Single versus multiple deficiencies of methionine, zinc, riboflavin, vitamin B-6 and choline elicit surprising growth responses in young chicks. (1/96)

A soy-protein isolate diet that was deficient in methionine (Met), zinc (Zn), riboflavin, vitamin B-6 and choline for chick growth (Assay 1) was used to study individual or multiple deficiencies of several of these nutrients. In all cases, adding all three deficient nutrients together resulted in growth responses that were superior to those resulting from supplementation with any pairs of deficient nutrients. In Assay 2, single addition of Zn but not of methionine or riboflavin produced a growth response, but the combination of either Zn and Met or Zn and riboflavin resulted in growth responses that were greater than the response elicited by Zn alone. Assay 3 involved individual or multiple deficiencies of choline, riboflavin and vitamin B-6, and individual additions suggested that choline was first limiting. Choline + riboflavin supplementation, however, produced marked growth and gain:food responses that were far greater than those resulting from supplemental choline or riboflavin alone. Moreover, the growth response to a combination of choline + pyridoxine (PN) was also greater than that obtained from any of the three nutrients fed alone; even PN + riboflavin (in the absence of choline) produced responses greater than those observed with the unsupplemented negative-control diet. In Assay 4, chicks responded to individual additions of riboflavin, PN or Met, and in Assay 5, to either riboflavin or PN; all two-way combinations resulted in growth rates that were far greater than those occurring with any single addition. The data from these experiments show that unlike the situation with three deficient amino acids, the expected responses to first-, second- and third-limiting B-vitamins or deficient vitamins combined with deficient levels of Zn or Met do not follow the expected pattern of response to first-, further response to first- and second- and an even further response to first-, second- and third-limiting nutrients.  (+info)

Low-dose vitamin B-6 effectively lowers fasting plasma homocysteine in healthy elderly persons who are folate and riboflavin replete. (2/96)

BACKGROUND: Current data suggest that physiologic doses of vitamin B-6 have no significant homocysteine-lowering effect. It is possible that an effect of vitamin B-6 was missed in previous trials because of a much greater effect of folic acid, vitamin B-12, or both. OBJECTIVE: The aim of this study was to investigate the effect of low-dose vitamin B-6 supplementation on fasting total homocysteine (tHcy) concentrations in healthy elderly persons who were made replete with folate and riboflavin. DESIGN: Twenty-two healthy elderly persons aged 63-80 y were supplemented with a low dose of vitamin B-6 (1.6 mg/d) for 12 wk in a randomized, double-blind, placebo-controlled trial after repletion with folic acid (400 microg/d for 6 wk) and riboflavin (1.6 mg/d for 18 wk); none of the subjects had a vitamin B-12 deficiency. RESULTS: Folic acid supplementation lowered fasting tHcy by 19.6% (P < 0.001). After folic acid supplementation, baseline tHcy concentrations ranged from 6.22 to 23.52 micromol/L and 10 subjects had suboptimal vitamin B-6 status (plasma pyridoxal-P < 20 nmol/L). Two-way analysis of variance showed that the significant improvement in vitamin B-6 status in response to vitamin B-6 supplementation (on the basis of both pyridoxal-P: and the erythrocyte aspartate aminotransferase activation coefficient) was reflected in a significant reduction in plasma tHcy of 7.5%. CONCLUSIONS: Low-dose vitamin B-6 effectively lowers fasting plasma tHcy in healthy subjects who are both folate and riboflavin replete. This suggests that any program aimed at the treatment or prevention of hyperhomocysteinemia should include vitamin B-6 supplementation.  (+info)

Riboflavin and mouse hepatic cell structure and function. Mitochondrial oxidative metabolism in severe deficiency states. (3/96)

Weanling mice were fed a riboflavin-deficient diet or the same diet with added galactoflavin. Both diets produced changes in hepatic mitochondrial morphology, the most striking of which was the development of giant mitochondria. The livers from these animals were fractionated, and the nuclear and mitochondrial fractions were examined by electron microscopy. The nuclear fraction contained giant mitochondria; the mitochondrial fraction contained the remaining normal to moderately enlarged mitochondria. Oxidative studies were carried out on the mitochondrial fractions. It was found that both experimental diets resulted in a marked reduction in fatty acid oxidation by the mitochondria. In addition, the mitochondria of mice with advanced riboflavin deficiency (induced simply by a riboflavin-free diet) showed a severely decreased state 3 (ADP-stimulated) respiration and depressed respiratory control ratios, but normal ADP/O ratios. In contrast, mitochondrial performance (aside from fatty acid oxidation) in galactoflavin-supplemented, riboflavin-deficient mice was related to the gross appearance, i.e., color, of the liver from which these organelles were derived. In mice fed this diet, the livers were either red or yellow. Mitochondria from yellow livers showed normal oxidative phosphorylation. Mitochondria from red livers showed a serious reduction in state 3 oxidation. This study demonstrates that in the mouse, riboflavin deficiency, however produced, not only results in altered mitochondrial morphology but also results in significantly impaired mitochondrial function.  (+info)

An evaluation of the role of leukocytes in the pathogenesis of experimentally induced corneal vascularization. (4/96)

Studies of corneal explants in the hamster cheek pouch chamber have demonstrated that blood vessels invade the cornea only if the tissue is first infiltrated by leukocytes. In view of this observation, a comparative study of the events that precede and accompany corneal vascularization was undertaken in various experimental models. A variety of established methods were used to induce corneal vascularization, including exposure of the cornea to noxious agents, intracorneal injection of antigens into sensitized animals, as well as maintaining animals on diets deficient in vitamin A or riboflavin. In all models studied, the corneal vascularization was a manifestation of the reparative phase of the inflammatory response. A conspicuous leukocytic infiltrate of the cornea preceded and accompanied the corneal vascularization in all of the models. Although the lesions varied in several respects in the different models, all models displayed three phases with regard to vascularization: an early prevascular phase of leukocytic infiltration, a second phase where blood vessels persisted in the cornea in the absence of leukocytes. The latent period that preceded vascularization was directly related to the time of the initial leukocytic infiltration. The models in which a delay occurred in the leukocytic invasion displayed a subsequent delay in the vascular ingrowth. Conversely, in experiments where there was a rapid and extensive leukocytic invasion, there was also an early and enhanced corneal vasoproliferative response. In the various modesl investigated, the sites of the leukocytic infiltration and subsequent vascular ingrowth into the cornea paralleled each other. The data further support the hypotheses that leukocytes are a prerequisite to corneal vascularization and that leukocytes produce one or more factors which stimulate directional vascular growth.  (+info)

Effects of riboflavin repletion during different developmental phases on behavioral patterns, brain nucleic acid and protein contents, and erythrocyte glutathione reductase activity of male rats. (5/96)

Effects of riboflavin repletion of rats at various stages of development were evaluated by biochemical and behavioral parameters. One group of dams received diets containing a suboptimal level of riboflavin, approximately 15 mug, and another group, control, received approximately 40 mug of the vitamin daily 2 weeks before mating. Rats fed the control diet received approximately 120 mug riboflavin daily during pregnancy and lactation; suboptimals received approximately 15 mug daily. Some rats fed the control diet were pair-fed to rats fed the suboptimal ration. A group of dams fed the suboptimal diet was switched to control after parturition. At weaning, male offspring were fed the same riboflavin levels their respective dams received before mating except one group, whose dams were fed the suboptimal diet, received the control diet. Male progeny of dams pair-fed the control diet to suboptimal rats were either pair-fed to offspring of suboptimal dams or to offspring riboflavin-repleted at weaning. Rats that always received the suboptimal diet had significantly higher general activity scores at 60 days of age than the scores of other animals. Brains from rats always fed the suboptimal diet and those receiving riboflavin repletion at weaning had lower, sometimes significantly, DNA, RNA, and protein contents than those from other animals. Riboflavin restriction during gestation and lactation, but not gestation alone, appeared to produce permanent alterations in general activity scores and brain nucleic acid and protein contents of male rat progeny.  (+info)

Dietary intake in the third trimester of pregnancy and birth weight of offspring among nonprivileged and priviledged women. (6/96)

The dietary intake during the third trimester of pregnancy among 20 nonprivileged and 10 privileged primigravidae in Addis Ababa was studied in a 2 day weighting inventory survey. With the exception of iron and thiamin, the nonprivileged group consumed a diet that was deficient in all nutrients, with an average daily protein and energy intake below 60% of the FAO/WHO Recommendations. The privileged group was found to meet the recommendations for all nutrients except for calcium and riboflavin. Infants born to the nonprivileged women had significantly lower mean birth weight when compared with the infants born to the privileged women.  (+info)

Angular stomatitis and riboflavin status among adolescent Bhutanese refugees living in southeastern Nepal. (7/96)

BACKGROUND: Between 1990 and 1993, fear of ethnic persecution led 83,000 ethnic Nepalese to flee from Bhutan to refugee camps in Nepal, where they remained at the time of this study. Reported cases of angular stomatitis (AS), ie, thinning or fissuring at the mouth angles, increased 6-fold from December 1998 to March 1999, from 5.5 to 35.6 cases per 1000 per month. This increase came after the removal of a fortified cereal from rations. OBJECTIVES: The main objectives were to assess the prevalence of AS and of low concentrations of riboflavin, folate, vitamin B-12, and iron by using biochemical measures; to determine whether riboflavin status was associated with AS; and to assess the potential of AS as a screening measure for low riboflavin concentrations. DESIGN: In October 1999, we performed a survey among a random sample of 463 adolescent refugees in which we conducted interviews and physical examinations and obtained blood specimens for riboflavin assessment. Riboflavin status was assessed with the erythrocyte glutathione reductase (EC 1.6.4.2) activity coefficient. After we excluded those adolescents who had taken vitamins during the past month, 369 were eligible for analyses. RESULTS: AS was common (26.8%; 95% CI: 22.3, 31.3), the prevalence of low riboflavin concentrations was high (85.8%; 80.7, 90.9), and riboflavin status was associated with AS. Adolescents with AS had significantly lower riboflavin concentrations than did adolescents without AS (P = 0.02). The adjusted odds ratio for AS and low riboflavin concentrations was 5.1 (1.55, 16.5). CONCLUSION: Globally, riboflavin deficiency is rare. Its emergence in food-dependent populations can be a harbinger of other B-vitamin deficiencies.  (+info)

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status. (8/96)

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.  (+info)

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