van der Voet G B
Toxicology Laboratory, University Hospital, Leiden, The Netherlands.
Ciba Found Symp. 1992;169:109-17; discussion 117-22.
The intestinal absorption of aluminium can contribute significantly to systemic exposure to this element. Aluminium can be absorbed not only from oral pharmaceuticals but also from solid food and drinking water. The absorption process is not restricted to patients with kidney disorders; other groups of patients and healthy subjects are not excluded. Details of the absorptive mechanism are mainly obtained from in vitro (everted gut sac) and animal studies (intestinal perfusion) rather than from controlled human studies and case reports. The process of absorption depends on the intraluminal speciation, the intraluminal quantity, the presence of competing (iron, calcium) or complexing (citrate) substances and the intraluminal pH. The condition of the exposed organism with respect to the gut also determines intestinal absorption (iron status, calcium [vitamin D, parathyroid hormone] status, age and kidney function). Various absorption sites and passage routes, both transcellular and paracellular, have been reported, each apparently related to a different aluminium species (hydrated ionic species, aluminium citrate complex etc.). No uniform mechanistic model allowing extrapolation to the clinical situation has yet emerged.
铝的肠道吸收对人体全身性接触该元素有显著影响。铝不仅可从口服药物中吸收，还能从固体食物和饮用水中吸收。吸收过程并不局限于肾病患者；其他患者群体和健康受试者也不排除在外。吸收机制的细节主要来自体外研究（外翻肠囊）和动物研究（肠道灌注），而非来自对照人体研究和病例报告。吸收过程取决于肠腔内的化学形态、肠腔内的量、竞争性物质（铁、钙）或络合物质（柠檬酸盐）的存在以及肠腔内的pH值。暴露生物体相对于肠道的状况也决定了肠道吸收（铁状态、钙[维生素D、甲状旁腺激素]状态、年龄和肾功能）。已报道了各种吸收部位和转运途径，包括跨细胞和细胞旁途径，每种途径显然与不同的铝物种（水合离子物种、柠檬酸铝络合物等）有关。目前尚未出现一个统一的、可外推至临床情况的机制模型。
