Srivastava R C, Hasan S K, Gupta J, Gupta S
Industrial Toxicology Research Centre, Lucknow, India.
Biochem Mol Biol Int. 1993 Jun;30(2):261-70.
Recent studies have focussed on the role of thiol rich proteins especially metallothionein (MT) in the therapeutic interventions against oxidative damage. In our previous communication we showed that reactive oxygen species arising via Fenton's reactions are the proximal lipid oxidant during nickel-toxicity. The purpose of the present communication is to evaluate the role of zinc, cadmium or silver-metallothioneins on the protection against nickel-induced peroxidative damage. Our results demonstrate that Zn-MT provided maximum protection against nickel-induced mortality in mice and also served as an efficient antagonist in inhibiting nickel-mediated lipid peroxidation compared to Cd-MT or Ag-MT. Zn-MT also provided protection against iron (II)-ascorbate induced microsomal lipid peroxidation and reversed nickel-mediated inhibition of calcium sequenstration. We conclude that Zn-MT could serve as an excellent physiological antioxidant against nickel-mediated oxidative.
最近的研究集中在富含硫醇的蛋白质尤其是金属硫蛋白（MT）在针对氧化损伤的治疗干预中的作用。在我们之前的交流中，我们表明通过芬顿反应产生的活性氧是镍中毒期间近端脂质氧化剂。本交流的目的是评估锌、镉或银金属硫蛋白在防止镍诱导的过氧化损伤中的作用。我们的结果表明，与镉金属硫蛋白或银金属硫蛋白相比，锌金属硫蛋白对小鼠镍诱导的死亡率提供了最大程度的保护，并且在抑制镍介导的脂质过氧化方面也是一种有效的拮抗剂。锌金属硫蛋白还提供了针对铁（II）-抗坏血酸诱导的微粒体脂质过氧化的保护，并逆转了镍介导的钙螯合抑制作用。我们得出结论，锌金属硫蛋白可以作为针对镍介导的氧化的出色生理抗氧化剂。
