Binding Studies as an Approach to the Study of Intestinal Transport

Eichholz, Alexander; Howell, Kathryn E.

doi:10.1016/s0016-5085(72)80052-0

Cited by 9 publications

(2 citation statements)

References 94 publications

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“…2 (around fraction number 6) was not very reproducible. Using this technique, the binding properties of fraction 2 were investigated arid found to be similar to those described by others in brush border fractions [2]. FoB instance, the bindinB exhibited a K m on the order of I0 lJmolar and was inhibited by SH reagents and sugar analogues, as will be shown later.…”

Section: Remits and Discussionsupporting

confidence: 67%

Bacterial contamination as a source of error in D‐glucose‐binding studies using intestinal brush border membrane preparations

1973

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Section: Remits and Discussionsupporting

confidence: 67%

Bacterial contamination as a source of error in D‐glucose‐binding studies using intestinal brush border membrane preparations

1973

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“…It is noteworthy that cysteamine-induced ulceration in rats occurs mainly in the proximal duodenum, within 10 mm of the pylorus, at the same site where most intestinal iron absorption takes place. The epithelial cell layer of the proximal duodenum is specialized for the uptake and transport of iron from the intestinal lumen to the systemic circulation (17,69). This raises the question whether the availability of dietary iron within the enterocytes of the proximal duodenum during iron absorption may play a role in ulcerogenesis induced by chemicals such as cysteamine.…”

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confidence: 99%

Role of iron in the pathogenesis of cysteamine-induced duodenal ulceration in rats

Khomenko¹,

Szabó²,

Deng³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Cysteamine induces perforating duodenal ulcers in rats within 24-48 h. This reducing aminothiol generates hydrogen peroxide in the presence of transition metals (e.g., ferric iron), producing oxidative stress, which may contribute to organ-specific tissue damage. Since most intestinal iron absorption takes place in the proximal duodenum, we hypothesized that cysteamine may disrupt regulation of mucosal iron transport, and iron may facilitate cysteamine-induced duodenal ulceration. We show here that cysteamine-induced ulceration was aggravated by pretreatment of rats with Fe(3+) or Fe(2+) compounds, which elevated iron concentration in the duodenal mucosa. In contrast, feeding rats an iron-deficient diet was associated with a 4.6-fold decrease in ulcer formation, accompanied by a 34% decrease (P < 0.05) in the duodenal mucosal iron concentration. Administration of deferoxamine inhibited ulceration by 65%. We also observed that the antiulcer effect of H2 receptor antagonist cimetidine included a 35% decrease in iron concentration in the duodenal mucosa. Cysteamine-induced duodenal ulcers were also decreased in iron-deficient Belgrade rats (P < 0.05). In normal rats, cysteamine administration increased the iron concentration in the proximal duodenal mucosa by 33% in the preulcerogenic stage but at the same time decreased serum iron (P < 0.05). Cysteamine also enhanced activation of mucosal iron regulatory protein 1 and increased the expression of divalent metal transporter 1 mRNA and protein. Transferrin receptor 1 protein expression was also increased, although mucosal ferroportin and ferritin remained almost unchanged. These results indicate an expansion of the intracellular labile iron pool in the duodenal mucosa, increasing its susceptibility to oxidative stress, and suggest a role for iron in the pathogenesis of organ-specific tissue injury such as duodenal ulcers.

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Characterization of bile acid binding to rat intestinal brush border membranes

Wilson

Treanor

1977

J. Membrain Biol.

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Studies were performed to characterize the binding1 of bile acids to intestinal brush border membranes. Total 14C-taurodeoxycholate binding was: 1) similar for brush borders prepared from jejunum and ileum, 2) linear with respect to monomer concentration, 3) uninhibited by a structural analog, and 4) not depressed by boiling or trypsin. A linear relationship existed between binding and the number of hydrogen bonds formed by a bile acid and the slope of the line corresponded to delta deltaF of 300 cal/mol. The binding of bile acids to the 105,000 x g supernatant fraction of sonicated brush borders was similar to the binding of phospholipid liposomes using gel chromatography. These data suggest that: 1) the kinetics and characteristics of binding of bile acid to ileal brush borders do not reflect the kinetics and characteristics of active ileal transport previously obtained in whole tissue preparations, but instead reflect the kinetics and characteristics of passive jejunal transport; 2) a determinant of binding is hydrogen bonding with water; 3) isolated intact brush borders are relatively polar membranes; and 4) binding to solubilized brush borders may represent partitioning between the aqueous phase and membrane lipid.

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Binding Studies as an Approach to the Study of Intestinal Transport

Cited by 9 publications

References 94 publications

Bacterial contamination as a source of error in D‐glucose‐binding studies using intestinal brush border membrane preparations

Bacterial contamination as a source of error in D‐glucose‐binding studies using intestinal brush border membrane preparations

Role of iron in the pathogenesis of cysteamine-induced duodenal ulceration in rats

Characterization of bile acid binding to rat intestinal brush border membranes

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