Foulkes E C, McMullen D M
Toxicology. 1986 Jan;38(1):35-42. doi: 10.1016/0300-483x(86)90170-8.
Nickel is taken up from the lumen of the perfused rat jejunum (step 1 of Ni absorption) by a mechanism closely resembling that responsible for step 1 of Cd absorption. Both processes are depressed to a similar extent by Zn or the constituents of dried skimmed milk. They procede at a rate proportional to concentration up to 20 microM; at higher levels they approach apparent saturation. In contrast to the slow movement of Cd from mucosa into the body (step 2 of absorption), Ni is not appreciably retained in the mucosa. Retention of Ni is not increased by induction of metallothionein synthesis, in agreement with its low affinity for this protein. Several observations suggest that basolateral membranes may be passively permeable to Ni: step 2 follows first order kinetics; Ni is also taken up by the mucosa from the serosal side, in vivo and in vitro; and no inhibitory effect of Zn could be shown. The ability of the mucosa to discriminate between the toxic, non-essential metal Cd and the essential metal Ni may depend therefore on the efficiency of mucosal trapping rather than the presence of Ni carriers on brush border or basolateral cell membranes.
镍从灌注的大鼠空肠肠腔中被吸收（镍吸收的步骤1），其机制与镉吸收的步骤1极为相似。锌或脱脂奶粉成分对这两个过程的抑制程度相似。在浓度高达20微摩尔时，两个过程的进行速率均与浓度成正比；浓度更高时，它们接近明显的饱和状态。与镉从黏膜缓慢进入体内（吸收步骤2）不同，镍在黏膜中没有明显的潴留。镍的潴留不会因金属硫蛋白合成的诱导而增加，这与其对该蛋白的低亲和力一致。多项观察结果表明，基底外侧膜可能对镍具有被动通透性：步骤2遵循一级动力学；在体内和体外，镍也可从浆膜侧被黏膜摄取；并且未显示锌有抑制作用。因此，黏膜区分有毒的非必需金属镉和必需金属镍的能力可能取决于黏膜捕获的效率，而非刷状缘或基底外侧细胞膜上镍载体的存在。
