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锌缺乏和长期炎症应激期间的血清碱性磷酸酶活性

Serum alkaline phosphatase activity during zinc deficiency and long-term inflammatory stress.

作者信息

Naber T H, Baadenhuysen H, Jansen J B, van den Hamer C J, van den Broek W

机构信息

Department of Medicine, University Hospital Nijmegen, The Netherlands.

出版信息

Clin Chim Acta. 1996 May 30;249(1-2):109-27. doi: 10.1016/0009-8981(96)06281-x.

Abstract

A decrease in serum zinc can be caused by a real zinc deficiency but can also be caused by an apparent zinc deficiency, e.g. in inflammatory stress. The aim of this study was to evaluate the diagnostic power of serum alkaline phosphatase (AP) activity in the discrimination between pathophysiologic states of "real" and "apparent" zinc deficiency. A decrease in serum zinc was induced in growing and adult rats, by providing a diet low in zinc and by causing inflammatory stress. AP activity was determined using reagents low or enriched in zinc. Serum AP was decreased in zinc-deficient adult rats (P < 0.01). In zinc-deficient growing rats AP activity was not different from normal rats but AP activity decreased rapidly. In the same growing rats a significant difference was found in AP activities determined using buffers low and enriched in zinc (P < 0.001) between both groups of rats. After inducing inflammatory stress a decrease in AP activity (P < 0.01) and serum zinc (P < 0.001) was seen during the first few days. After the initial phase of inflammation AP activity normalized, serum zinc showed a rise which after correction for the decrease in serum albumin reached the level of the control rats. A difference in AP activity in buffers low and enriched in zinc was observed only during the first few days after induction of inflammatory stress (P < 0.001). Probably the method of measurement of the difference in enzyme activity, using buffers low and enriched in zinc, can be used as an indication for zinc deficiency in situations with changing AP enzyme concentrations. AP activity is decreased during the initial phase of inflammatory stress due to a decrease in serum zinc.

摘要

血清锌降低可能是由真正的锌缺乏引起的,但也可能是由明显的锌缺乏导致的,例如在炎症应激状态下。本研究的目的是评估血清碱性磷酸酶(AP)活性在区分“真正的”和“明显的”锌缺乏病理生理状态方面的诊断能力。通过提供低锌饮食并引发炎症应激,在生长中的大鼠和成年大鼠中诱导血清锌降低。使用锌含量低或高的试剂测定AP活性。锌缺乏的成年大鼠血清AP降低(P < 0.01)。在锌缺乏的生长大鼠中,AP活性与正常大鼠无差异,但AP活性迅速降低。在同一批生长大鼠中,两组大鼠使用低锌和高锌缓冲液测定的AP活性存在显著差异(P < 0.001)。诱导炎症应激后,最初几天内AP活性降低(P < 0.01),血清锌降低(P < 0.001)。在炎症初始阶段过后,AP活性恢复正常,血清锌升高,在纠正血清白蛋白降低后达到对照大鼠的水平。仅在诱导炎症应激后的最初几天观察到使用低锌和高锌缓冲液时AP活性的差异(P < 0.001)。在AP酶浓度变化的情况下,使用低锌和高锌缓冲液测量酶活性差异的方法可能可作为锌缺乏的一个指标。在炎症应激的初始阶段,由于血清锌降低,AP活性降低。

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