scholarly journals A biochemical evaluation of the erythrocyte glutathione reductase (EC1.6.4.2) test for riboflavin status

1981 ◽  
Vol 45 (1) ◽  
pp. 37-52 ◽  
Author(s):  
A. M. Prentice ◽  
C. J. Bates
Keyword(s):  
Glutathione Reductase ◽  
Dehydrogenase Activity ◽  
Early Stage ◽  
Mean Value ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Biochemical Evaluation ◽  
Final Extent ◽  
Riboflavin Status ◽  
Deficient Group

1. Acute riboflavin deficiency was produced in weanling rats by feeding a deficient diet and using tailcups to prevent refection. Animals were killed at weekly interval for 7 weeks, by the end of which they had become severely deficient, and mortality was high.2. Growth of the deficient animals virtually ceased in the early stages of deficiency; food intake was severely and progressively depressed. Liver: body-weight increased markedly; packed cell volume fell at a late stage only. Pathological signs accumulated throughout the deficiency but were not closely related to the biochemical changes within the deficient group.3. The activation coefficient (stimulated: basal activity; AC) of glutathione oxidoreductase (EC 1.6.4.2; glutathione reductase; GR) in erythrocytes rose to a mean value of 3–8 after 3 weeks, and subsequently remained almost constant: this change was not seen in pair-fed or ud lib.-fed controls. Both deficient and pair-fed animals exhibited a twofold reduction in FAD-stimulated erythrocyteGR activity at an early stage. In liver, both deficient and pair-fed groups showed a major progressive fall in FAD-stimulated GR activity, but only the deficient group showed an increase in AC, which occurred towards the later stages of the experiment. In skin, too, the deficient group showed an increase in AC during the terminal stages.4. Hepatic, intestinal and brain succinate: (acceptor) oxidoreductase (EC 1.3.99,1; succinate dehydrogenase) activity fell relatively early during deficiency; in liver and intestine this was at least partly shared by the pair-fed group, and therefore attributable to inanition. Changes in hepatic NADH:(acceptor) oxidoreductase (EC I.6.99.3; NADH dehydrogenase) activity appeared to be entidy attributable to inanition.5. An early reduction was observed in hepatic ATP: riboflavin 5-phosphotransferase (EC2.7.1.26; flavo- kinase) activity in the deficient group, values falling by nearly half within 1 week, and then remaining almost constant. Similar but smaller changes were seen in renal flavokinase activity. Hepatic ATP: FMN adenylyltrans- ferase (EC2.7.7.2; FAD pyrophosphorylase) was unchanged until the third week, at which point it rose sharply to a new plateau in the deficient group; in kidney it did not respond. These changes were not observed in pair-fed or ad-lib.-fed controls.6. Hepatic flavin levels fell dramatically during the first 2 weeks of deficiency, FAD being conserved at the expense of FMN. Smaller changes were observed in kidney.7. Of the processes which are affected by riboflavin deficiency, AC of erythrocyte GR (EGRAC) responds earlier, more dramatically and more specifically than most others, with the possible exception of hepatic flavin levels and flavokinase. Potentially, it is therefore a good index of over-all body riboflavin status, but in acute deficiency the rate of response of many variables is not related to the final extent of response; consequently the correlation between EGRAC and other riboflavin-sensitive processes is less satisfactory than it would be in an equilibrium situation.

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 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 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 Serum surfactant protein D in COVID-19 is elevated and correlated with disease severity

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ming Tong ◽  
Ying Xiong ◽  
Chen Zhu ◽  
Hong Xu ◽  
Qing Zheng ◽  
...  
Keyword(s):  
Acute Phase ◽  
Early Stage ◽  
Recovery Period ◽  
Serum Levels ◽  
Surfactant Protein ◽  
Mean Value ◽  
Multivariate Logistic Regression Model ◽  
Surfactant Protein D ◽  
Multivariate Logistic Regression ◽  
Roc Curve Analysis

Abstract Background The serum surfactant protein D (SP-D) level is suggested to be a useful biomarker for acute lung injuries and acute respiratory distress syndrome. Whether the serum SP-D level could identify the severity of coronavirus disease 2019 (COVID-19) in the early stage has not been elucidated. Methods We performed an observational study on 39 laboratory-confirmed COVID-19 patients from The Fourth People’s Hospital of Yiyang, Hunan, China. Receiver operating characteristic (ROC) curve analysis, correlation analysis, and multivariate logistic regression model analysis were performed. Results In the acute phase, the serum levels of SP-D were elevated significantly in severe COVID-19 patients than in mild cases (mean value ± standard deviation (SD), 449.7 ± 125.8 vs 245.9 ± 90.0 ng/mL, P<0.001), while the serum levels of SP-D in the recovery period were decreased dramatically than that in the acute phase (mean value ± SD, 129.5 ± 51.7 vs 292.9 ± 130.7 ng/ml, P<0.001), and so were for the stratified patients. The chest CT imaging scores were considerably higher in the severe group compared with those in the mild group (median value, 10.0 vs 9.0, P = 0.011), while markedly lower in the recovery period than those in the acute phase (median value, 2.0 vs 9.0, P<0.001), and so were for the stratified patients. ROC curve analysis revealed that areas under the curve of lymphocyte counts (LYM), C-reaction protein (CRP), erythrocyte sedimentation rate (ESR), interleukin-6 (IL-6), and SP-D for severe COVID-19 were 0.719, 0.833, 0.817, 0.837, and 0.922, respectively. Correlation analysis showed that the SP-D levels were negatively correlated with LYM (r = − 0.320, P = 0.047), while positively correlated with CRP (r = 0.658, P<0.001), IL-6 (r = 0.471, P = 0.002), the duration of nucleic acid of throat swab turning negative (r = 0.668, P<0.001), chest CT imaging score on admission (r = 0.695, P<0.001) and length of stay (r = 0.420, P = 0.008). Multivariate logistic regression model analysis showed that age (P = 0.041, OR = 1.093) and SP-D (P = 0.008, OR = 1.018) were risk factors for severe COVID-19. Conclusions Elevated serum SP-D level was a potential biomarker for the severity of COVID-19; this may be useful in identifying patients whose condition worsens at an early stage.

Effect of Riboflavin Deficiency on the Metabolism of Oxypurines in Chicks

1971 ◽  
Vol 49 (12) ◽  
pp. 1059-1062 ◽  
Author(s):  
S. T. Chou
Keyword(s):  
Uric Acid ◽  
Acid Synthesis ◽  
Xanthine Dehydrogenase ◽  
Broiler Chicks ◽  
Uric Acid Concentration ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
High Incidence ◽  
Liver And Kidney ◽  
Riboflavin Deficient

Day-old broiler chicks of both sexes were used in three experiments to determine the effect of riboflavin deficiency on oxypurine metabolism catalyzed by xanthine dehydrogenase, a riboflavin-containing enzyme. Chicks fed a riboflavin-deficient diet (1.38 mg/kg) for 3 weeks exhibited depressed growth and a high incidence of curled-toe paralysis (higher than 80%) as compared to control chicks (15.1 mg riboflavin per kilogram diet; no incidence of curled-toe paralysis). In addition, the precursors of uric acid, hypoxanthine and/or xanthine, accumulated in the liver and kidney of deficient chicks showing curled-toe paralysis. These observations show that dietary riboflavin being incorporated into xanthine dehydrogenase is essential for oxypurine metabolism. Moreover in the chick, the liver and the kidney may be important sites of uric acid synthesis. The low uric acid concentration in the plasma of the deficient chicks appeared to be indicative of a disturbance in uric acid synthesis in the liver and kidney.

Enhancement of reflection and backscattering components by plane wave imaging for estimation of surface roughness

2021 ◽  
Author(s):  
Kazuhiro Tochigi ◽  
Ryo Nagaoka ◽  
Jens Erik Wilhjelm ◽  
Hideyuki Hasegawa
Keyword(s):  
Surface Roughness ◽  
Plane Wave ◽  
Arterial Wall ◽  
Early Stage ◽  
Mean Value ◽  
Luminal Surface ◽  
Ultrasonic Echo ◽  
Wave Imaging ◽  
The Mean ◽  
Reflection Component

Abstract In the early stage of atherosclerosis, the luminal surface of the arterial wall becomes rough. Methods for distinguishing between the reflected and backscattered components in the ultrasonic echo from the arterial wall has the potential to be used as a method for assessment of the roughness of the arterial wall. In this study, we proposed a method to distinguish between the reflected and backscattered components using a technique based on plane wave compounding. This method was evaluated by experiments using planar phantoms with rough surfaces made of polyurethane rubber. The coefficient of variation calculated from the mean value of the reflection component and the standard deviation of the backscattering component was proportional to the roughness of the rubber phantom. This result shows the potential usefulness of this method for analyzing surface roughness of the arterial wall.

EXCRETION OF 4(5)-AMINO-5(4)-IMIDAZOLECARBOXAMIDE AND FORMIMINO-L-GLUTAMIC ACID IN FOLIC ACID AND VITAMIN B12 DEFICIENT RATS

1965 ◽  
Vol 43 (8) ◽  
pp. 1367-1374 ◽  
Author(s):  
P. L. McGeer ◽  
N. P. Sen ◽  
D. A. Grant
Keyword(s):  
Folic Acid ◽  
Glutamic Acid ◽  
Fold Increase ◽  
Urocanic Acid ◽  
Vitamin B ◽  
Deficient Diet ◽  
Intraperitoneal Dose ◽  
Group A ◽  
Acid Load ◽  
Deficient Group

The excretion of 4(5)-amino-5(4)-imidazolecarboxamide (AIC) in the urines of normal rats, rats raised on a folic acid deficient diet, and rats raised on a vitamin B12 deficient diet was measured. The AIC excretion was elevated 3-fold above normal in the B12 deficient group and 1.5-fold above normal in the folic acid deficient group.No evidence could be found that the raised AIC excretion was associated with a block in the conversion of AIC to purines. The recovery of radioactive AIC in the urine after an intraperitoneal dose of 2 μmoles AIC per kg was not increased over normal in any of the deficient groups, and was significantly less than normal in the B12-deficient group. Most of the urinary radioactivity in all groups was in allantoin, uric acid, and purines.When a load of 220 μmoles of AIC per kg was administered there was no difference between the vitamin B12 deficient and the normal groups in AIC recovery in the urine. When a load of 220 μmoles of urocanic acid per kg was administered, however, the B12-deficient group had an 18-fold increase over normal in Figlu excretion, and the folic acid deficient group a 17-fold increase. Thus, a substantial block in formimino-L-glutamic acid (Figlu) metabolism, but not in AIC metabolism, existed in the vitamin-deficient groups.Feeding a B12-deficient group a 2% methionine supplement reduced the Figlu excretion after a urocanic acid load to less than half that observed in B12-deficient groups without methionine supplementation, but had no influence on the AIC excretion.

scholarly journals Glutathione peroxidase (EC 1.11.1.9) and superoxide dismutase (EC 1.15.1.1) activities in riboflavin-deficient rats infected with Plasmodium berghei malaria

1998 ◽  
Vol 79 (3) ◽  
pp. 305-309 ◽  
Author(s):  
D. A. Adelekan ◽  
D. I. Thurnham
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Plasmodium Berghei ◽  
Control Group ◽  
Riboflavin Deficiency ◽  
Sod Activity ◽  
Parasite Protein ◽  
Riboflavin Deficient ◽  
Gpx Activity ◽  
Deficient Group

Riboflavin deficiency interferes with the growth and multiplication of malaria parasites as well as the host response to malaria. The objective of the present work was to determine the effects of riboflavin deficiency on erythrocyte glutathione peroxidase (EC1.11.1.9; GPx) and superoxide dismutase (EC1.15.1.1; SOD) in rats infected withPlasmodium bergheimalaria. Riboflavin in its co-enzyme form, FAD, is required by glutathione reductase (EC1.6.4.1) to regenerate GSH and GSH is an important cellular antioxidant both in its own right and also as a substrate for the enzyme GPx. Weanling rats were deprived of riboflavin for 8 weeks before intraperitoneal injection of 1 × 106P. bergheiparasites. Control animals were weight-matched to the respective riboflavin-deficient group. At 10d post-infection, parasite counts were higher in the weight-matched control group than the riboflavin-deficient group (P= 0.004). GPx activity was higher in erythrocytes of rats parasitized withP. bergheithan comparable non-infected rats regardless of riboflavin status (P< 0.05). As mature erythrocytes do not synthesize new protein, the higher GPx activities were probably due to the presence of the parasite protein. In erythrocytes from riboflavin-deficient rats, GPx activity tended to be lower than in those rats fed on diets adequate in riboflavin (weight-matched controls) whether parasitized or not, but the difference was not significant. Neither riboflavin deficiency nor malaria had any effect on erythrocyte SOD activity. It was concluded that riboflavin deficiency has no marked effect on erythrocyte GPx or SOD activity in the rat.

THE ROLE OF RIBOFLAVIN IN MONOAMINE OXIDASE ACTIVITY

1963 ◽  
Vol 41 (1) ◽  
pp. 57-64 ◽  
Author(s):  
M. H. Wiseman-Distler ◽  
T. L. Sourkes
Keyword(s):  
Monoamine Oxidase ◽  
De Novo ◽  
Intraperitoneal Administration ◽  
Enzymatic System ◽  
Irreversible Inhibitor ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Hydroxyindoleacetic Acid

The role of riboflavin in the activity of monoamine oxidase (MAO) was investigated by omitting the vitamin from the diet of rats which were further treated with iproniazid, an irreversible inhibitor of the enzyme. The rate of recovery from the inhibition, presumably reflecting de novo synthesis of the enzyme, was estimated by measuring the excretion of the acidic metabolites formed after intraperitoneal administration of serotonin (5 HT) and dopamine. Consumption of the deficient diet did not impair the action of MAO on these amines. After injection of iproniazid, return to control levels of MAO activity was slower when measured by the oxidation of dopamine than of 5 HT; there was a small but significant effect of riboflavin deficiency upon the conversion of 5 HT to 5-hydroxyindoleacetic acid. This was probably due to enhanced inhibition of MAO observed in deficient rats, an effect that was also obtained when inhibitors other than iproniazid were used in vivo. Similarly, disappearance of 5 HT during incubation with a supernatant prepared from liver of deficient rats was also affected to a greater extent by these inhibitors than when the enzymatic system was prepared from control livers. This finding suggests that riboflavin deficiency renders MAO more susceptible to inhibition.

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