Salvarezza R C, De Mele M F, Videla H A
Life Support Syst. 1984 Apr-Jun;2(2):137-44.
Film formation during the pitting corrosion of aluminium in human plasma is studied using conventional electrochemical techniques complemented with scanning electron microscopy as well as energy-dispersive x-ray, electron microprobe and immunoelectrophoresis analysis. The anodic polarization curve of aluminium in human plasma at 37 degrees C shows a passive region related to a low corrosion rate that extends up to -0.66 V (s.c.e.). At more positive potential values than -0.66 V, the breakdown of the oxide protective film occurs due to the chloride anions, leading to an intense localized dissolution of the metal (pitting corrosion). Scanning electron microscopy of the metal surface reveals a thick non-adherent precipitate covering pits of a crystallographic feature. Energy-dispersive x-ray and the microprobe analysis show the presence of aluminium, chloride and carbon signals. Immunoelectrophoresis of the precipitate resuspended in physiological solution shows a strong protein denaturization. Results suggest that the corrosion products are formed during pitting by the interaction of the saturated AlCl3 salt present within the pits and the adsorbed plasma proteins.
采用传统电化学技术,并辅以扫描电子显微镜以及能量色散X射线、电子微探针和免疫电泳分析,研究了铝在人体血浆中发生点蚀时的成膜情况。铝在37℃人体血浆中的阳极极化曲线显示出一个与低腐蚀速率相关的钝化区,该钝化区一直延伸到-0.66V(饱和甘汞电极)。在比-0.66V更正的电位值下,由于氯离子的作用,氧化保护膜发生击穿,导致金属强烈的局部溶解(点蚀)。金属表面的扫描电子显微镜显示,有一层厚厚的非附着沉淀物覆盖着具有晶体学特征的蚀坑。能量色散X射线和微探针分析表明存在铝、氯和碳信号。将沉淀物重新悬浮在生理溶液中的免疫电泳显示出强烈的蛋白质变性。结果表明,点蚀过程中形成的腐蚀产物是由蚀坑内存在的饱和AlCl₃盐与吸附的血浆蛋白相互作用产生的。