Jasim S, Tjälve H
Toxicol Lett. 1986 Jun;31(3):249-55. doi: 10.1016/0378-4274(86)90133-5.
Intravenous administration of 63Ni2+ (as 63NiCl2) together with potassium ethylxanthate resulted in highly increased levels of 63Ni2+ in several tissues of mice in comparison with animals given 63Ni2+ alone. However, this effect was not observed when 63Ni2+ and potassium ethylxanthate were given orally. Sodium diethyldithiocarbamate was active in increasing 63Ni2+ concentrations after both intravenous and oral administration. Both ethylxanthate and diethyldithiocarbamate can form highly lipophilic complexes with nickel and a facilitated penetration of these complexes through the cellular membranes of the tissues probably explains the increased uptake of the metal. Xanthates are unstable at acid pH and degradation in the acid milieu of the stomach probably underlies the lack of effect at oral administration.
与单独给予63Ni2+(以63NiCl2形式)的动物相比,静脉注射63Ni2+(以63NiCl2形式)与乙基黄原酸钾一起导致小鼠多个组织中63Ni2+水平大幅升高。然而,当63Ni2+和乙基黄原酸钾口服给药时,未观察到这种效应。二乙基二硫代氨基甲酸钠在静脉注射和口服给药后均能有效提高63Ni2+浓度。乙基黄原酸盐和二乙基二硫代氨基甲酸盐都能与镍形成高度亲脂性的络合物,这些络合物通过组织细胞膜的促进渗透可能解释了金属摄取的增加。黄原酸盐在酸性pH值下不稳定,在胃的酸性环境中降解可能是口服给药无效的原因。