The longitudinal gradient of intestinal iron transfer was investigated in normal and iron-deficient male Sprague-Dawley rats in vitro and in vivo. In normal rats in vitro iron transfer in the duodenum was approximately 3 times higher than in the jejunum and decreased in the ileum to approximately half the jejunal values. Compared to the controls in vitro iron transfer was increased 3–4 times in the duodenum and in the first jejunal segment and 2–3 times in the second jejunal segment. No significant adaptation to iron deficiency was found in the rest of the small intestine. Iron transfer rates showed the same longitudinal pattern when iron was chelated with nitrilotriacetic acid (NTA) or with ascorbate. The absorbed iron quantities, however, were approximately 5 times lower when Fe-ascorbate was used, which might be due to differences in bioavailability. Omission of Fe-NTA and Fe-ascorbate had no impact on the vitality of the segments. Glucose transfer was used as vitality criterion. It was not significantly different between corresponding iron-deficient and control segments. To control these results in vivo mesenteric blood was collected from duodenal and jejunal segments in situ. Corresponding to in vitro findings iron transfer was close to linear over the experimental period. In iron deficient duodenal segments iron transfer increased approximately 3 times as compared to controls while no adaptational changes were found in the distal jejunum. No significant longitudinal gradient was found in the mucosal content of ferritin and nonheme iron. Both parameters were decreased in iron deficiency by about half. The mucosal transferrin content showed no longitudinal gradient in control animals. In iron deficiency transferrin was significantly increased in the duodenum and in the three most proximal jejunal segments. The results indicate that in rats adaptation of iron absorption to the demand can only be expected in the duodenum and in the proximal 20 cm of the jejunum. Because this process shows a steep gradient in the proximal small intestine, studies on the adaptation of intestinal iron transfer to the demand should use short and well-defined segments in order to provide reproducible results.

1 The interaction between As and three toxic metals (Cd, Ni and Pb) and Cu (an essential trace metal) in the kidney was investigated in the rat by feeding diets containing various concentrations of As whilst maintaining constant concentrations of the other elements. After 1, 3, 7 and 15 weeks of feeding, metal contents in the renal cortex and medulla, red blood cells and plasma were determined by atomic emission spectrometry (ICP-AES). 2 As accumulated in the whole kidney, whereas Cu accumulated only in the cortex. Accumulation of Cu was found to depend on the feeding period and dietary As concentration. 3 As was also accumulated in red blood cells, where saturation was found at 550 μg As g-1 cells. 4 Although Cd was also accumulated in the cortex, its accumulation was independent of the dietary As concentration. Ni and Pb were not detected by ICP-AES. 5 Chromatography of the supernatants from cortical homogenates of control and As-treated rat kidney suggested that Cu accumulated in renal metallothionein (MT). Its accumulation in this fraction was independent of that of Cd, indicating that the As-Cu interaction was not a result of MT induction, but rather that it might result from altered renal handling of Cu with subsequent incorporation into MT.

No abstract

To further characterize the role of ferritin in regulating iron absorption, uptake of an oral dose of 59Fe (0.2 mg Fe/kg body wt.) into duodenal and hepatic ferritin of control and iron-deficient (ID) rats was studied. Retention and uptake of 59Fe from Fe(II)-sulfate, Fe(III)-chloride, or Fe(III)-polymaltose were measured up to 28 h after dosing. Ferritin was determined by radioimmunoassay (RIA) and 59Fe ferritin-iron by gel electrophoresis. Retention and liver content of 59Fe was higher in ID rats than in controls. The mucosa of ID rats, however, retained only one third of the amount of 59Fe retained by the mucosa of controls. The mucosal and hepatic ferritin levels were lower in ID rats than in controls. The percentage of orally administered 59Fe found in the liver ferritin was therefore higher in control than in ID rats. However, when expressed as per unit of ferritin, iron uptake was eight times higher in ID rats. In contrast, mucosa ferritin of ID rats contained one-third of 59Fe per unit of ferritin than that of controls. Assuming no change in the mechanism of iron uptake into ferritin of control and ID rats, the differential uptake of oral iron into mucosa and liver ferritin indicates either a different compartmentation of the tissue ferritin or differences in the iron transport processes, but mucosal ferritin does not withdraw iron from intestinal absorption.

Mucosal transferrin was determined as transferrin-like immunoreactivity (TLIR) by means of a 2-site immunoradiometric assay (IRMA). Scraped-off mucosal tissue as well as isolated mucosal cells from the duodenum and jejunum of normal and iron-deficient rats before and after a washing procedure were examined. In iron-deficient rats there was about twice as much TLIR in scraped-off mucosal tissue as in the untreated animals. In the duodenum and jejunum of normal and iron-deficient rats, TLIR contents of the isolated cells in the magnitude of 320-510 ng/mg dry weight were found. Washing isolated cells three times in ice-cold Hank's solution resulted in a nearly tenfold decrease of TLIR content in all groups. In contrast the cells' RNA content remained unchanged.