Acta vitaminologica et enzymologica最新文献

The Authors studied the effectiveness and safety of a commercial hypocaloric diet on 11 obese postmenopausal women. During the experimental period 1 meal/day has been replaced with a chemically defined low calories product. Different parameters have been evaluated to assess the nutritional status 1), anthropometric: weight, skinfold thickness, arm muscle circumference; 2) biochemical total plasma proteins, transferrin, vitamins A, E, C, B12, folic acid; plasma iron, hemoglobin, MCV, RBC; 3) immune status (T lymphocytes and immunoglobulins). Moreover blood sugar, cholesterol and triglyceride levels, as well as blood pressure have been taken into account. All the possible side effects and the diet acceptance for all the patients have been scored. After 1 month all the abnormal conditions (weight, cholesterol, blood pressure) improved, while the nutritional status and immune response remained at an optimal level.

The effect of vitamin A status on colon and liver glutathione content and the activity of glutathione S-transferase was studied in rats. Animals were fed diets with or without vitamin A for 4-5 weeks. There was no difference in the weight gains of control and deficient animals. Hepatic and colonic level of vitamin A was significantly reduced in vitamin A deficient animals. Hepatic glutathione content was below control values (31%); whereas activity of glutathione S-transferase was enhanced in deficient animals (41.2%). Contrary to this, colon glutathione S-transferase activity was significantly reduced (40.7%) and glutathione content remained unchanged in vitamin A deficiency.

The present study represents a contribution to the knowledge of secondary hyperparathyroidism (SHP) in patients treated with anticonvulsant drugs (AC). In these subjects alterations of the calcium: phosphorus metabolism as rickets and osteomalacia are frequent; however literature data on SHP are scarce. Our research carried out on 29 adult patients under treatment with one or more AC for periods ranging from 9 months to 12 years confirmed that 25-OHD levels in the serum are low, especially in patients treated for longer times. The iPTH levels in the serum are increased with respect to normal controls, while blood calcium and phosphate levels are normal as are urine calcium and phosphate. The 25-OHD levels in serum present the same seasonal variations as the normal controls. The administration of 25-OHD3 (20 micrograms/day for 3 months) to 12 of these patients who had the lowest 25-OHD spring levels rendered the 25-OHD levels attain normal values. Cyclic AMP was normalized; serum and urine calcium and phosphorus and urinary hydroxyproline were not modified significantly. On the basis of the present data it is recommended that chronic AC treatment should be accompanied by long term administration of 25-OHD3 for prophylaxis and/or for treatment of SHP.

Male rats fed on pellet diet to an average weight of 105 g were placed on a vitamin E deficient diet containing 20% coconut oil for a period of 12 weeks at two dietary protein levels, 20% and 10% casein. Rats on 20% casein diet showed a definite weight loss but not so at the 10% casein level. A marked increase in the liver in vitro lipid peroxidation was observed at both protein levels. Feeding of retinyl palmitate at 100,000 IU/100 g body weight for 4 consecutive days inhibited the liver, brain and kidney in vitro peroxidation; megadoses of ascorbic acid produced less inhibition of the liver peroxidation, but the same degree of inhibition for brain and kidney peroxidation as in vitamin A loaded rats. Both dietary palmitate or ascorbic acid. Acetylcholine esterase and ATPase, two of the membrane enzymes of erythrocytes, were depressed in all the groups. The glutathione content of erythrocytes was increased in rats given ascorbic acid. In all the groups the higher dietary protein levels produced greater loss of body and tissue weights. It is concluded vitamin E deficient diet supplemented with dietary coconut oil (saturated fat) induces increased in vitro lipid peroxidation and oxidative lysis of erythrocytes and that megadoses of vitamin A or C suppress the in vitro lipid peroxidation but enhance the lysis.

Recent developments in riboflavin statis assessment suggest the possibility of satisfactory replacement of the method based on the determination of glutathione reductase (GRe) (EC 1, 6, 4, 2) activity in erythrocytes by one on whole blood. The advantages would be the elimination of the steps of separation and washing of the erythrocytes, which may be of problematic execution under the difficult logistic conditions of field studies. In order to verify the interchangeability of the two methods, we have undertaken a comparison of the results obtained on 81 subjects. Our data show that the results of the whole blood method closely replicate those obtained on the erythrocytes and that all cases are correctly classified in terms of riboflavin status assessment. A linear regression analysis shows that the two methods overlap perfectly, with a highly significant (P less than 1%) correlation coefficient (r = 0.82). Sixty five percent of the variance of the dependent variable (CA GRsi) is accounted for by the variation of the independent variable CA GRe).

The association between serum transferrin and serum biochemical indicators of vitamin A and protein nutriture was investigated in 295 preschool children. Their levels of retinol and RBP correlated positively and significantly with transferrin, iron, total iron binding capacity (TIBC), total proteins and albumin. However, when removing those cases having unacceptable levels of total proteins (less than or equal to 6.4 g/dl) and/or albumin (less than or equal to 3.5 g/dl), the significant correlation between retinol (or RBP) and transferrin disappeared. It is concluded that transferrin levels are not directly related to the vitamin A nutritional status. The significance of this observation in relation to the known interaction between vitamin A and iron is discussed.

The second order rate constant for the reaction between ascorbic acid and superoxide at pH 7.4 using the xanthine-xanthine oxidase system was estimated to be 5.4 x 10(6) M-1 sec-1. The results indicate that the efficacies of superoxide dismutase and ascorbic acid for catalyzing the decay of superoxide radical in animal tissues are similar. The significance of ascorbic acid as a scavenger of superoxide is discussed from the point of view of evolution of ascorbic acid synthesizing capacity in the terrestrial vertebrates.

Escherichia coli wild strain K12 and the vitamin B6 requiring mutant strain KG980 were compared with respect to the growth inhibition by L-penicillamine and the reversal of inhibition with pyridoxine. The growth of KG980 was much more severely inhibited than that of K12 by relatively low concentrations of L-penicillamine, when KG980 was grown with a usually sufficient concentration of pyridoxine. The following findings indicated that this was because L-penicillamine caused vitamin B6 deficiency in KG980; (a) addition of excess pyridoxine significantly reversed the inhibition, (b) comparison of the growth with various concentrations of pyridoxine showed that the vitamin requirement became higher upon addition of L-penicillamine. Examination of cellular vitamin B6 compounds showed that pyridoxal 5'-phosphate was markedly decreased when L-penicillamine was present, in agreement with the probable reaction of the inhibitor with the coenzyme. On the other hand, the growth inhibition of K12 appeared independent of vitamin B6 deficiency, and the cellular pyridoxal 5,-phosphate was found not to be markedly reduced by the presence of L-penicillamine, while the total of vitamin B6 compounds, probably including the product formed by the coenzyme and the inhibitor, increased clearly. The results, therefore, suggest that the wild strain of E. coli can avoid the deficiency of vitamin B6 by enhancing its biosynthesis, although L-penicillamine acts as an antivitamin B6.

Transformed cells (Balb/c, 3T12-3), induced to increase their adhesion to the substrate by treatment with retinoic acid, display higher incorporation of (2-(3)H)-mannose into both lipids and glycoproteins than untreated controls. Stimulation of (2-(3)H)-mannose incorporation into manno-lipids is evident 8 hr after exposing the cells to retinoic acid, and stimulation of tritiated mannose incorporation into glycoproteins occurs slightly later. SDS-PAGE of (2-(3)H)-mannose labelled glycoproteins indicates that both retinoic acid and retinol treatments stimulate the incorporation of the radiolabelled sugar into a glycoprotein with subunit MW 180,000 (Gp 180) and, to a lesser extent, into other glycoproteins. 3H-leucine incorporation into a protein banding at the same position as the 3H-mannose labelled Gp 180 does not appear to be affected by retinoid treatment. A retinoic acid induced increase in the amount of Gp 180 can also be shown by lactoperoxidase catalyzed radioiodination of cultured 3T12 cells, and controlled trypsin digestion experiments indicate that Gp 180 is a component of the cell surface. On the contrary, the increased cell adhesion to the substrate induced by retinoic acid is not accompanied, in this system, by an increase in the amount of fibronectin, as judged by iodination of the cell surface components followed by SDS-PAGE.