Van Wouwe J P, Hoogenkamp S, Van den Hamer C J
Department of Radiochemistry, Interfaculty Reactor Institute, Technical University, Delft, The Netherlands.
Biol Trace Elem Res. 1990 Mar;24(3):207-16. doi: 10.1007/BF02917208.
The effects of histidine on the zinc status are controversial. In mice, we studied the effects of a moderate histidine supplement on the regulation of the zinc status using subcutaneously administered 65Zn. In animals fed a zinc-adequate diet, histidine supplement did not cause changes in the zinc status (zinc concentrations, 65Zn tissue distribution, and tissue specific activities). Neither effects on the regulation of the zinc status (65Zn retention, excretion and biological half-life) could be demonstrated. However, the combination of a low zinc diet and moderate histidine supplementation caused changes in the regulation of the zinc status (lower 65Zn retention, associated with increased fecal excretion and a shorter biological half-life), aggravating the dietary deficiency (lower bone zinc, a shift in the 65Zn tissue distribution). Reviewing the literature, it seems that only a molar histidine/zinc ration of 2,000 or higher will cause zinc deficiency.
组氨酸对锌状态的影响存在争议。在小鼠中,我们使用皮下注射的65Zn研究了适量补充组氨酸对锌状态调节的影响。在喂食锌充足饮食的动物中,补充组氨酸并未导致锌状态发生变化(锌浓度、65Zn组织分布和组织比活性)。也未显示出对锌状态调节(65Zn保留、排泄和生物半衰期)有影响。然而,低锌饮食与适量补充组氨酸相结合会导致锌状态调节发生变化(65Zn保留降低,伴有粪便排泄增加和生物半衰期缩短),加重饮食缺乏(骨骼锌含量降低,65Zn组织分布发生变化)。回顾文献,似乎只有组氨酸/锌摩尔比达到2000或更高时才会导致锌缺乏。