The effect of vitamin B6 on dexamethasone-induced depression in mice model of despair

2018 ◽  
Vol 22 (10) ◽  
pp. 744-749 ◽  
Author(s):  
Azadeh Mesripour ◽  
Fatima Alhimma ◽  
Valiollah Hajhashemi
Keyword(s):  
Vitamin B6 ◽  
Mice Model

scholarly journals Pyridoxine Response in Mouse Alas2 Knock-in Models of X-Linked Sideroblastic Anemia and X-Linked Protoporphyria

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 925-925
Author(s):  
Sarah Ducamp ◽  
Paul J Schmidt ◽  
Dean R Campagna ◽  
Mark D. Fleming
Keyword(s):  
Flow Cytometry ◽  
Vitamin B6 ◽  
Aminolevulinic Acid ◽  
Microcytic Anemia ◽  
Normal Diet ◽  
Growth Delay ◽  
Loss Of Function ◽  
Mice Model ◽  
Sideroblastic Anemia ◽  
Control Male

Abstract Introduction. Pyridoxal 5' Phosphate (PLP) is the cofactor form of vitamin B6 in ~60 human enzymes. The first enzyme of the heme biosynthesis pathway, delta-aminolevulinic acid synthase (ALAS), that catalyzes the condensation of glycine and succinyl-CoA to form 5-ALA the sole precursor of porphyrins and heme, is PLP dependent. The erythroid specific isoform of ALAS is ALAS2. Inherited ALAS2 mutations cause two rare diseases: X-linked Sideroblastic Anemia (XLSA), due to loss-of-function mutations located throughout the gene, and X-linked Protoporphyria (XLPP), due to gain-of-function mutations specifically located in the C-terminal domain. Male XLSA patients have a microcytic hypochromic anemia of variable severity characterized by abnormal erythroid mitochondrial iron deposits, in nucleated and enucleate cells (ring sideroblasts and siderocytes). XLPP patients develop acute photosensitivity, due to an abnormal erythroid accumulation of free protoporphyrin IX (PPIX), the substrate of ferrochelatase, the last enzyme in the pathway. In two-thirds of XLSA patients, the anemia is responsive to oral pyridoxine supplementation. Isoniazid, an antituberculosis agent, that can cause sideroblastic anemia by limiting PLP availability to ALAS2, may limit free PPIX accumulation in protoporphyric patients. While being well tolerated, isoniazid treatment of protoporphyric patients did not reduce erythroid free PPIX accumulation. Given these clinical findings, we sought to explore the effects of dietary supplementation and restriction of vitamin B6 in animal models of the diseases. Methodology. Using CRISPR-CAS9 editing technology, we generated C57BL/6N mouse models of p.R170H, p.R452H and p.R411H found in XLSA patients with B6-sensitive or -refractory disease, and p. Q548X, a XLPP allele. Fed our normal chow containing 8ppm of pyridoxine, XLSA mouse males develop phenotypes ranging from severe (p.R411H) to trivial (p.R170H) anemia; XLPP animals have the expected protoporphyric phenotype. At weaning, we fed XLSA, XLPP and control male littermates with diets with defined amounts of B6 (Envigo: 0ppm, 2ppm or 10ppm). We performed complete blood counts (CBC) and quantified erythroid free PPIX by flow cytometry after 2, 5 and 8 weeks on diet and evaluated steady state and stress erythropoiesis by flow cytometry at 8 weeks. Results. B6-depleted animals have a growth delay that is more severe in the XLSA animals. Similarly treated control and XLPP animals develop a mild microcytic anemia with siderocytes only after 8 weeks. XLPP depleted animals accumulate less free PPIX compared to normal diet, while a 2 ppm B6 diet did not affect free PPIX accumulation. On 0 ppm B6, all XLSA depleted animals developed a very severe anemia characterized by profound reticulocytopenia and massive splenomegaly. Blood smears revealed many fragmented red blood cells and siderocytes. Flow cytometry analyses reveal a blockage of erythropoiesis, at early stages of differentiation, in both the marrow and the spleen. Feeding with 2ppm B6, demonstrated variable responses in each of the three mutants, with the p.R411H being the most severe and the R170H being the least. Conclusion. All XLSA mutations are sensitive to B6 depletion. Thus, the tendency to develop B6 deficiency with age may account for later clinical presentations in patients with pyridoxine-sensitive mutations. The limited PPIX response and development of siderocytic anemia in B6 deficient XLPP animals may suggest why the B6 inhibitor isoniazid had limited clinical efficacy. Thus our novel XLSA and XLPP mice model the each disease accurately and have demonstrated their potential for evaluating experimental treatments. Disclosures Schmidt: Disc Medicine, Inc.: Research Funding. Fleming: Disc Medicine: Current holder of stock options in a privately-held company, Membership on an entity's Board of Directors or advisory committees.

Membrane-associated microtubular areays induced in proximal myelinated processes of dorsal root ganglia by large doses of vitamin B6

1986 ◽  
Vol 44 ◽  
pp. 368-369
Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin
Keyword(s):  
Animal Model ◽  
Endoplasmic Reticulum ◽  
Dorsal Root Ganglia ◽  
Rough Endoplasmic Reticulum ◽  
Dorsal Root ◽  
Vitamin B6 ◽  
Morphological Changes ◽  
Model System ◽  
Sensory Nerves ◽  
Peripheral Sensory

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.

The Weight Loss Effects of Branched Chain Amino Acids and Vitamin B6: A Randomized Controlled Trial on Obese and Overweight Women

2018 ◽  
Vol 88 (1-2) ◽  
pp. 80-89 ◽  
Author(s):  
Zahra Shakibay Novin ◽  
Saeed Ghavamzadeh ◽  
Alireza Mehdizadeh
Keyword(s):  
Amino Acids ◽  
Weight Loss ◽  
Body Composition ◽  
Vitamin B6 ◽  
Controlled Trial ◽  
Density Lipoprotein ◽  
Branched Chain Amino Acids ◽  
Model Assessment ◽  
Waist To Hip Ratio ◽  
Branched Chain

Abstract. Branched chain amino acids (BCAA), with vitamin B6 have been reported to improve fat metabolism and muscle synthesis. We hypothesized that supplementation with BCAA and vitamin B6 would result in more weight loss and improve body composition and blood markers related to cardiovascular diseases. Our aim was to determine whether the mentioned supplementation would affect weight loss, body composition, and cardiovascular risk factors during weight loss intervention. To this end, we performed a placebo-controlled randomized clinical trial in 42 overweight and obese women (BMI = 25–34.9 kg/m2). Taking a four-week moderate deficit calorie diet (–500 kcal/day), participants were randomized to receive BCAA (6 g/day) with vitamin B6 (40 mg/day) or placebo. Body composition variables measured with the use of bioelectrical impedance analysis, homeostatic model assessment, and plasma insulin, Low density lipoprotein, High density lipoprotein, Total Cholesterol, Triglyceride, and fasting blood sugar were measured. The result indicated that, weight loss was not significantly affected by BCAA and vitamin B6 supplementation (–2.43 ± 1.02 kg) or placebo (–1.64 ± 1.48 kg). However, significant time × treatment interactions in waist to hip ratio (P = 0.005), left leg lean (P = 0.004) and right leg lean (P = 0.023) were observed. Overall, supplementation with BCAA and vitamin B6 could preserve legs lean and also attenuated waist to hip ratio.

Mice model melanoma

Nature ◽  
2001 ◽  
Author(s):  
John Whitfield
Keyword(s):  
Mice Model

Ginger, Vitamin B6 Ease Nausea in Pregnancy

2007 ◽  
Vol 37 (23) ◽  
pp. 30
Author(s):  
SHERRY BOSCHERT
Keyword(s):  
Vitamin B6 ◽  
In Pregnancy

Diagnostik und Therapie der Homocystinurie

2009 ◽  
Vol 09 (05) ◽  
pp. 289-293
Author(s):  
B. Reulecke ◽  
J. Denecke
Keyword(s):  
Vitamin B12 ◽  
Vitamin B6 ◽  
Sich Eine ◽  
Diagnostik Und Therapie

ZusammenfassungDie Homocystinurie ist eine seltene angeborene Erkrankung des Methioninstoffwechsels, die mit einer pathologischen Erhöhung der nicht proteinogenen Aminosäure Homocystein und der Ausscheidung ihres Disulfids Homocystin über den Urin einhergeht. Mehrere biochemische und genetische Defekte können zu einer deutlichen Homocysteinerhö-hung führen, darunter Störungen des Vita-min-B6-, Folsäure- und Vitamin-B12-Stoffwechsels, sodass der Terminus Homocystinurie eine Erkrankungsgruppe zusammenfasst. Die häufigste Ursache der Homocystinurie, auch klassische Homocystinurie oder Homo-cystinurie Typ I genannt, stellt die hereditäre Cystathionin-β-Synthase-Defizienz dar, die mit einer Erhöhung von Homocystein und Methionin im Blut einhergeht. Die Diagnose wird durch Bestimmung von Homocystein im Plasma gestellt und kann biochemisch und genetisch gesichert werden. Unbehandelt zeigen sich eine erhebliche Morbidität und Mortalität, die durch Ausschöpfung der therapeutischen Optionen, bestehend aus Vitamin B6, Folsäure, Vitamin B12, Betain und einer Proteinrestriktion mit Aminosäuresupplementie-rung, erheblich reduziert werden können.

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