1.e27
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
McClain,CJ
中科院分区：
文献类型：
--
作者：
Goldblum,SE;Cohen,DA;Jay,M;McClain,CJ
The mechanism(s) of stress-induced hypoferremia and hypozincemia remains unclear. We studied the role of granulocytes and lactoferrin (LF) in endotoxin and murine interleukin 1 (IL-1)-induced depression of serum Fe and Zn concentrations in both rabbits and rats. Both endotoxin and IL-1 administration induced significant hypoferremia (P less than 0.01) and hypozincemia (P less than 0.01) after 6 h in both species. Granulocyte depletion before IL-1 infusion significantly (P less than 0.01) diminished the hypoferremia but not the hypozincemia. Moreover, infusion of 5 or 15 mg of human LF into rabbits caused significant hypoferremia (P less than 0.005) without hypozincemia. Significant hypozincemia (P less than 0.01) could only be demonstrated after a 75-mg infusion. In contrast, infusions of human transferrin at equivalent doses (5, 15, and 75 mg) induced neither hypoferremia nor hypozincemia. Therefore endotoxin and IL-1-induced hypoferremia and, to a much lesser degree, hypozincemia are granulocyte dependent. Granulocyte released LF is a specific carrier molecule for transport and removal of Fe from the circulation during the acute phase response. The data suggest a mechanistic dissociation of IL-1-induced hypoferremia and hypozincemia with LF-independent mechanisms for Zn.
