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Ronenn Roubenoff - One of the best experts on this subject based on the ideXlab platform.
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Inflammation causes tissue-specific depletion of vitamin B_6
Arthritis Research & Therapy, 2005Co-Authors: En-pei Chiang, Donald E Smith, Jacob Selhub, Gerard Dallal, Yi-cheng Wang, Ronenn RoubenoffAbstract:Previously we observed strong and consistent associations between vitamin B_6 status and several indicators of inflammation in patients with rheumatoid arthritis. Clinical indicators, including the disability score, the length of morning stiffness, and the degree of pain, and biochemical markers, including the erythrocyte sedimentation rate and C-reactive protein levels, were found to be inversely correlated with circulating vitamin B_6 levels. Such strong associations imply that impaired vitamin B_6 status in these patients results from inflammation. In the present study we examined whether inflammation directly alters vitamin B_6 tissue contents and its excretion in vivo . A cross-sectional case-controlled human clinical trial was performed in parallel with experiments in an animal model of inflammation. Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-Pyridoxic Acid excretion, and the activity coefficient of erythrocyte aspartate aminotransferase were compared between patients and healthy subjects. Adjuvant arthritis was induced in rats for investigating hepatic and muscle contents as well as the urinary excretion of vitamin B_6 during acute and chronic inflammation. Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and urinary 4-Pyridoxic Acid excretion. Adjuvant arthritis in rats did not affect 4-Pyridoxic Acid excretion or muscle storage of pyridoxal 5'-phosphate, but it resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in liver during inflammation. Inflammation induced a tissue-specific depletion of vitamin B_6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are unlikely to be due to insufficient intake or excessive vitamin B_6 excretion. Possible causes of decreased levels of vitamin B_6 are discussed.
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Inflammation causes tissue-specific depletion of vitamin B6.
Arthritis research & therapy, 2005Co-Authors: En-pei Chiang, Donald E Smith, Jacob Selhub, Gerard Dallal, Yi-cheng Wang, Ronenn RoubenoffAbstract:Previously we observed strong and consistent associations between vitamin B6 status and several indicators of inflammation in patients with rheumatoid arthritis. Clinical indicators, including the disability score, the length of morning stiffness, and the degree of pain, and biochemical markers, including the erythrocyte sedimentation rate and C-reactive protein levels, were found to be inversely correlated with circulating vitamin B6 levels. Such strong associations imply that impaired vitamin B6 status in these patients results from inflammation. In the present study we examined whether inflammation directly alters vitamin B6 tissue contents and its excretion in vivo. A cross-sectional case-controlled human clinical trial was performed in parallel with experiments in an animal model of inflammation. Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-Pyridoxic Acid excretion, and the activity coefficient of erythrocyte aspartate aminotransferase were compared between patients and healthy subjects. Adjuvant arthritis was induced in rats for investigating hepatic and muscle contents as well as the urinary excretion of vitamin B6 during acute and chronic inflammation. Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and urinary 4-Pyridoxic Acid excretion. Adjuvant arthritis in rats did not affect 4-Pyridoxic Acid excretion or muscle storage of pyridoxal 5'-phosphate, but it resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in liver during inflammation. Inflammation induced a tissue-specific depletion of vitamin B6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are unlikely to be due to insufficient intake or excessive vitamin B6 excretion. Possible causes of decreased levels of vitamin B6 are discussed.
Stephen P Coburn - One of the best experts on this subject based on the ideXlab platform.
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Use of chlorite to improve HPLC detection of pyridoxal 5'-phosphate.
Journal of chromatography. B Analytical technologies in the biomedical and life sciences, 2005Co-Authors: Karen L. Ericson, J. Dennis Mahuren, Yvonne Zubovic, Stephen P CoburnAbstract:The sensitivity of fluorescent detection of the biologically active form of Vitamin B-6, pyridoxal 5'-phosphate (PLP), in biological samples has been improved approximately four-fold by adopting chlorite as a post-column derivatization reagent (instead of bisulfite) in high-performance liquid chromatography (HPLC) separation. Chlorite oxidizes PLP to the more fluorescent 4-Pyridoxic Acid 5'-phosphate, and avoids the toxicity and heating of the cyanide procedure. Detection of another major metabolite, 4-Pyridoxic Acid (4-PA), is not effected. Detection of pyridoxal (PL) is slightly lowered due to eluting at a lower pH.
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Elevated plasma 4-Pyridoxic Acid in renal insufficiency
The American journal of clinical nutrition, 2002Co-Authors: Stephen P Coburn, J. Dennis Mahuren, Robert D. Reynolds, W E Schaltenbrand, Yao Wang, Karen L. Ericson, Michael P. Whyte, Yvonne Zubovic, Paula J. Ziegler, David L. CostillAbstract:BACKGROUND Renal insufficiency is associated with altered vitamin B-6 metabolism. We have observed high concentrations of 4-Pyridoxic Acid, the major catabolite of vitamin B-6 metabolism, in plasma during renal insufficiency. OBJECTIVE The objective was to evaluate the renal handling of 4-Pyridoxic Acid and the effects of renal dysfunction on vitamin B-6 metabolism. DESIGN We measured the renal clearance of 4-Pyridoxic Acid and creatinine in 17 nonpregnant, 17 pregnant, and 16 lactating women. We then examined the influence of vitamin B-6 or alkaline phosphatase activity on the ratio of 4-Pyridoxic Acid to pyridoxal (PA:PL) in plasma in 10 men receiving a low (0.4 mg pyridoxine.HCl/d) or high (200 mg pyridoxine.HCl/d) vitamin B-6 intake for 6 wk, in 10 healthy subjects during a 21-d fast, in 1235 plasma samples from 799 people screened for hypophosphatasia, and in 67 subjects with a range of serum creatinine concentrations. RESULTS Renal clearance of 4-Pyridoxic Acid was 232 +/- 94 mL/min in nonpregnant women, 337 +/- 140 mL/min in pregnant women, and 215 +/- 103 mL/min in lactating healthy women. These values were approximately twice the creatinine clearance, indicating that 4-Pyridoxic Acid is at least partially eliminated by tubular secretion. Elevated plasma creatinine concentrations were associated with marked elevations in 4-Pyridoxic Acid and PA:PL. PA:PL was not affected by wide variations in vitamin B-6 intake or by the wide range of pyridoxal-P concentrations encountered while screening for hypophosphatasia. CONCLUSIONS Plasma 4-Pyridoxic Acid concentrations are markedly elevated in renal insufficiency. Plasma PA:PL can distinguish between increases in 4-Pyridoxic Acid concentrations due to increased dietary intake and those due to renal insufficiency.
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Measurement of the turnover of glycogen phosphorylase by GC/MS using stable isotope derivatives of pyridoxine (vitamin B6).
Biochemical Journal, 1996Co-Authors: Robert J. Beynon, Richard P. Evershed, Deborah M. Leyland, Richard H. T. Edwards, Stephen P CoburnAbstract:The majority of vitamin B 6 in the body is in skeletal muscle, bound as the cofactor pyridoxal 5´-phosphate to one abundant protein, glycogen phosphorylase. Previous work has established that radiolabelled vitamin B 6 can be used as a turnover label for glycogen phosphorylase. In this study, a stable isotope derivative of pyridoxine {dideuterated pyridoxine; 3-hydroxy-4-(hydroxymethyl)-5-[ hydroxymethyl - 2 H 2 ]-2-methylpyridine} ([ 2 H 2 ]PN) has been used as a metabolic tracer to study the kinetics of labelling of the body pools of vitamin B 6 in mice. A non-invasive method was developed in which the isotope abundance of the urinary excretory product of vitamin B 6 metabolism, 4-Pyridoxic Acid, was analysed by GC/MS. The change in isotope abundance of urinary 4-Pyridoxic Acid following administration of [ 2 H 2 ]PN reflects the kinetics of labelling of the body pools of vitamin B 6 , and yields, non-invasively, the rate of degradation of glycogen phosphorylase.
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Pyridoxic Acid excretion during low vitamin B-6 intake, total fasting, and bed rest
The American journal of clinical nutrition, 1995Co-Authors: Stephen P Coburn, J D Mahuren, K G Thampy, H W Lane, P S Conn, P J Ziegler, D L Costill, W J Fink, D R Pearson, W E SchaltenbrandAbstract:Vitamin B-6 metabolism in 10 volunteers during 21 d of total fasting was compared with results from 10 men consuming a diet low only in vitamin B-6 (1.76 mumol/d) and with men consuming a normal diet during bed rest. At the end of the fast mean plasma concentrations of vitamin B-6 metabolites and urinary excretion of 4-Pyridoxic Acid tended to be higher in the fasting subjects than in the low-vitamin B-6 group. The fasting subjects lost approximately 10% of their total vitamin B-6 pool and approximately 13% of their body weight. The low-vitamin B-6 group lost only approximately 4% of their vitamin B-6 pool. Compared with baseline, urinary excretion of Pyridoxic Acid was significantly increased during 17 wk of bed rest. There was no increase in Pyridoxic Acid excretion during a second 15-d bed rest study. These data suggest the possibility of complex interactions between diet and muscle metabolism that may influence indexes that are frequently used to assess vitamin B-6 status.
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Identification of 5-Pyridoxic Acid and 5-Pyridoxic Acid lactone as metabolites of vitamin B6 in humans
The Journal of Nutritional Biochemistry, 1991Co-Authors: J. Dennis Mahuren, Thomas A. Pauly, Stephen P CoburnAbstract:Abstract Plasma and urine from individuals ingesting large amounts of vitamin B 6 contain several unidentified vitamin B 6 metabolites. Based on movement in 6 TLC solvents, elution in HPLC, and ultraviolet and infrared spectra, two of these metabolites have been identified as 5-Pyridoxic Acid and its lactone. These two compounds can account for 10–20% of the urinary vitamin B 6 metabolites.
En-pei Chiang - One of the best experts on this subject based on the ideXlab platform.
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Inflammation causes tissue-specific depletion of vitamin B_6
Arthritis Research & Therapy, 2005Co-Authors: En-pei Chiang, Donald E Smith, Jacob Selhub, Gerard Dallal, Yi-cheng Wang, Ronenn RoubenoffAbstract:Previously we observed strong and consistent associations between vitamin B_6 status and several indicators of inflammation in patients with rheumatoid arthritis. Clinical indicators, including the disability score, the length of morning stiffness, and the degree of pain, and biochemical markers, including the erythrocyte sedimentation rate and C-reactive protein levels, were found to be inversely correlated with circulating vitamin B_6 levels. Such strong associations imply that impaired vitamin B_6 status in these patients results from inflammation. In the present study we examined whether inflammation directly alters vitamin B_6 tissue contents and its excretion in vivo . A cross-sectional case-controlled human clinical trial was performed in parallel with experiments in an animal model of inflammation. Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-Pyridoxic Acid excretion, and the activity coefficient of erythrocyte aspartate aminotransferase were compared between patients and healthy subjects. Adjuvant arthritis was induced in rats for investigating hepatic and muscle contents as well as the urinary excretion of vitamin B_6 during acute and chronic inflammation. Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and urinary 4-Pyridoxic Acid excretion. Adjuvant arthritis in rats did not affect 4-Pyridoxic Acid excretion or muscle storage of pyridoxal 5'-phosphate, but it resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in liver during inflammation. Inflammation induced a tissue-specific depletion of vitamin B_6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are unlikely to be due to insufficient intake or excessive vitamin B_6 excretion. Possible causes of decreased levels of vitamin B_6 are discussed.
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Inflammation causes tissue-specific depletion of vitamin B6.
Arthritis research & therapy, 2005Co-Authors: En-pei Chiang, Donald E Smith, Jacob Selhub, Gerard Dallal, Yi-cheng Wang, Ronenn RoubenoffAbstract:Previously we observed strong and consistent associations between vitamin B6 status and several indicators of inflammation in patients with rheumatoid arthritis. Clinical indicators, including the disability score, the length of morning stiffness, and the degree of pain, and biochemical markers, including the erythrocyte sedimentation rate and C-reactive protein levels, were found to be inversely correlated with circulating vitamin B6 levels. Such strong associations imply that impaired vitamin B6 status in these patients results from inflammation. In the present study we examined whether inflammation directly alters vitamin B6 tissue contents and its excretion in vivo. A cross-sectional case-controlled human clinical trial was performed in parallel with experiments in an animal model of inflammation. Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-Pyridoxic Acid excretion, and the activity coefficient of erythrocyte aspartate aminotransferase were compared between patients and healthy subjects. Adjuvant arthritis was induced in rats for investigating hepatic and muscle contents as well as the urinary excretion of vitamin B6 during acute and chronic inflammation. Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and urinary 4-Pyridoxic Acid excretion. Adjuvant arthritis in rats did not affect 4-Pyridoxic Acid excretion or muscle storage of pyridoxal 5'-phosphate, but it resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in liver during inflammation. Inflammation induced a tissue-specific depletion of vitamin B6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are unlikely to be due to insufficient intake or excessive vitamin B6 excretion. Possible causes of decreased levels of vitamin B6 are discussed.
Ivo Fridolin - One of the best experts on this subject based on the ideXlab platform.
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4-Pyridoxic Acid in the Spent Dialysate: Contribution to Fluorescence and Optical Monitoring
PloS one, 2016Co-Authors: Sigrid Kalle, Risto Tanner, Jürgen Arund, Ruth Tomson, Merike Luman, Ivo FridolinAbstract:Aim In this work we estimated the contribution of the fluorescence of 4-Pyridoxic Acid (4-PA) to the total fluorescence of spent dialysate with the aim of evaluating the on-line monitoring of removal of this vitamin B-6 metabolite from the blood of patients with end-stage renal disease (ESRD). Methods Spectrofluorometric analysis of spent dialysate, collected from hemodialysis and hemodiafiltration sessions of 10 patients receiving regularly pyridoxine injections after dialysis treatment, was performed in the range of Ex/Em 220–500 nm. 4-PA in dialysate samples was identified and quantified using HPLC with fluorescent and MS/MS detection. Results Averaged HPLC chromatogram of spent dialysate had many peaks in the wavelength region of Ex320/Em430 nm where 4-PA was the highest peak with contribution of 42.2±17.0% at the beginning and 47.7±18.0% in the end of the dialysis. High correlation (R = 0.88–0.95) between 4-PA concentration and fluorescence intensity of spent dialysate was found in the region of Ex310-330/Em415-500 nm, respectively. Conclusion 4-PA elimination from the blood of ESRD patients can be potentially followed using monitoring of the fluorescence of the spent dialysate during dialysis treatments.
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Optical measurement of 4-Pyridoxic Acid in the spent dialysate: Algorithm Development
2016 15th Biennial Baltic Electronics Conference (BEC), 2016Co-Authors: Sigrid Kalle, Risto Tanner, Jürgen Arund, Ruth Tomson, Ivo FridolinAbstract:The aim of this study was to develop an algorithm suitable for the estimation of 4-Pyridoxic Acid (4PA) concentration removed during dialysis through fluorescence measurements in spent dialysate. 4PA is the major urinary catabolite of vitamin B-6 (B6), that is regularly injected to dialysis patients. 4PA could be used to estimate B6 nutritional status of the patients. For the study 10 hemodialysis patients during 40 dialysis sessions were studied. Full fluorescence spectra of spent dialysates were recorded with the spectrofluorophotometer RF-5301 by Shimadzu (Kyoto, Japan) and 4-Pyridoxic Acid concentrations were measured with HPLC system. Two single wavelength models were developed were correlation coefficients for Ex/Em 320/430 nm were 0.931 and 0.853 and for Ex/Em 310/460 nm were 0.944 and 0.931 for calibration and validation set, respectively. In summary, 4PA concentration can be estimated through fluorescence measurements from spent dialysate.
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Dependence of the correlation between fluorescence intensity of spent dialysate and 4-Pyridoxic Acid concentration on the excitation-emission wavelength conditions.
2016Co-Authors: Sigrid Kalle, Risto Tanner, Jürgen Arund, Ruth Tomson, Merike Luman, Ivo FridolinAbstract:Dependence of the correlation between fluorescence intensity of spent dialysate and 4-Pyridoxic Acid concentration on the excitation-emission wavelength conditions.
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Comparison of mass spectra (negative ionization) of A) biggest fluorescent peak (no 2, Fig 2) and B) 4-Pyridoxic Acid reference.
2016Co-Authors: Sigrid Kalle, Risto Tanner, Jürgen Arund, Ruth Tomson, Merike Luman, Ivo FridolinAbstract:Comparison of mass spectra (negative ionization) of A) biggest fluorescent peak (no 2, Fig 2) and B) 4-Pyridoxic Acid reference.
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Example of an averaged Ex320/Em430 nm chromatogram of the spent dialysate (N = 10).
2016Co-Authors: Sigrid Kalle, Risto Tanner, Jürgen Arund, Ruth Tomson, Merike Luman, Ivo FridolinAbstract:Samples were collected 7–10 min after the start of the dialysis. Compound 2 was identified as 4-Pyridoxic Acid. Raised chromatogram is of a reference 4-Pyridoxic Acid solution (1 μM).
Yi-cheng Wang - One of the best experts on this subject based on the ideXlab platform.
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Inflammation causes tissue-specific depletion of vitamin B_6
Arthritis Research & Therapy, 2005Co-Authors: En-pei Chiang, Donald E Smith, Jacob Selhub, Gerard Dallal, Yi-cheng Wang, Ronenn RoubenoffAbstract:Previously we observed strong and consistent associations between vitamin B_6 status and several indicators of inflammation in patients with rheumatoid arthritis. Clinical indicators, including the disability score, the length of morning stiffness, and the degree of pain, and biochemical markers, including the erythrocyte sedimentation rate and C-reactive protein levels, were found to be inversely correlated with circulating vitamin B_6 levels. Such strong associations imply that impaired vitamin B_6 status in these patients results from inflammation. In the present study we examined whether inflammation directly alters vitamin B_6 tissue contents and its excretion in vivo . A cross-sectional case-controlled human clinical trial was performed in parallel with experiments in an animal model of inflammation. Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-Pyridoxic Acid excretion, and the activity coefficient of erythrocyte aspartate aminotransferase were compared between patients and healthy subjects. Adjuvant arthritis was induced in rats for investigating hepatic and muscle contents as well as the urinary excretion of vitamin B_6 during acute and chronic inflammation. Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and urinary 4-Pyridoxic Acid excretion. Adjuvant arthritis in rats did not affect 4-Pyridoxic Acid excretion or muscle storage of pyridoxal 5'-phosphate, but it resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in liver during inflammation. Inflammation induced a tissue-specific depletion of vitamin B_6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are unlikely to be due to insufficient intake or excessive vitamin B_6 excretion. Possible causes of decreased levels of vitamin B_6 are discussed.
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Inflammation causes tissue-specific depletion of vitamin B6.
Arthritis research & therapy, 2005Co-Authors: En-pei Chiang, Donald E Smith, Jacob Selhub, Gerard Dallal, Yi-cheng Wang, Ronenn RoubenoffAbstract:Previously we observed strong and consistent associations between vitamin B6 status and several indicators of inflammation in patients with rheumatoid arthritis. Clinical indicators, including the disability score, the length of morning stiffness, and the degree of pain, and biochemical markers, including the erythrocyte sedimentation rate and C-reactive protein levels, were found to be inversely correlated with circulating vitamin B6 levels. Such strong associations imply that impaired vitamin B6 status in these patients results from inflammation. In the present study we examined whether inflammation directly alters vitamin B6 tissue contents and its excretion in vivo. A cross-sectional case-controlled human clinical trial was performed in parallel with experiments in an animal model of inflammation. Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-Pyridoxic Acid excretion, and the activity coefficient of erythrocyte aspartate aminotransferase were compared between patients and healthy subjects. Adjuvant arthritis was induced in rats for investigating hepatic and muscle contents as well as the urinary excretion of vitamin B6 during acute and chronic inflammation. Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and urinary 4-Pyridoxic Acid excretion. Adjuvant arthritis in rats did not affect 4-Pyridoxic Acid excretion or muscle storage of pyridoxal 5'-phosphate, but it resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in liver during inflammation. Inflammation induced a tissue-specific depletion of vitamin B6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are unlikely to be due to insufficient intake or excessive vitamin B6 excretion. Possible causes of decreased levels of vitamin B6 are discussed.
