Novelli E L, Rodrigues N L, Ribas B O
Department of Chemistry, Universidade Estadual Paulista, UNESP, São Paulo, Brazil.
Bol Estud Med Biol. 1993 Jan-Dec;41(1-4):28-32.
The effect of nickel from soluble NiCl2 on Cu-Zn superoxide dismutase (SOD) activity, as well as on rate of nitro blue tetrazolium reduction, was studied in vitro since lipid peroxidation has been implicated in cell damage by nickel insoluble compounds, whose toxicity and carcinogenicity are well established. The physical and chemical nature of nickel compounds is one of the key determinations of its toxicity. Soluble nickel freely enter cells, but is just as readily excreted reducing the opportunity for production of lipid damage. Nickel from NiCl2 strongly activated SOD activity. In vitro addition of nickel chloride to a crude lung preparation altered the KM for SOD without changing the Vmax. Nickel chloride produced increased enzyme affinity to the substrate, because decreased (O2-) concentration that yields half-maximal velocity. The combination of nickel and SOD may contribute to stabilization of the particular conformation of SOD responsible for maximal catalytically activity.
由于脂质过氧化与不溶性镍化合物导致的细胞损伤有关，且此类化合物的毒性和致癌性已得到充分证实，因此研究了可溶性氯化镍中的镍对铜锌超氧化物歧化酶（SOD）活性以及对硝基蓝四唑还原速率的体外影响。镍化合物的物理和化学性质是其毒性的关键决定因素之一。可溶性镍可自由进入细胞，但同样容易被排出，从而减少了产生脂质损伤的机会。氯化镍中的镍强烈激活了SOD活性。在体外向粗制肺制剂中添加氯化镍会改变SOD的米氏常数（KM），而不改变最大反应速度（Vmax）。氯化镍使酶与底物的亲和力增加，因为产生最大反应速度一半时的（超氧阴离子）（O2-）浓度降低。镍与SOD的结合可能有助于稳定负责最大催化活性的SOD特定构象。
