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Frontiers in Cellular and Infection... 2023B vitamins are essential micro-organic compounds for the development of humans and animals. Vitamin B6 comprises a group of components including pyridoxine, pyridoxal,...
B vitamins are essential micro-organic compounds for the development of humans and animals. Vitamin B6 comprises a group of components including pyridoxine, pyridoxal, and pyridoxamine. In addition, vitamin B6 acts as the coenzymes in amino acid biosynthesis, decarboxylation, racemic reactions, and other biological processes. In this study, we found that the expressions of a gene encoding pyridoxine biosynthesis protein () were significantly upregulated in the early infectious stages in . Furthermore, deletion of slowed vegetative growth on different media, especially on MM media, and the growth defect was rescued when MoPdx1-protein was expressed in mutants strains and when commercial VB6 (pyridoxine) was added exogenously. However, VB6 content in different strains cultured in CM media has no significant difference, suggested that MoPdx1 was involved in VB6 biosynthesis not in uptake process, and VB6 regulates the vegetative growth of . The Δ mutants presented abnormal appressorium turgor, slowed invasive growth and reduced virulence on rice seedlings and sheath cells. MoPdx1 was located in the cytoplasm and present in spore and germ tubes at 14 hours post inoculation (hpi) and then transferred into the appressorium at 24 hpi. Addition of VB6 in the conidial suspentions could rescue the defects of appressorium turgor pressure at 14 hpi or 24 hpi, invasive growth and pathogenicity of the deletion mutants. Indicated that MoPdx1 affected the appressorium turgor pressure, invasive growth and virulence mainly depended on VB6, and VB6 was biosynthesized in conidia, then transported into the appressorium, which play important roles in substances transportation from conidia to appressorium thus to regulate the appressorium turgor pressure. However, deletion of did not affect the ability that scavenge ROS produced by rice cells, and the mutant strains were unable to activate host defense responses. In addition, co-immunoprecipitation (Co-IP) assays investigating potential MoPdx1-interacting proteins suggested that MoPdx1 might take part in multiple pathways, especially in the ribosome and in biosynthesis of some substances. These results indicate that vitamins are involved in the development and pathogenicity of .
Topics: Humans; Virulence; Pyridoxine; Fungal Proteins; Magnaporthe; Oryza; Plant Diseases; Spores, Fungal; Gene Expression Regulation, Fungal
PubMed: 36824685
DOI: 10.3389/fcimb.2023.1099967 -
MedEdPORTAL : the Journal of Teaching... Sep 2018Treatment of seizures in the neonatal patient is urgent and time sensitive. Effective and timely treatment of this life-threatening condition is vital in preventing...
INTRODUCTION
Treatment of seizures in the neonatal patient is urgent and time sensitive. Effective and timely treatment of this life-threatening condition is vital in preventing mortality and long-term morbidity. This simulation-based curriculum involves the identification and management of a seizure in a 4-day-old neonate with pyridoxine-dependent epilepsy. The target audience is emergency medicine and pediatric residents, pediatric emergency medicine fellows, and medical students.
METHODS
The primary objectives for this simulation are to (1) rapidly initiate stabilization techniques for a seizing neonate, (2) recognize the importance of checking a glucose level in a seizing neonate, (3) demonstrate understanding of antiepileptic medications and dosing, and (4) identify status epilepticus and initiate pyridoxine once initial seizure management has failed. The goals of this simulation are for residents to treat a seizing infant in an emergency department setting, identify status epilepticus, develop a differential diagnosis that includes vitamin B6 deficiency, and correctly administer pyridoxine. Requirements of this simulation include a high-fidelity patient simulator, medical supplies, a patient simulator operator, and one actor.
RESULTS
This simulation case was performed at the simulation lab at the State University of New York Upstate Medical University with emergency medicine and pediatric residents. Feedback evaluations for the case showed that it improved resident education and clinical skills.
DISCUSSION
This simulation case was well received and helped residents develop a systematic approach to seizure management of a newborn. Residents reported increased confidence in treating a seizing neonate and increased comprehension of pyridoxine-dependent epilepsy.
Topics: Clinical Competence; Emergency Medicine; Epilepsy; High Fidelity Simulation Training; Humans; Infant; Infant, Newborn; New York; Pediatric Emergency Medicine; Pyridoxine; Seizures; Vitamin B Complex
PubMed: 30800953
DOI: 10.15766/mep_2374-8265.10753 -
Journal of the American Society of... Dec 2021Primary hyperoxaluria type 1 (PH1) is an inborn error of glyoxylate metabolism, characterized by increased endogenous oxalate production. The metabolic pathways...
BACKGROUND
Primary hyperoxaluria type 1 (PH1) is an inborn error of glyoxylate metabolism, characterized by increased endogenous oxalate production. The metabolic pathways underlying oxalate synthesis have not been fully elucidated, and upcoming therapies require more reliable outcome parameters than the currently used plasma oxalate levels and urinary oxalate excretion rates. We therefore developed a stable isotope infusion protocol to assess endogenous oxalate synthesis rate and the contribution of glycolate to both oxalate and glycine synthesis in vivo .
METHODS
Eight healthy volunteers and eight patients with PH1 (stratified by pyridoxine responsiveness) underwent a combined primed continuous infusion of intravenous [1- 13 C]glycolate, [U- 13 C 2 ]oxalate, and, in a subgroup, [D 5 ]glycine. Isotopic enrichment of 13 C-labeled oxalate and glycolate were measured using a new gas chromatography-tandem mass spectrometry (GC-MS/MS) method. Stable isotope dilution and incorporation calculations quantified rates of appearance and synthetic rates, respectively.
RESULTS
Total daily oxalate rates of appearance (mean [SD]) were 2.71 (0.54), 1.46 (0.23), and 0.79 (0.15) mmol/d in patients who were pyridoxine unresponsive, patients who were pyridoxine responsive, and controls, respectively ( P =0.002). Mean (SD) contribution of glycolate to oxalate production was 47.3% (12.8) in patients and 1.3% (0.7) in controls. Using the incorporation of [1- 13 C]glycolate tracer in glycine revealed significant conversion of glycolate into glycine in pyridoxine responsive, but not in patients with PH1 who were pyridoxine unresponsive.
CONCLUSIONS
This stable isotope infusion protocol could evaluate efficacy of new therapies, investigate pyridoxine responsiveness, and serve as a tool to further explore glyoxylate metabolism in humans.
Topics: Humans; Oxalates; Tandem Mass Spectrometry; Pyridoxine; Hyperoxaluria, Primary; Glycolates; Glycine; Glyoxylates; Hyperoxaluria
PubMed: 34686543
DOI: 10.1681/ASN.2021060729 -
Cellular Physiology and Biochemistry :... Jun 2022Besides their physiological properties, vitamins, such as vitamin C (ascorbic acid) and B (pyridoxine), ameliorate the symptoms of allergic disorders. Because exocytosis...
BACKGROUND/AIMS
Besides their physiological properties, vitamins, such as vitamin C (ascorbic acid) and B (pyridoxine), ameliorate the symptoms of allergic disorders. Because exocytosis in mast cells can be detected electrophysiologically by the changes in the membrane capacitance (Cm), its continuous monitoring in the presence of these vitamins would determine their mast cell-stabilizing, anti-allergic properties.
METHODS
Employing the whole-cell patch-clamp technique in rat peritoneal mast cells, we examined the effects of ascorbic acid and pyridoxine on the degranulation of mast cells and the increase in the Cm during exocytosis.
RESULTS
Both ascorbic acid and pyridoxine dose-dependently suppressed the GTP-γ-S-induced increase in the Cm and inhibited the degranulation from mast cells. Surprisingly enough, relatively low concentrations of pyridoxine (1, 2 mM) synergistically enhanced the suppressive effect of 2 mM ascorbic acid on mast cell degranulation.
CONCLUSION
These results provided electrophysiological evidence for the first time that ascorbic acid and pyridoxine inhibited the process of exocytosis in a dose-dependent manner. At relatively lower concentrations, these vitamins were not enough to stabilize mast cells. However, such concentrations of pyridoxine synergistically potentiated the mast cell-stabilizing property of ascorbic acid.
Topics: Animals; Ascorbic Acid; Exocytosis; Mast Cells; Pyridoxine; Rats; Vitamins
PubMed: 35781358
DOI: 10.33594/000000534 -
Journal of Clinical Neuromuscular... Sep 2014Pyridoxine deficiency and excess have been implicated as a cause for peripheral neuropathy. As a result, unrelated neuropathies are often treated with pyridoxine based... (Review)
Review
Pyridoxine deficiency and excess have been implicated as a cause for peripheral neuropathy. As a result, unrelated neuropathies are often treated with pyridoxine based on questionable evidence. However, neurological practitioners frequently discourage patients from taking pyridoxine in excess of 50 mg/d given concerns around the development of a toxic sensory neuronopathy. There is no systematic review to support either of the 2 practices. To address this gap in knowledge, we reviewed the available literature on neuropathy attributed to pyridoxine deficiency and excess. Based on the current limited data, it can be concluded that very low doses of daily pyridoxine are required to prevent peripheral neuropathy. There is inadequate evidence to support routine pyridoxine supplementation in patients with disorders of peripheral nervous system. Supplementation with pyridoxine at doses greater than 50 mg/d for extended duration may be harmful and should be discouraged.
Topics: Clinical Trials as Topic; Evidence-Based Medicine; Female; Humans; Male; Peripheral Nervous System Diseases; PubMed; Pyridoxine; Vitamin B 6 Deficiency
PubMed: 25137514
DOI: 10.1097/CND.0000000000000049 -
Journal of Cosmetic Dermatology Feb 2023Individual B vitamins have many favorable effects on the skin and are common cosmetic ingredients. However, their formulation is demanding due to stability issues, which...
BACKGROUND
Individual B vitamins have many favorable effects on the skin and are common cosmetic ingredients. However, their formulation is demanding due to stability issues, which consequently affect the products' quality.
AIMS
We aimed to determine the quality (labeling accuracy, content determination, and content-related quality control) and stability under long-term and accelerated storage conditions of a representative sample of commercial cosmetics containing the most common B vitamins - nicotinamide, dexpanthenol, pyridoxine, and cyanocobalamin.
METHODS
Cyanocobalamin was determined by a previously published stability-indicating HPLC- diode array detector (DAD) method for the simultaneous determination of all hydrophilic vitamins. This method was additionally simplified and adjusted for the time-effective analysis of nicotinamide, dexpanthenol, and pyridoxine. Both methods were properly validated.
RESULTS
All labeled B vitamins were present in the 36 tested products, mostly in contents, reported effective on the skin. Thus, a straightforward correlation between vitamin contents and product prices were not observed. The content-related quality control of eight products, which quantitively specify their content, revealed significantly lower nicotinamide contents (47% and 57%) in two products and appropriate or higher nicotinamide (102%-112%) and dexpanthenol (100%-104%) contents than declared in the remaining products. The 6-month long-term and accelerated stability studies demonstrated the products' physical stability, but also revealed dexpanthenol, pyridoxine, and cyanocobalamin degradation, while nicotinamide was mostly stable in the tested products.
CONCLUSIONS
The obtained results provide an inside into the quality of commercial vitamin B cosmetics and highlight the importance of stability testing in the formulation of quality, efficient, and safe cosmetics.
Topics: Humans; Vitamin B Complex; Pyridoxine; Vitamin A; Niacinamide; Vitamin K; Vitamin B 12
PubMed: 35997631
DOI: 10.1111/jocd.15321 -
Frontiers in Cellular and Infection... 2023Although tremendous success has been achieved in the development and deployment of effective COVID-19 vaccines, developing effective therapeutics for the treatment of...
BACKGROUND
Although tremendous success has been achieved in the development and deployment of effective COVID-19 vaccines, developing effective therapeutics for the treatment of those who do come down with the disease has been with limited success. To repurpose existing drugs for COVID-19, we previously showed, qualitatively, that erythromycin, retapamulin, pyridoxine, folic acid, and ivermectin inhibit SARS-COV-2-induced cytopathic effect (CPE) in Vero cells.
AIM
This study aimed to quantitatively explore the inhibition of SARS-CoV-2-induced CPE by erythromycin, retapamulin, pyridoxine, folic acid, and ivermectin and to determine the effect of these drugs on SARS-CoV-2 papain-like protease and 3CL protease (M) enzymes.
METHODS
Neutral red (3-amino-7-dimethylamino-2-methyl-phenazine hydrochloride) cell viability assay was used to quantify CPE after infecting pre-treated Vero cells with clinical SARS-Cov-2 isolates. Furthermore, SensoLyte 520 SARS-CoV-2 papain-like protease and SensoLyte 520 SARS-CoV-2 M activity assay kits were used to evaluate the inhibitory activity of the drugs on the respective enzymes.
RESULTS
Erythromycin, retapamulin, pyridoxine, folic acid, and ivermectin dose-dependently inhibit SARS-CoV-2-induced CPE in Vero cells, with inhibitory concentration-50 (IC) values of 3.27 µM, 4.23 µM, 9.29 µM, 3.19 µM, and 84.31 µM, respectively. Furthermore, erythromycin, retapamulin, pyridoxine, folic acid, and ivermectin dose-dependently inhibited SARS-CoV-2 papain-like protease with IC values of 0.94 µM, 0.88 µM, 1.14 µM, 1.07 µM, and 1.51 µM, respectively, and inhibited the main protease (M) with IC values of 1.35 µM, 1.25 µM, 7.36 µM, 1.15 µM, and 2.44 µM, respectively.
CONCLUSION
The IC for all the drugs, except ivermectin, was at the clinically achievable plasma concentration in humans, which supports a possible role for the drugs in the management of COVID-19. The lack of inhibition of CPE by ivermectin at clinical concentrations could be part of the explanation for its lack of effectiveness in clinical trials.
Topics: Animals; Chlorocebus aethiops; Humans; SARS-CoV-2; COVID-19; Papain; Ivermectin; Pyridoxine; Peptide Hydrolases; Vero Cells; COVID-19 Vaccines; Erythromycin; Folic Acid; Antiviral Agents; Protease Inhibitors
PubMed: 38089816
DOI: 10.3389/fcimb.2023.1273982 -
Nutrients Aug 2020Nutritional optic neuropathy is a cause of bilateral, symmetrical, and progressive visual impairment with loss of central visual acuity and contrast sensitivity,... (Review)
Review
Nutritional optic neuropathy is a cause of bilateral, symmetrical, and progressive visual impairment with loss of central visual acuity and contrast sensitivity, dyschromatopsia, and a central or centrocecal scotoma. The clinical features are not pathognomonic, since hereditary and toxic forms share similar signs and symptoms. It is becoming increasingly common due to the widespread of bariatric surgery and strict vegetarian or vegan diets, so even the scientific interest has recently increased. In particular, recent studies have focused on possible pathogenetic mechanisms, and on novel diagnostic and therapeutic strategies in order to prevent the onset, make a prompt diagnosis and an accurate nutritional supplementation, and to avoid irreversible optic nerve atrophy. Nowadays, there is clear evidence of the role of cobalamin, folic acid, thiamine, and copper, whereas further studies are needed to define the role of niacin, riboflavin, and pyridoxine. This review aims to summarize the etiology, diagnosis, and treatment of nutritional optic neuropathy, and it is addressed not only to ophthalmologists, but to all physicians who could come in contact with a patient with a possible nutritional optic neuropathy, being a fundamental multidisciplinary approach.
Topics: Copper; Folic Acid; Humans; Niacin; Optic Neuritis; Pyridoxine; Riboflavin; Thiamine; Vision Disorders; Visual Acuity; Vitamin B 12
PubMed: 32878163
DOI: 10.3390/nu12092653 -
Obstetrics and Gynecology Feb 2015
Topics: Doxylamine; Female; Humans; Morning Sickness; Ondansetron; Pregnancy; Pyridoxine
PubMed: 25611628
DOI: 10.1097/AOG.0000000000000651 -
Molecular Genetics & Genomic Medicine Oct 2022Typical patients with KCNQ2 (OMIM# 602235) epileptic encephalopathy present early neonatal-onset intractable seizures with a burst suppression EEG pattern and severe... (Review)
Review
BACKGROUND
Typical patients with KCNQ2 (OMIM# 602235) epileptic encephalopathy present early neonatal-onset intractable seizures with a burst suppression EEG pattern and severe developmental delay or regression, and those patients always fail first-line treatment with sodium channel blockers. Vitamin B6, either pyridoxine or pyridoxal 50-phosphate, has been demonstrated to improve seizure control in intractable epilepsy.
METHODS
Here, we collected and summarized the clinical data for four independent cases diagnosed with pyridoxine-responsive epileptic encephalopathy, and their exome sequencing data. Moreover, we reviewed all published cases and summarized the clinical features, genetic variants, and treatment of pyridoxine-responsive KCNQ2 epileptic encephalopathy.
RESULTS
All four cases showed refractory seizures during the neonatal period or infancy, accompanied by global development delay. Four pathogenetic variants of KCNQ2 were uncovered and confirmed by Sanger sequencing: KCNQ2 [NM_172107.4: c.2312C > T (p.Thr771Ile), c.873G > C (p.Arg291Ser), c.652 T > A (p.Trp218Arg) and c.913-915del (p. Phe305del)]. Sodium channel blockers and other anti-seizure medications failed to control their seizures. The frequency of seizures gradually decreased after treatment with high-dose pyridoxine. In case 1, case 2, and case 4, clinical seizures relapsed when pyridoxine was withdrawn, and seizures were controlled again when pyridoxine treatment was resumed.
CONCLUSION
Our study suggests that pyridoxine may be a promising adjunctive treatment option for patients with KCNQ2 epileptic encephalopathy.
Topics: Electroencephalography; Epilepsy, Generalized; Humans; Infant, Newborn; KCNQ2 Potassium Channel; Phosphates; Pyridoxal; Pyridoxine; Sodium Channel Blockers
PubMed: 35906921
DOI: 10.1002/mgg3.2024