[Evaluation of inclusion of specialized carbohydrate-protein product with vitamins and mineral substances in the diet therapy of gastrointestinal and osteopenia diseases].

It has been shown that inclusion of the specialized product containing 50% from recommended daily consumption of calcium, 20%--of protein, 17-60%--of 11 mineral substances and 11 vitamins in the diet of patients suffering from diseases of gastroenteric tract and osteopenia within 6 months lead to increasing of bone mineral density while it has not liquidated the existing vitamin B2 and vitamin D deficiency. The data obtained confirm the expediency of the development of specialized products of the set chemical composition intended for a concrete category of patients, and their inclusion in the diet.

A novel dairy product fermented with Propionibacterium freudenreichii improves the riboflavin status of deficient rats.

OBJECTIVE: Riboflavin deficiency is common in many parts of the world, particularly in developing countries. The use of riboflavin-producing strains in the production of dairy products such as fermented milk, yogurt, and cheese is feasible and economically attractive because it would decrease the costs involved during conventional vitamin fortification and satisfy consumer demands for healthier foods. The present study in a rat bioassay assessed the response of administration of yogurt containing a riboflavin-producing strain of Propionibacterium freudenreichii on the riboflavin status of deficient rats. METHODS: Propionibacterium freudenreichii NIZO B2336 is a spontaneous roseoflavin-resistant mutant derived from P. freudenreichii B374 that produces larger amounts of riboflavin than the parental stain. Rats were fed a riboflavin-deficient diet for 21 d (depletion period), after which this same diet was supplemented with conventional yogurt, yogurt containing the riboflavin-producing strain (B2336), or the parental non-producing strain (B374) and fed to animals for 28 d (repletion period). As controls, rats were fed the same diet with different concentrations of commercial riboflavin. RESULTS: The novel fermented product containing P. freudenreichii B2336, with increased levels of riboflavin, eliminated most physiologic manifestations of ariboflavinosis such as stunted growth, high erythrocyte glutathione reductase activation coefficient values, and hepatomegaly that were observed when using a riboflavin depletion-repletion model, whereas the product fermented with the non-riboflavin-producing strain did not show this beneficial effect. CONCLUSIONS: Consumption of such products with increased levels of riboflavin on a regular basis may help prevent deficiencies of this essential vitamin.

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status.

OBJECTIVE: To investigate the effect of riboflavin supplementation on plasma homocysteine (tHcy) concentrations in healthy elderly people with sub-optimal riboflavin status. DESIGN: A double-blind, randomized, placebo-controlled riboflavin supplementation trial. SETTING: Community based study in Northern Ireland. SUBJECTS: From a screening sample of 101 healthy elderly people, 52 had sub-optimal riboflavin status (erythrocyte glutathione reductase activation coefficient, EGRAC>or=1.20) and were invited to participate in the study. INTERVENTION: The intervention had two parts. Part 1 was a 12 week randomized double blind, placebo-controlled intervention with riboflavin (1.6 mg/day). Following completion of part 1, the placebo group went on to part 2 of the study which involved supplementation with folic acid (400 micro g/day) for 6 weeks followed by folic acid and riboflavin (1.6 mg/day) for a further 12 weeks, with a 16 week washout period post-supplementation. The purpose of part 2 was: (a) to address the possibility that homocysteine-lowering in response to riboflavin may be obscured by a much greater effect of folate, and that, once folate status was optimized, a dependence of homocysteine on riboflavin might emerge; and (b) to demonstrate that these subjects had homocysteine concentrations which could be lowered by nutritional intervention. RESULTS: Although riboflavin supplementation significantly improved riboflavin status in both parts 1 and 2 of the study (P<0.001 for each), tHcy concentrations were unaffected (P=0.719). In contrast, folic acid supplementation (study part 2) resulted in a homocysteine lowering of 19.6% (P=0.001). CONCLUSION: Despite the metabolic dependency of tHcy on riboflavin, it did not prove to be an effective homocysteine-lowering agent, even in the face of sub-optimal riboflavin status.

Interpretation of erythrocyte glutathione reductase activation test values for assessing riboflavin status.

The erythrocyte glutathione reductase activation test (EGR-AC) is considered to be the best method to assess riboflavin nutritional status. Riboflavin supplementation studies carried out in India have raised doubts about the validity of currently available interpretive guidelines for interpreting the EGR-AC test. Changes in EGR-AC values in response to graded doses of riboflavin supplementation were investigated in schoolchildren, aged 7-11 years, belonging to the low-income group. For comparison, unsupplemented well-to-do schoolchildren of similar age group were also examined. The results of the study based on the measurement of EGR-AC by the procedure of Bayoumi and Rosalki (Clinical Chemistry, 1976, Vol. 22, pp. 327-335) with an incubation period of 15 min suggest that the cut-off value for EGR-AC to discriminate between riboflavin-deficient and normal children cannot be less than 1.5.

Glutathione and related indices in rat lenses, liver and red cells during riboflavin deficiency and its correction.

Biochemical changes in lenses and at other sites in adult rats were investigated during the induction and correction of riboflavin deficiency. Riboflavin deficient (D), 1-day-repleted (R1), 2-days-repleted (R2), 16-days-repleted (R3), food-restricted, weight-matched controls (CFR) and ad libitum-fed controls (CAL) were compared. Activation coefficients of erythrocyte and lens glutathione reductase, which became abnormal in the deficient (D) animals, were corrected to varying extents in the repleted (R) groups. Hepatic flavin concentrations were lowered in the groups with raised glutathione. Inter-group differences in hepatic glutathione concentrations were not simply related to tissue flavin depletion or its reversal, but were complicated by changes in liver: body-weight ratios. Inter-group differences in lenticular glutathione levels were very small. In both liver and lens, sorbitol concentrations were lowest in group R3 and highest in groups D, R1 and R2. Lens ascorbate levels and the lens enzymes, aldose reductase, sorbitol dehydrogenase, glutathione peroxidase and superoxide dismutase, were not significantly affected by diet. Thiobarbituric acid-reactive substances were increased in riboflavin-deficient rat lenses but were lowered in riboflavin-deficient plasma samples. The results suggest overall that while riboflavin deficiency may affect certain biochemical indices, such as sorbitol and thiobarbituric-reactive substances, in the lens and other tissues, these changes are not the result of lowered glutathione levels. They also clearly demonstrate the importance of inanition as a confounding factor in the interpretation of changes resulting from riboflavin deficiency in experimental animals.

Glutathione reductase in the south-western province of Saudi Arabia--genetic variation vs. acquired deficiency.

The activity of glutathione reductase (GR) is closely associated with the riboflavin level in diet. Dietary deficiency of this water-soluble vitamin causes glutathione reductase deficiency. Furthermore, a variable frequency of GR variants with reduced activity has been reported in several populations. In an attempt to determine GR deficiency due to genetic (GR variant) and acquired causes (riboflavin deficiency), red cell GR activity was estimated in 461 male and female Saudis from the South-Western province of Saudi Arabia. The frequency of genetic GR deficiency (GR variant) was 24.5% in Saudi males and 20.3% in females. The frequency of acquired GR deficiency (riboflavin deficiency) was 17.8% and 22.4%, respectively. Interaction between genetic GR deficiency and other genetic abnormalities, i.e. sickle cell gene and glucose-6-phosphate dehydrogenase deficiency were also estimated. No specific link could be demonstrated.

Effect of diet on vitamin deficiencies in retarded individuals receiving drugs.

A population of mentally retarded and physically disabled individuals on long-term therapy with anticonvulsant drugs had a high prevalence of folic acid and riboflavin deficiency, 20% and 17%, respectively, as they entered an institution devoted to their care. Their previous diet was probably nutritionally marginal, as it was cooked and prepared to baby food consistency, and milk was rarely given. They were fed in the recumbent position, resulting in frequent vomiting. In this institution, a carefully planned dietary regimen that was adequate in essential nutrients was fed by trained personnel. Drug therapy was continued. After a year no signs of folic acid or riboflavin deficiency were evident. We conclude that these weak vitamin antagonists may precipitate deficiencies on marginally adequate diets. A good dietary regimen prevented the appearance of these vitamin deficiencies.

Efficacy of a food supplement in correcting riboflavin deficiency in pregnant Gambian women.

Pregnant women living in rural Gambian villages, whose natural riboflavin intake is about 0.5 mg/d, have abnormal biochemical riboflavin status and signs of clinical deficiency. A vitamin-fortified food supplement given in one village which increased the riboflavin intake to about 1.3 mg/d was followed by a substantial improvement in biochemical status, although seasonally-related variations in status somewhat complicated the picture. It was calculated that the amount of riboflavin needed to satisfy the requirement, for normal biochemical status, of the majority of pregnant women throughout pregnancy and throughout the year, is about 2.6 mg/d. Clinical signs associated with riboflavin deficiency, especially atrophic lingual papillae, showed significantly reduced incidence in the supplemented, compared with an unsupplemented, village. Cord blood values of the activation coefficient of erythrocyte glutathione reductase were in the abnormal range for 84 per cent of infants before introduction of the supplement, but were abnormal for only one of 12 infants after its introduction. Thus even a suboptimal maternal riboflavin intake of about 1.3 mg/d appears to be sufficient to prevent biochemical deficiency in cord blood, and to reduce considerably the incidence of clinical deficiency signs during pregnancy.

Effect of riboflavin supplementation on riboflavin nutriture of a secondary school population in Nigeria.

Riboflavin status was assessed in 42 secondary school students before and after supplementing the food intake with 5 mg riboflavin daily for 7 days. Energy, protein, and riboflavin intakes were determined on foods actually consumed by each student. Riboflavin nutriture was based on urinary riboflavin excretion and erythrocyte glutathione reductase activity coefficient. The energy and riboflavin intakes of the students were 68 to 82% and 80 to 88%, respectively, of the recommended allowance. The basal urinary riboflavin excretion was 0.335 mg/g creatinine and increased significantly to 3.51 mg/g creatinine after supplementation. The basal erythrocyte glutathione reductase activity coefficient values indicated an overall prevalence of 38% biochemical ariboflavinosis (erythrocyte glutathione reductase activity coefficient greater than 1.30) and dropped significantly (p less than 0.001) from 1.26 to 1.08. The results confirm that urinary riboflavin is of limited value in the assessment of riboflavin status while erythrocyte glutathione reductase activity coefficient more precisely assesses metabolic availability of riboflavin and more accurately detects biochemical ariboflavinosis.

An automated flavin adenine dinucleotide-dependent glutathione reductase assay for assessing riboflavin nutriture.

An automated AutoAnalyzer method using 5:5'-dithiobis-2-nitrobenzoic acid is described for determining whole blood glutathione reductase (BGR) activity and for measuring in vitro activation of BGR with flavin adenine dinucleotide (FAD). BGR activity is expressed as mumoles glutathione regenerated from oxidized glutathione per ml of whole blood (WB) or per g of hemoglobin. The stimulatory effect of FAD on BGR activity divided by the activity without FAD determined the activity coefficient (AC). We found that NADPH and oxidized glutathione assay concentrations of 0.100 mmole/liter and 0.250 mmole/liter, respectively, in 0.1 mole/liter phosphate buffer, pH 7.4, gave consistent results when WB, before assay, was diluted 20-fold. WB samples to be stored are initially diluted 10-fold with distilled water and frozen. Prior to assay, two aliquots of the sample are diluted 2-fold, one aliquot with distilled water and another with 46 mumole/liter FAD. With sample and manifold dilutions the assay FAD concentrations is 1.0 mumole/liter: assay concentrations greater than 5.0 mumole FAD/liter were shown to be inhibitory. We examined blood samples from 617 children in the age range 6 to 60 months and determined the normal AC range to be between 1.00 and 1.35. Six weaned rats (23 days of age), maintained on a riboflavin-deficient diet, showed a mean AC of 1.23, 1.54, 2.02, and 2.41 at 23, 26, 30, and 36 days of age, respectively. Six control rats maintained an AC of 1.23 +/- 0.05 (SD) during the same period.