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The present study was performed to determine the respective involvement of the cellular and paracellular routes in ileal Ca2+ transport. Two groups of rats were either fed a normal Ca2+ diet (1. 0%) or a Ca2+-deficient diet (0.02%) for 14 days. Ileal Ca2+ absorption was determined using both an in situ method of continuous luminal perfusion and an in vitro method (Ussing chamber model). The low-Ca2+ diet stimulated net Ca2+ flux in the ileum twofold, associated with a twofold increase of the mucosal-to-serosal Ca2+ flux in both models. This effect was observed in the absence of concomitant changes in Na+ or water flux in the in situ model or mannitol flux in the in vitro model, excluding the participation of the paracellular pathway in Ca2+ transport. Thus only cellular Ca2+ flux was stimulated. These data suggest that the ileum plays a major role in the adaptation to low dietary Ca2+. Whereas under physiological conditions with usual Ca2+ intakes the transcellular pathway of Ca2+ transport is negligible, it becomes of major importance in the case of Ca2+ deficiency, at least under the present conditions of severe Ca2+ deprivation.

Objectives: The aim of this study was to study the effect of sorbitol on sodium, water and calcium fluxes in rat ileum in situ perfused loop., Methods: Net water, sodium and calcium fluxes, and one-way calcium fluxes were measured in situ in a perfused rat ileal loop in the presence of varying concentrations of sorbital., Results: High concentrations of sorbitol in perfused ileal solution induced a decrease of sodium and water fluxes and a concomitant increase of lumen to mucosa calcium flux associated with an increase of net calcium flux, using a solution containing either 8.0 or 1.25 mM calcium. These effects were independent of absolute initial values of water and sodium fluxes. They were observed in the presence of 25 mM glucose, 10 mM theophyllin or after treatment of rats with dexamethasone., Conclusion: These effects of sorbitol on calcium flux are not compatible with a stimulation of paracellular pathway. By contrast, they can be explained by a stimulation of transcellular calcium pathway in ileum associated with the hyperpolarisation of the cells induced by the decrease of luminal sodium concentration necessary in the presence of sorbitol to maintain unchanged osmolarity of perfusate.

To further define the mechanism of interaction among phenytoin, folates and cobalamins in rats, we studied the effect of phenytoin (60 mg/(kg.day)) with or without folic acid supplementation and with or without cobalamin deficiency, as well as the effect of supplementing with folic acid (200 mg/kg diet) with or without a cobalamin deficiency, on the tissue concentrations of folates and phenytoin (determined respectively by HPLC and fluorescence polarization). The major tissues (liver, intestinal mucosae, blood and brain) were studied. A folic acid overload (estimated at about 2 mg/day) increased folate levels in the liver, the intestinal mucosae and blood, while there was no effect on cerebral levels. Phenytoin had no significant effect on folate tissue concentration. The major finding was that a folic acid overload caused a considerable decrease in the hepatic and cerebral concentrations of phenytoin. This decrease could be responsible for the increased frequency of epileptic fits in patients treated with this anticonvulsant drug when combined with a folic acid supplement. Concentration changes of the drug in cobalamin-replete or -deficient rats, with or without folic acid supplementation, suggest that the interaction between the anticonvulsant and the two vitamins (folates and cobalamins) occurs at the level of transmethylation reactions.

The authors measured the activities of four enzymes (L.D.H., acid phosphatase, B glucuronidase, and lysozyme) and the contents of AMPc and GMPc in the synovial fluid in 35 patients with rheumatic disease. In those with various forms of inflammatory rheumatism, they found negative correlation between AMPc and the enzymes, whereas in rheumatoid arthritis they observed a positive correlation between GMPc and these enzymes.

The native fluorescence of the main biological derivatives of folic acid is maximal at acidic pH. The intensities obtained with 5-methyltetrahydrofolic acid, tetrahydrofolic acid, and formyltetrahydrofolic acid are in the ratio 10/5/1. After separating the metabolites by reversed phase high-performance liquid chromatography, the fluorometric detection limit varied between 0.4 and 20 pmol per injection. Rat liver extract (about 2 g/50 ml of 1% ascorbate solution) could be analyzed after incubation at 37 degrees C overnight, deproteinizing with acetone, and purification and concentration in an ion exchange column. The concentrations obtained varied from 1.27 to 7.96 nmol/g depending on the derivative. Recovery varied from 89 to 113%.