Chen C Y, Lin T H
Department of Medical Technology, Foo-Yin Institute of Technology, Kaohsiung, Taiwan, Republic of China.
J Toxicol Environ Health A. 2001 Mar 23;62(6):431-8. doi: 10.1080/00984100150501169.
This study was undertaken to examine the effects of nickel (Ni) on human platelet function. In a (concentration-dependent manner, Ni significantly inhibited the function of platelet aggregation induced by collagen. The phenomenon of lipid peroxidation was involved as Ni significantly increased malondialdehyde (MDA) levels with reduction in platelet reduced glutathione (GSH) and alpha-tocopherol content. Further, platelet thromboxane B2, formation was markedly inhibited and the levels of cyclic AMP were significantly elevated by Ni. Treatment with ascorbic acid (Vit C) significantly lowered the levels of MDA and increased the content of alpha-tocopherol and reduced GSH. Vit C also significantly increased platelet aggregation and thromboxane B2 when coincubated with Ni. Data show that Ni is toxic as evidenced by lipid peroxidative damage and inhibition of human platelet aggregation, but that ascorbic acid provides protection, at least partially, against this metal.
本研究旨在探讨镍（Ni）对人血小板功能的影响。镍以浓度依赖的方式显著抑制胶原蛋白诱导的血小板聚集功能。脂质过氧化现象参与其中，因为镍显著增加丙二醛（MDA）水平，同时血小板还原型谷胱甘肽（GSH）和α-生育酚含量降低。此外，镍显著抑制血小板血栓素B2的形成，并显著提高环磷酸腺苷水平。用抗坏血酸（维生素C）处理可显著降低MDA水平，增加α-生育酚含量并提高还原型GSH水平。当与镍共同孵育时，维生素C还显著增加血小板聚集和血栓素B2。数据表明，镍具有毒性，脂质过氧化损伤和人血小板聚集受抑制可证明这一点，但抗坏血酸至少可部分提供针对这种金属的保护作用。
