scholarly journals Riboflavin deficiency: early effects on post-weaning development of the duodenum in rats

2001 ◽  
Vol 86 (5) ◽  
pp. 593-599 ◽  
Author(s):  
Catherine A Yates ◽  
Gareth S. Evans ◽  
Hilary J. Powers
Keyword(s):  
Wistar Rats ◽  
Developmental Changes ◽  
Riboflavin Deficiency ◽  
Show Evidence ◽  
Activation Coefficient ◽  
Early Effects ◽  
Riboflavin Deficient ◽  
Rates Of Growth ◽  
Riboflavin Status

The aim of this present study was to identify the earliest point at which riboflavin deficiency affects post-weaning bowel development in rats. After weaning, eighty Wistar rats were weight-matched as pairs, one animal being fed a normal synthetic diet and the other being fed the same diet but deficient in riboflavin. Body weight, feeding and rates of growth were monitored and eight pairs of animals were taken for analysis at 45, 69, 93, 117 and 141 h. Riboflavin status was monitored by determining the erythrocyte glutathione reductase activation coefficient (EGRAC), and hepatic flavins were measured by a fluorescence assay. Changes to the number and dimensions of villi and crypts in the duodenum were determined, as well as crypt division (bifurcation) and the DNA synthesis index of the crypt epithelium by bromodeoxyuridine (BrdU) labelling. Riboflavin deficiency was established in the experimental rats, as demonstrated by a significant increase in EGRAC after 45 h (P<0·001) and decreased liver flavins after 96 h (P<0·001). After 96 h a significant increase in the size and cellularity of the crypts (P<0·001 in both cases) was seen in these riboflavin-deficient animals, with a decreased incidence of bifurcating crypts and of BrdU-labelled cells. No changes to villus number or size were observed. The present study has demonstrated that developmental changes to the duodenal crypt arise shortly after circulating riboflavin measurements show evidence of deficiency. These changes primarily affect cell proliferation and crypt bifurcation, and precede long-term changes such as the reduction of villus number.

scholarly journals Effect of riboflavin deficiency on reproductive performance and on biochemical indices of riboflavin status in the rat

1985 ◽  
Vol 53 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Julia M. Duerden ◽  
C. J. Bates
Keyword(s):  
Post Partum ◽  
Basal Diet ◽  
Young Female ◽  
Female Rats ◽  
Riboflavin Deficiency ◽  
Diet Control ◽  
Activation Coefficient ◽  
Riboflavin Deficient ◽  
Biochemical Indices ◽  
Riboflavin Status

1. Young female rats were made riboflavin-deficient by feeding a purified diet containing casein (210 g/kg). This basal diet provided 0.40 mg riboflavin/kg diet, to which was added additional riboflavin at 0, 0.12 or 0.25 mg/kg diet. Control animals received the same diet with 15 mg added riboflavin/kg. The diets were given for 4 weeks before mating, then throughout pregnancy and for 15 d of lactation.2. With no added riboflavin in the diet, reproduction was severely impaired and fetal resorption was usually observed. With 0.12 mg added riboflavin/kg diet, however, reproduction was usually successful, and the growth of dams and pups was only marginally depressed in comparison with pair-fed controls optimally supplied with riboflavin.3. The activation coefficient (stimulated: basal activity) of erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2)was high, and the concentration of riboflavin in the liver was correspondingly low in the dams receiving diets containing 0.12 or 0.25 mg added riboflavin/kg and in their sucking pups at 15 d post partum. Riboflavin levels in the milk from both groups of dams were about eightfold lower than in controls. There was little evidence that the sucking pups could maintain their riboflavin level at the expense of that in the maternal tissues.

scholarly journals Refection in rats fed on a sucrose-based, riboflavin-deficient diet

1980 ◽  
Vol 43 (1) ◽  
pp. 171-177 ◽  
Author(s):  
A. M. Prentice ◽  
C. J. Bates
Keyword(s):  
Biochemical Tests ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Biochemical Effects ◽  
Severe Deficiency ◽  
Riboflavin Deficient ◽  
Riboflavin Status

1. Refection, resulting in an increased supply of riboflavin to riboflavin-deficient rats through coprophagy, was demonstrated on a sucrose-based diet when sensitive biochemical tests of riboflavin status were employed: these included measurements of NAD(P)H2:glutathione oxidoreductase (EC 1.6.4.2); succinate:(acceptor) oxidoreductase (EC 1.3.99.1) and NADH:(acceptor) oxidoreductase (EC 1.6.99.3).2. The use of tail-cups to eliminate coprophagy, and hence refection, resulted in a more rapid and reproducible progress into severe deficiency.3. The occurrence of refection on a sucrose-based diet may account for hitherto unexplained differences between previous publications on the biochemical effects of riboflavin deficiency.

scholarly journals The effect of riboflavin deficiency on methylenetetrahydrofolate reductase (NADPH)(EC 1.5.1.20) and folate metabolism in the rat

1986 ◽  
Vol 55 (2) ◽  
pp. 455-464 ◽  
Author(s):  
C. J. Bates ◽  
N. J. Fuller
Keyword(s):  
Methylenetetrahydrofolate Reductase ◽  
Folate Metabolism ◽  
Hepatic Tissue ◽  
Riboflavin Deficiency ◽  
Weanling Rats ◽  
Metabolizing Enzyme ◽  
Riboflavin Deficient ◽  
Riboflavin Status

1. Riboflavin deficiency at two levels of severity was produced in weanling rats by feeding deficient diets for 6 weeks and using neck collars to prevent coprophagy. The severity of deficiency was monitored by growth, liver flavin levels and the activation coefficient of erythrocyte glutathione oxidoreductase (NAD(P)H) (EC 1. 6. 4. 2 ) Control groups, receiving the same diet with ample added riboflavin, were fed either ad lib., or were pair-fed with the deficient animals.2. The hepatic flavoenzyme, methylenetetrahydrofolate reductase (NADPH) (EC 1.5.1.20), was very markedly affected by severe riboflavin deficiency and was significantly, but less markedly, affected by the intermediate level of deficiency. This reduction in activity was due primarily to the direct effect of the diminished supply of riboflavin, and occurred to only a small extent as a result of inanition, demonstrated by a moderate reduction in activity in the more severely food-restricted of the two pair-fed groups. Since the enzyme is assayed in the presence of its flavin cofactor, FAD, it clearly cannot be reactivated in vitro, as some other depleted flavoenzymes can. The discriminatory ability in distinguishing between severe and moderate riboflavin deficiency in vivo confers some potential advantages on this oxidoreductase as a possible index of riboflavin status.3. The hepatic activity of another key folate-metabolizing enzyme, dihydrofolate reductase (EC 1.5.1.3), was not diminished by riboflavin deficiency in the present study.4. The ratio, labelled 5-methyltetrahydrofolic acid: other labelled compounds derived from intraperitoneally injected pteroylglutamic acid in extracts of hepatic tissue was significantly reduced in the riboflavin-deficient groups, indicating the possibility of an effect of riboflavin deficiency on folate metabolism in vivo.

scholarly journals Effects of methodological variation on assessment of riboflavin status using the erythrocyte glutathione reductase activation coefficient assay

2008 ◽  
Vol 102 (2) ◽  
pp. 273-278 ◽  
Author(s):  
Marilyn H. E. Hill ◽  
Angela Bradley ◽  
Sohail Mushtaq ◽  
Elizabeth A. Williams ◽  
Hilary J. Powers
Keyword(s):  
Glutathione Reductase ◽  
Intervention Study ◽  
Flavin Adenine Dinucleotide ◽  
Riboflavin Deficiency ◽  
Study Results ◽  
Erythrocyte Enzyme ◽  
Activation Coefficient ◽  
The Uk ◽  
Riboflavin Status

Riboflavin status is usually measured as thein vitrostimulation with flavin adenine dinucleotide of the erythrocyte enzyme glutathione reductase, and expressed as an erythrocyte glutathione reductase activation coefficient (EGRAC). This method is used for the National Diet and Nutrition Surveys (NDNS) of the UK. In the period between the 1990 and 2003 surveys of UK adults, the estimated prevalence of riboflavin deficiency, expressed as an EGRAC value ≥ 1·30, increased from 2 to 46 % in males and from 1 to 34 % in females. We hypothesised that subtle but important differences in the detail of the methodology between the two NDNS accounted for this difference. We carried out an evaluation of the performance of the methods used in the two NDNS and compared against an ‘in-house’ method, using blood samples collected from a riboflavin intervention study. Results indicated that the method used for the 1990 NDNS gave a significantly lower mean EGRAC value than both the 2003 NDNS method and the ‘in-house’ method (P < 0·0001). The key differences between the methods relate to the concentration of FAD used in the assay and the duration of the period of incubation of FAD with enzyme. The details of the EGRAC method should be standardised for use in different laboratories and over time. Additionally, it is proposed that consideration be given to re-evaluating the basis of the EGRAC threshold for riboflavin deficiency.

scholarly journals A biochemical evaluation of the erythrocyte glutathione reductase (EC 1.6.4.2) test for riboflavin status

1981 ◽  
Vol 45 (1) ◽  
pp. 53-65 ◽  
Author(s):  
A. M. Prentice ◽  
C. J. Bates
Keyword(s):  
Glutathione Reductase ◽  
Liver Weight ◽  
Strongly Correlated ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Serial Measurement ◽  
Weanling Rats ◽  
Biochemical Evaluation ◽  
Activation Coefficient ◽  
Riboflavin Status

1. Chronic marginal riboflavin deficiency was induced in groups of weanling rats by feeding a deficient diet supplemented with 0, 0·5, 1·0 and 1·5 mg riboflavin/kg diet. Ad lib.- and pair-fed controls received 3·0 and 15 mg riboflavin/kg diet respectively.2. Serial measurement of erythrocyte NAD(P)H2 glutathione oxidoreductase (glutathione reductase; EC 1.6.4.2) and its activation coefficient revealed that after 12 weeks a steady-state of deficiency had been reached following initial fluctuations in status; the animals were then killed, and their tissues analysed.3. Food intake, growth rate and the appearance of pathological signs were directly proportional to riboflavin content; however relative liver weight was increased above control levels only in the most-severelydeficient group, and anaemia was not detected in any group.4. The activation coefficient of glutathione reductase in erythrocytes and liver was closely related to dietary riboflavin content; that of skin responded maximally even in the least-severelydepleted animals.5. Hepatic and renal flavin contents were directly proportional to dietary riboflavin, FAD being conserved at the expense of ribotlavin and FMN. ATP: riboflavin 5-phosphotransferase (flavokinase; EC 2.7.1.26) activity was reduced, even in the least-severely deficient animals; ATP: FMN adenylyltransferase (FAD pyrophosphory1ase; EC 2.7.7.2) was increased in liver, but only in the most-severely-deficient animals.6. Hepatic succinate: (acceptor) oxidoreductase (succinate dehydrogenase; EC 1. 3.99.1) activity fell sharply between 1·5 and 0·5 mg riboflavin/kg diet, producing an S-shaped dose-response curve; it showed smaller or less specific changes in other tissues such as brain, skin and intestine. NADH: (acceptor) oxidoreductase (NADH dehydrogenase; EC 1.6.99.3) activity declined in liver and intestine, but not in skin or brain.7. Theactivation coefficient of glutathione reductase was correlated strongly with nearly all the riboflavin-sensitive variables measured, once equilibrium had been reached in this chronic deficiency model, and it was particularly strongly correlated with hepatic and renal FAD levels. Under equilibrium conditions, therefore, it appears to represent a good index of the extent of riboflavin deficiency, and significant changes in flavin levels and enzymes in the internal organs were detected even under conditions of marginal deficiency, associated with relatively small increases in the activation coefficient.

scholarly journals Cytokinetic and structural responses of the rat small intestine to riboflavin depletion

1996 ◽  
Vol 75 (2) ◽  
pp. 315-324 ◽  
Author(s):  
E. A. Williams ◽  
R. D. E. Rumsey ◽  
H. J. Powers
Keyword(s):  
Small Intestine ◽  
Wistar Rats ◽  
Rat Small Intestine ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Structural Responses ◽  
Normal Increase ◽  
Riboflavin Deficient

Abstract:The impaired absorption and metabolism of Fe seen in riboflavin defiaency is attributed, at least in part, to a hyperproliferative response in the small intestine, associated with an altered morphology. Studies were conducted in female weanling Wistar rats to explore further the effect of riboflavin deficiency on the cytokinetics and structure of the small intestine. Feeding a riboflavin-deficient diet for 8 weeks from weaning resulted in a significantly lower villus number, a significant increase in villus length and an increased rate of transit of enterocytes along the villi, compared with weight-matched controls. A second experiment focused on the 3 weeks after weaning and showed that riboflavin deficiency inhibits the increase in villus number observed in control animals over this period. We suggest that riboflavin deficiency induced at weaning impairs the normal increase in villus number and that prolonged deficiency leads to an adaptive increase in length of villi and depth of crypts.

The Stability of the WHO Reference Thromboplastin NIBS & C 67/40

1979 ◽  
Vol 42 (04) ◽  
pp. 1135-1140 ◽  
Author(s):  
G I C Ingram
Keyword(s):  
Human Brain ◽  
Collaborative Study ◽  
Calibration Constant ◽  
Long Term Stability ◽  
Freeze Dried ◽  
Show Evidence ◽  
Human Material ◽  
Reference Preparation ◽  
The Stability

SummaryThe International Reference Preparation of human brain thromboplastin coded 67/40 has been thought to show evidence of instability. The evidence is discussed and is not thought to be strong; but it is suggested that it would be wise to replace 67/40 with a new preparation of human brain, both for this reason and because 67/40 is in a form (like Thrombotest) in which few workers seem to use human brain. A �plain� preparation would be more appropriate; and a freeze-dried sample of BCT is recommended as the successor preparation. The opportunity should be taken also to replace the corresponding ox and rabbit preparations. In the collaborative study which would be required it would then be desirable to test in parallel the three old and the three new preparations. The relative sensitivities of the old preparations could be compared with those found in earlier studies to obtain further evidence on the stability of 67/40; if stability were confirmed, the new preparations should be calibrated against it, but if not, the new human material should receive a calibration constant of 1.0 and the new ox and rabbit materials calibrated against that.The types of evidence available for monitoring the long-term stability of a thromboplastin are discussed.

Russia’s Development Strategy: Guidelines and Restrictions

2008 ◽  
pp. 119-130 ◽  
Author(s):  
V. Senchagov
Keyword(s):  
Economic Development ◽  
Development Strategy ◽  
Conceptual Basis ◽  
The Core ◽  
Economic Development Strategy ◽  
Socio Economic Development ◽  
Rates Of Growth

The core of Russia’s long-term socio-economic development strategy is represented by its conceptual basis. Having considered debating points about the essence and priority of the strategy, the author analyzes the logic and stages of its development as well as possibilities, restrictions and risks of high GDP rates of growth.

scholarly journals CD34+ human marrow cells that express low levels of Kit protein are enriched for long-term marrow-engrafting cells

Blood ◽  
1996 ◽  
Vol 87 (10) ◽  
pp. 4136-4142 ◽  
Author(s):  
I Kawashima ◽  
ED Zanjani ◽  
G Almaida-Porada ◽  
AW Flake ◽  
H Zeng ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Marrow Cell ◽  
In Utero ◽  
Fetal Sheep ◽  
Hematopoietic Stem ◽  
Show Evidence ◽  
Marrow Cells

Using in utero transplantation into fetal sheep, we examined the capability of human bone marrow CD34+ cells fractionated based on Kit protein expression to provide long-term in vivo engraftment. Twelve hundred to 5,000 CD34+ Kit-, CD34+ Kit(low), and CD34+ Kit(high) cells were injected into a total of 14 preimmune fetal sheep recipients using the amniotic bubble technique. Six fetuses were killed in utero 1.5 months after bone marrow cell transplantation. Two fetuses receiving CD34+ Kit(low) cells showed signs of engraftment according to analysis of CD45+ cells in their bone marrow cells and karyotype studies of the colonies grown in methylcellulose culture. In contrast, two fetuses receiving CD34+ Kit(high) cells and two fetuses receiving CD34+ Kit- cells failed to show evidence of significant engraftment. Two fetuses were absorbed. A total of six fetuses receiving different cell populations were allowed to proceed to term, and the newborn sheep were serially examined for the presence of chimerism. Again, only the two sheep receiving CD34+ Kit(low) cells exhibited signs of engraftment upon serial examination. Earlier in studies of murine hematopoiesis, we have shown stage-specific changes in Kit expression by the progenitors. The studies of human cells reported here are in agreement with observations in mice, and indicate that human hematopoietic stem cells are enriched in the Kit(low) population.

Notch signalling becomes transiently attenuated during long-term memory consolidation in adult Wistar rats

2007 ◽  
Vol 88 (3) ◽  
pp. 342-351 ◽  
Author(s):  
Lisa Conboy ◽  
Claire M. Seymour ◽  
Marco P. Monopoli ◽  
Niamh C. O’Sullivan ◽  
Keith J. Murphy ◽  
...  
Keyword(s):  
Memory Consolidation ◽  
Wistar Rats ◽  
Notch Signalling ◽  
Long Term Memory ◽  
Term Memory
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