F. Weber

Glutathione reductase test with whole blood, a convenient procedure for the assessment of the riboflavin status in humans

Eine vereinfachte Variante des Glutathionreduktasetests zur Erfassung des Riboflavinstatus wird beschrieben, für die nur 0,05 ml Gesamtblut anstelle von gewaschenen Erythrozyten benötigt werden. Beim Vergleich der Stimulierbarkeit der Glutathionreduktase durch das Coenzym FAD ergab sich eine sehr gute Korrelation zwischen den Aktivierungskoeffizienten bei Verwendung von Gesamtblut und Erythrozyten. Diese zeigten statistisch signifikante Korrelationen zum Flavingehalt im Blut.

Metabolism of Vitamin A and the Determination of Vitamin A Status

Publisher Summary This chapter describes the metabolism of vitamin A and the determination of vitamin A status. Estimations of the vitamin A status of humans and animals usually are based upon determinations of the vitamin A concentration in plasma. The plasma vitamin A level is correlated to the amount in the liver, the main site of storage of the vitamin in the body, only in cases of extreme hypo- and hypervitaminosis A but is constant over a wide range of intermediate vitamin A levels in the liver. The rate of urinary excretion of radioactive metabolites after a loading dose of labeled vitamin A, was studied in rats possessing different vitamin A reserves. It is possible to calculate the amount of vitamin A metabolites excreted in the urine in terms of vitamin A equivalents on the bases of the urinary radioactivity and of the specific radioactivity of the vitamin A contained in the liver when excretion of urinary vitamin A-derived radioactivity had reached a constant rate about 7 days after treatment with labeled vitamin A. Positive results for a reliable determination of the vitamin A status of rats were obtained by an isotopic dilution technique consisting of an intravenous administration of a physiological dose of radioactive vitamin A acetate and the determination of the specific radioactivity of the plasma vitamin A after a certain equilibration period.

Na+-dependent, potential-sensitive L-ascorbate transport across brush border membrane vesicles from kidney cortex.

l-Ascorbate is taken up into brush border vesicles from kidney cortex of rat, rabbit and guinea pig by an efficient, Na+-dependent and potential-sensitive transport process. This uptake shows saturation (Km:0.1–0.3 mM) and is strongly stimulated by low concentrations of N3−. Erythorbate (d-isoascorbate) seems to be another, but poorer, substrate of the same transporter.

Biochemical Pathology of Vitamin B6 Deficiency

Publisher Summary Various pyridoxal phosphate enzymes are affected differently by vitamin B 6 depletion. Enzymes involved in the degradation of tryptophan and of the sulfur amino acids are impaired at an early stage of the deficiency. Therefore, alterations of the metabolism of these amino acids are the first signs of the vitamin B 6 deficiency state. The apoenzyme synthesis of pyridoxal phosphate-containing enzymes seems to be induced and regulated by pyridoxal phosphate. Consequently, organs with a high protein turnover lose their pyridoxal phosphate enzymes more rapidly by vitamin B 6 depletion than those with a low protein turnover. Correlations exist between cerebral symptoms produced by vitamin B 6 depletion, the reduction of the pyridoxal phosphate content in the brain and the activity of its enzymes dependent on pyridoxal phosphate.

Uptake and release of [1-14C]ascorbic acid and [1-14C]dehydroascorbic acid by erythrocytes of guinea pigs

Abstract The uptake and release of [1- 14 C] ascorbic acid and [1- 14 C]dehydroascorbic acid by erythrocytes of guinea pigs kept on a normal diet and of those on an ascorbic acid-deficient diet was studied in vitro . Results strongly suggest that the erythrocyte membrane is permeable to both ascorbic acid and dehydroascorbic acid in either direction. Mean ratios of the uptake of dehydroascorbic acid to ascorbic acid by the erythrocytes of normally fed guinea pigs (2.03 ± 0.69) and of vitamin C-deficient animals (2.49 ± 0.44) are given. After incubation with [1- 14 C]ascorbic acid, only ascorbic acid was found in the erythrocytes and only ascorbic acid was released during reincubation. In the case of [1- 14 C]dehydroascorbic acid, mainly dehydroascorbic acid was found to be present in the erythrocyte, but some ascorbic acid was always detectable. Both dehydroascorbic acid and ascorbic acid were released, mainly, however, dehydroascorbic acid.

Site of intestinal absorption of ascorbic acid in guinea pigs and rats

Abstract The site of absorption of ascorbic acid by the small intestine was studied in vivo in guinea pigs, normal and hypophysectomized rats after oral application of 14C-ascorbic acid. A species-specific difference was revealed. The site of absorption in the guinea pig was located in the duodenal and proximal small intestinal wall, whereas the rat showed highest absorption in the ileum. Hypophysectomy in rats caused a shift of the absorption site from the ileum to the jejunum. No absorption was observed in the duodenum and ileum. A regulatory role of the pituitary gland in the absorption of ascorbic acid by the small intestine is discussed.

Ethanol selectively affects Na+-gradient dependent intestinal transport systems

Moderate concentrations of ethanol reduce the velocity of uptake of three representative Na+‐symport systems (D‐glucose, L‐alanine, L‐ascorbate), whether electrogenic (the first two) or electroneutral (L‐ascorbate). This ‘inhibition’ is observed only if these transport systems are tested in the presence of an initial Na+ gradient (out > in); no inhibition is found in tracer‐equilibrium exchange measurements. A representative Na+‐independent system (D‐fructose) is not inhibited by ethanol. ‘Passive diffusion’ (measured as uptake of L‐glucose) is increased somewhat by alcohol. All these observations can be rationalized [as suggested by Tillotson et al. (1981) Arch. Biochem. Biophys. 207, 360–370] by an effect of ethanol on passive diffusion, which leads to a faster collapse of the Na+ gradient, with the resulting reduction of the uptake velocities of Na+‐dependent transport systems when tested with the added driving force of an Na+ out → in gradient.

Studies on the uptake of [1-14C]ascorbic acid and [1-14C]-dehydroascorbic acid by platelets of guinea pigs

Abstract Ascorbic acid as well as dehydroascorbic acid were shown to penetrate the platelet membrane in vitro. The percentage uptake by platelets of control guinea pigs (ascorbic acid 0.22 ± 0.014; dehydroascorbic acid 0.54 ± 0.033; p = 0.001) as well as of vitamin C-deficient animals (ascorbic acid 0.40 ± 0.026; dehydroascorbic acid 0.88 ± 0.060; p = 0.001 SEM given) were found to be significantly different. The uptake of ascorbic acid as well as of dehydroascorbic acid were significantly enhanced compared to control animals (p = 0.001). However, the ratios of uptake of dehydroascorbic acid to ascorbic acid were unaffected (control animals 2.30 ± 0.24; vitamin C-deficient animals (2.30 ± 0.17). The uptake of ascorbic acid was found to be fairly dependent on the concentration and was not influenced by ouabain. On the contrary, the uptake of dehydroascorbic acid did not show a linear dependency on the concentration and was inhibited by 10−3 M ouabain. These findings suggest an active transport mechanism for the uptake of dehydroascorbic acid whereas in case of ascorbic acid the facilitated diffusion mechanism is discussed. After incubation of platelets of control and vitamin C-deficient animals with [1-14C]ascorbic acid as well as with [1-14C]dehydroascorbic acid only [1-14C] ascorbic acid was detectable in the platelets and only [1-14C]ascorbic acid was released by the platelets.

Uptake and release of [I-14C]ascorbic acid and [I-14C]dehydro-ascorbic acid by leucocytes of guinea pigs

Abstract The leucocyte membrane was found to be permeable to both ascorbic acid and dehydroascorbic acid in either direction. Mean ratios of uptake of dehydroascorbic acid to ascorbic acid by leucocytes of normally fed guinea pigs (1.41 ± 0.16) and of vitamin C-deficient animals (1.91 ± 0.22) are given. No difference in uptake behaviour was observed using leucocytes of animals depleted of vitamin C for up to 16 days. However, ratios for uptake decreased rapidly in leucocytes of such animals being depleted for longer than 20 days, but this was most probably due to inanition and resulting metabolic disorders. After incubation with ascorbic acid, in both groups, only ascorbic acid was found in leucocytes and only ascorbic acid was released during re-incubation. After incubation with dehydroascorbic acid only ascorbic acid was found to be present in leucocyctes of the control group, whereas in the deficient group both, ascorbic acid and dehydroascorbic acid, were found and both compounds were released. After incubation with dehydroascorbic acid in the control group, mainly ascorbic acid was released.

Influence of erythorbic acid on the vitamin C status in guinea-pigs

Eine Verabreichung von Erythorbinsäure (d-Isoascorbinsäure,d-Araboascorbinsäure) vermindert die Aufnahme von Ascorbinsäure (Vitamin C) in verschiedenen Organen des Meerschweinchens. Da Erythorbinsäure nur eine sehr geringe Vitamin-C-Aktivität besitzt, wird bei einer gleichzeitigen Einnahme von Erythorbinsäure und Ascorbinsäure die Verfügbarkeit des Vitamin C für den Tierorganismus signifikant reduziert.