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铜依赖性对某些生物聚合物的酶促降解和吞噬细胞诱导降解的控制,这可能是与全身炎症的一种联系。

Copper dependent control of the enzymic and phagocyte induced degradation of some biopolymers, a possible link to systemic inflammation.

作者信息

Hartmann H J, Gärtner A, Weser U

出版信息

Clin Chim Acta. 1985 Oct 31;152(1-2):95-103. doi: 10.1016/0009-8981(85)90180-9.

Abstract

The role of copper during inflammation is unknown. An attempt was made to examine the reactivity of copper on the oxygen free radical induced depolymerization of hyaluronic acid and synovial fluid. Thionein-copper and CuSO4 at 2 mumol/l concentrations inhibited the degradation of this biopolymer successfully. Translation of the enzymically generated excited oxygen species onto a cellular level was performed. Activated PMN cells were used to decompose hyaluronic acid in the presence of CuSO4, Cu-thionein and ceruloplasmin not exceeding physiological levels. All employed copper compounds inhibited the depolymerizing process. Furthermore, PMN cell induced bleaching of cytochrome c was also affected in the presence of both CuSO4 and thionein-copper.

摘要

铜在炎症过程中的作用尚不清楚。我们尝试研究铜对氧自由基诱导的透明质酸和滑液解聚反应的影响。2μmol/L浓度的硫蛋白铜和硫酸铜成功抑制了这种生物聚合物的降解。我们还将酶促产生的活性氧转化到细胞水平进行了研究。在不超过生理水平的硫酸铜、铜硫蛋白和铜蓝蛋白存在的情况下,使用活化的中性粒细胞来分解透明质酸。所有使用的铜化合物均抑制了解聚过程。此外,在硫酸铜和硫蛋白铜存在的情况下,中性粒细胞诱导的细胞色素c漂白也受到了影响。

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