Abstract
Mice were made iron-deficient by feeding a semisynthetic low-iron diet, by bleeding, or by a combination of both methods. Dietary-induced iron deficiency, by itself, enhanced iron absorption from an. intragastric dose to a much greater extent than did bleeding mice fed an iron-supplemented diet. Enhanced lead absorption was seen in the former but not in the latter group. Bleeding was effective, however, in raising lead absorption when mice were fed the iron-deficient diet. Additionally, the kinetics of lead absorption were studied by using an openended duodenal perfusion technique. When lead was perfused in solutions containing either 0.15 M sodium chloride or 0.15 M sodium ascorbate, irondeficient animals took up more lead into the mucosa and transferred more to the body than mice fed an iron-supplemented diet. Intestinal uptake of lead from both perfusates in iron-sufficient animals appeared to occur by a process that was primarily dependent on the luminal lead concentration. Lead uptake from the saline perfusate in iron-deficient mice was also directly related to the lead concentration of the perfusate, whereas uptake from the ascorbate perfusate was proportionally greater from lowerthan from higher-lead concentrations, giving rise to saturation-type kinetics. Lead transfer to the body from both types of perfusate also displayed saturation kinetics in both iron-sufficient and iron-deficient animals. When iron and lead were perfused together in 0.15 M sodium ascorbate, iron inhibited lead up take and transfer at Fe/Pb molar ratios as low as 0.5:1, whereas lead inhibited iron uptake and transfer at a Pb/Fe ratio of 5:1. These mutually inhibitory effects were not as easily demonstrated with a saline perfusate. Our results suggest that lead absorption occurs by two simultaneous processes: the first is a diffusion-type mechanism, and the second is a carrier-mediated process, which is enhanced by feeding a low-iron diet. Lead appeared to have less affinity than iron for the latter mechanism.
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