5-Methyltetrahydrofolic acid (BioDeep_00000001267)
Secondary id: BioDeep_00000016512, BioDeep_00000180451, BioDeep_00001868257
human metabolite PANOMIX_OTCML-2023 Endogenous blood metabolite
代谢物信息卡片
化学式: C20H25N7O6 (459.1866)
中文名称: L-5-甲基四氢叶酸
谱图信息:
最多检出来源 Homo sapiens(blood) 16.59%
Last reviewed on 2024-08-14.
Cite this Page
5-Methyltetrahydrofolic acid. BioDeep Database v3. PANOMIX ltd, a top metabolomics service provider from China.
https://query.biodeep.cn/s/5-methyltetrahydrofolic_acid (retrieved
2024-12-22) (BioDeep RN: BioDeep_00000001267). Licensed
under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0).
分子结构信息
SMILES: c1([nH]c(=O)c2c(n1)NC[C@@H](N2C)CNc1ccc(cc1)C(=O)N[C@H](CCC(=O)O)C(=O)O)N
InChI: InChI=1S/C20H25N7O6/c1-27-12(9-23-16-15(27)18(31)26-20(21)25-16)8-22-11-4-2-10(3-5-11)17(30)24-13(19(32)33)6-7-14(28)29/h2-5,12-13,22H,6-9H2,1H3,(H,24,30)(H,28,29)(H,32,33)(H4,21,23,25,26,31)/t12-,13+/m0/s1
描述信息
5 methyltetrahydrofolic acid (5-MTHF) is the most biologically active form of the B-vitamin known as folic acid, also known generically as folate. 5-MTHF functions, in concert with vitamin B12, as a methyl-group donor involved in the conversion of the amino acid homocysteine to methionine. Methyl (CH3) group donation is vital to many bodily processes, including serotonin, melatonin, and DNA synthesis. Therapeutically, 5-MTHF is instrumental in reducing homocysteine levels, preventing neural tube defects, and improving vascular endothelial function. Research on folate supplementation suggests it plays a key role in preventing cervical dysplasia and protecting against neoplasia in ulcerative colitis. Folic acid also shows promise as part of a nutritional protocol to treat vitiligo, and may reduce inflammation of the gingiva. Furthermore, certain neurological, cognitive, and psychiatric presentations may be secondary to folate deficiency. Such presentations include depression, peripheral neuropathy, myelopathy, restless legs syndrome, insomnia, dementia, forgetfulness, irritability, endogenous depression, organic psychosis, and schizophrenia-like syndromes. After ingestion, the process of conversion of folic acid to the metabolically active coenzyme forms is relatively complex. Synthesis of the active forms of folic acid requires several enzymes, adequate liver and intestinal function, and adequate supplies of riboflavin (B2), niacin (B3), pyridoxine (B6), zinc, vitamin C, and serine. After formation of the coenzyme forms of the vitamin in the liver, these metabolically active compounds are secreted into the small intestine with bile (the folate enterohepatic cycle), where they are reabsorbed and distributed to tissues throughout the body. Human pharmacokinetic studies indicate folic acid has high bioavailability, with large oral doses of folic acid substantially raising plasma levels in healthy subjects in a time and dose dependent manner. Red blood cells (RBCs) appear to be the storage depot for folic acid, as RBC levels remain elevated for periods in excess of 40 days following discontinuation of supplementation. Folic acid is poorly transported to the brain and rapidly cleared from the central nervous system. The primary methods of elimination of absorbed folic acid are fecal (through bile) and urinary. Despite the biochemical complexity of this process, evidence suggests oral supplementation with folic acid increases the bodys pool of 5-MTHF in healthy individuals. However, enzyme defects, mal-absorption, digestive system pathology, and liver disease can result in impaired ability to activate folic acid. In fact, some individuals have a severe congenital deficiency of the enzyme Methyl tetrahydrofolate reductase (5-MTHFR), which is needed to convert folic acid to 5-MTHF. Milder forms of this enzyme defect likely interact with dietary folate status to determine risk for some disease conditions. In individuals with a genetic defect of this enzyme (whether mild or severe), supplementation with 5- MTHF might be preferable to folic acid supplementation. (PMID: 17176169).
5 methyltetrahydrofolic acid (5-MTHF) is the most biologically active form of the B-vitamin folic acid, also known generically as folate. 5-MTHF functions, in concert with vitamin B12, as a methyl-group donor involved in the conversion of the amino acid homocysteine to methionine. Methyl (CH3) group donation is vital to many bodily processes, including serotonin, melatonin, and DNA synthesis. Therapeutically, 5-MTHF is instrumental in reducing homocysteine levels, preventing neural tube defects, and improving vascular endothelial function. Research on folate supplementation suggests it plays a key role in preventing cervical dysplasia and protecting against neoplasia in ulcerative colitis. Folic acid also shows promise as part of a nutritional protocol to treat vitiligo, and may reduce inflammation of the gingiva. Furthermore, certain neurological, cognitive, and psychiatric presentations may be secondary to folate deficiency. Such presentations include depression, peripheral neuropathy, myelopathy, restless legs syndrome, insomnia, dementia, forgetfulness, irritability, endogenous depression, organic psychosis, and schizophrenia-like syndromes. After ingestion, the process of conversion of folic acid to the metabolically active coenzyme forms is relatively complex. Synthesis of the active forms of folic acid requires several enzymes, adequate liver and intestinal function, and adequate supplies of riboflavin (B2), niacin (B3), pyridoxine (B6), zinc, vitamin C, and serine. After formation of the coenzyme forms of the vitamin in the liver, these metabolically active compounds are secreted into the small intestine with bile (the folate enterohepatic cycle), where they are reabsorbed and distributed to tissues throughout the body. Human pharmacokinetic studies indicate folic acid has high bioavailability, with large oral doses of folic acid substantially raising plasma levels in healthy subjects in a time and dose dependent manner. Red blood cells (RBCs) appear to be the storage depot for folic acid, as RBC levels remain elevated for periods in excess of 40 days following discontinuation of supplementation. Folic acid is poorly transported to the brain and rapidly cleared from the central nervous system. The primary methods of elimination of absorbed folic acid are fecal (through bile) and urinary. Despite the biochemical complexity of this process, evidence suggests oral supplementation with folic acid increases the bodys pool of 5-MTHF in healthy individuals. However, enzyme defects, mal-absorption, digestive system pathology, and liver disease can result in impaired ability to activate folic acid. In fact, some individuals have a severe congenital deficiency of the enzyme Methyl tetrahydrofolate reductase (5-MTHFR), which is needed to convert folic acid to 5-MTHF. Milder forms of this enzyme defect likely interact with dietary folate status to determine risk for some disease conditions. In individuals with a genetic defect of this enzyme (whether mild or severe), supplementation with 5- MTHF might be preferable to folic acid supplementation. (PMID: 17176169) [HMDB]
5-Methyltetrahydrofolic acid (5-Methyl THF) is a biologically active form of folic acid. 5-Methyltetrahydrofolic acid is a methylated derivate of tetrahydrofolate. 5-Methyltetrahydrofolic acid is the predominant natural dietary folate and the principal form of folate in plasma and cerebrospinal fluid[1].
Levomefolic acid (5-MTHF) is an orally active, brain-penetrant natural active form of folic acid and is one of the most widely used folic acid food supplements[1][2].
同义名列表
39 个代谢物同义名
(2R)-2-[(4-{[(2-amino-5-methyl-4-oxo-3,4,5,6,7,8-hexahydropteridin-6-yl)methyl]amino}phenyl)formamido]pentanedioic acid; (2R)-2-[(4-{[(2-amino-5-methyl-4-oxo-3,6,7,8-tetrahydropteridin-6-yl)methyl]amino}phenyl)formamido]pentanedioic acid; N-(4-(((2-Amino-1,4,5,6,7,8-hexahydro-5-methyl-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-L-glutamic acid; N-(4-(((2-Amino-1,4,5,6,7,8-hexahydro-5-methyl-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-L-glutamate; 5-Methyltetrahydrofolate, methyl-(14)C-labeled, (DL-glu)-isomer; 5-Methyltetrahydrofolate, methyl-(14)C-labeled, (L-glu)-isomer; 5-Methyltetrahydrofolate, calcium salt (1:1), (L-glu)-isomer; N-(5-Methyl-5,6,7,8-tetrahydropteroyl)-L-glutamic acid; N-(5-Methyl-5,6,7,8-tetrahydropteroyl)-L-glutamate; [(6S)-5-Methyl-5,6,7,8-tetrahydropteroyl]glutamate; 5-Methyltetrahydrofolate, (L-glu)-(S)-isomer; 5-Methyltetrahydrofolate, (L-glu)-(R)-isomer; N5-Methyltetrahydropteroyl mono-L-glutamate; 5-Methyltetrahydrofolate, (DL-glu)-isomer; 5-Methyltetrahydropteroylglutamate; 5-Methyl-5,6,7,8-tetrahydrofolate; N(5)-Methyltetrahydrofolic acid; N5-Methyl-tetrahydrofolic acid; 5-Methyltetrahydrofolic acid; N( 5)-Methyltetrahydrofolate; N5-Methyl-tetrahydrofolate; 5-Methyl-tetrahydrofolate; 5-Methyl tetrahydrofolate; N5-Methyltetrahydrofolate; 5-Methyltetrahydrofolate; Methyl-tetrahydrofolate; Levomefolic acid; L-Methyl folate; L-Methylfolate; Methyl folate; 5-Methyl-THF; Mefolinate; Prefolic a; methyl-THF; CH3-FH4; Deplin; 5-Methyl THF; 5-MTHF; 5-Methyltetrahydrofolate
数据库引用编号
26 个数据库交叉引用编号
- ChEBI: CHEBI:136009
- ChEBI: CHEBI:15641
- KEGG: C00440
- KEGGdrug: D09353
- PubChem: 135402010
- PubChem: 135398561
- HMDB: HMDB0001396
- Metlin: METLIN6215
- DrugBank: DB11256
- ChEMBL: CHEMBL1231574
- Wikipedia: Levomefolic acid
- KNApSAcK: C00007252
- foodb: FDB022600
- chemspider: 388371
- CAS: 31690-09-2
- CAS: 134-35-0
- PMhub: MS000000234
- PDB-CCD: C2F
- PDB-CCD: THH
- 3DMET: B04681
- NIKKAJI: J356.349I
- RefMet: 5-Methyl-THF
- medchemexpress: HY-113046
- medchemexpress: HY-14781
- PubChem: 3729
- KNApSAcK: 15641
分类词条
相关代谢途径
Reactome(0)
BioCyc(6)
PlantCyc(0)
代谢反应
74 个相关的代谢反应过程信息。
Reactome(13)
- Metabolism:
1-3-oxo-THA-CoA + CoA-SH ⟶ DHA-CoA + propionyl CoA
- Metabolism of vitamins and cofactors:
H2O + Oxygen + PXL ⟶ H2O2 + PDXate
- Metabolism of water-soluble vitamins and cofactors:
H2O + Oxygen + PXL ⟶ H2O2 + PDXate
- Cobalamin (Cbl, vitamin B12) transport and metabolism:
Cbl + H+ + Homologues of MMACHC + TPNH ⟶ MMACHC:cob(II)alamin + TPN
- Metabolism of water-soluble vitamins and cofactors:
H2O + Oxygen + PXL ⟶ H2O2 + PDXate
- Metabolism:
2MACA-CoA + CoA ⟶ Ac-CoA + PROP-CoA
- Metabolism of vitamins and cofactors:
H2O + Oxygen + PXL ⟶ H2O2 + PDXate
- Metabolism of water-soluble vitamins and cofactors:
H2O + Oxygen + PXL ⟶ H2O2 + PDXate
- Metabolism of folate and pterines:
ATP + HCOOH + THF ⟶ 10-formyl-THF + ADP + Pi
- Metabolism:
2MACA-CoA + CoA ⟶ Ac-CoA + PROP-CoA
- Metabolism of vitamins and cofactors:
H2O + Oxygen + PXL ⟶ H2O2 + PDXate
- Metabolism of folate and pterines:
ATP + HCOOH + THF ⟶ 10-formyl-THF + ADP + Pi
- Metabolism of folate and pterines:
FOLA + Homologues of FOLR2 ⟶ FOLR2:FOLA
BioCyc(7)
- formylTHF biosynthesis I:
H+ + NAD+ + gly + tetrahydrofolate ⟶ 5,10-methylenetetrahydrofolate + CO2 + NADH + ammonia
- folate metabolism:
H+ + ser + tetrahydrofolate ⟶ 5,10-methylene-THF + H2O + gly
- formylTHF biosynthesis II:
H+ + NAD+ + gly + tetrahydrofolate ⟶ 5,10-methylenetetrahydrofolate + CO2 + NADH + ammonia
- methionine biosynthesis:
H2O + L-cystathionine ⟶ H+ + L-homocysteine + ammonia + pyruvate
- aspartate superpathway:
ATP + ammonia + nicotinate adenine dinucleotide ⟶ AMP + H+ + NAD+ + diphosphate
- superpathway of lysine, threonine and methionine biosynthesis I:
H2O + L-cystathionine ⟶ H+ + L-homocysteine + ammonia + pyruvate
- methionine biosynthesis I:
H2O + L-cystathionine ⟶ H+ + L-homocysteine + ammonia + pyruvate
WikiPathways(3)
- Folate-alcohol and cancer pathway hypotheses:
Cysteine ⟶ Cystathionine
- MTHFR deficiency:
Choline ⟶ Phosphocholine
- Disorders of folate metabolism and transport:
Folic acid ⟶ DHF
Plant Reactome(0)
INOH(2)
- Folate metabolism ( Folate metabolism ):
6-Pyruvoyl-5,6,7,8-tetrahydro-pterin + NADPH ⟶ 5,6,7,8-Tetrahydro-biopterin + NADP+
- Methionine and Cysteine metabolism ( Methionine and Cysteine metabolism ):
H2O + L-Cystathionine ⟶ 2-Oxo-butanoic acid + L-Cysteine + NH3
PlantCyc(0)
COVID-19 Disease Map(0)
PathBank(49)
- Methylenetetrahydrofolate Reductase Deficiency (MTHFRD):
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- S-Adenosylhomocysteine (SAH) Hydrolase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Homocystinuria-Megaloblastic Anemia Due to Defect in Cobalamin Metabolism, cblG Complementation Type:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Folate Malabsorption, Hereditary:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Betaine Metabolism:
S-Adenosylhomocysteine + Water ⟶ Adenosine + Homocysteine
- Folate Metabolism:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Methionine Metabolism:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Betaine Metabolism:
S-Adenosylhomocysteine + Water ⟶ Adenosine + Homocysteine
- Folate Metabolism:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Methionine Metabolism:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Folate Metabolism:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Methionine Metabolism:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Methotrexate Action Pathway:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Methionine Metabolism:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Sarcosine Oncometabolite Pathway:
L-Serine + Tetrahydrofolic acid ⟶ 5,10-Methylene-THF + Glycine + Water
- Sarcosine Oncometabolite Pathway:
L-Serine + Tetrahydrofolic acid ⟶ 5,10-Methylene-THF + Glycine + Water
- Cystathionine beta-Synthase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Glycine N-Methyltransferase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Hypermethioninemia:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Methionine Adenosyltransferase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Methylenetetrahydrofolate Reductase Deficiency (MTHFRD):
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- S-Adenosylhomocysteine (SAH) Hydrolase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Homocystinuria-Megaloblastic Anemia Due to Defect in Cobalamin Metabolism, cblG Complementation Type:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- One Carbon Pool by Folate:
S-Aminomethyldihydrolipoylprotein; + Tetrahydrofolic acid ⟶ 5,10-Methylene-THF + Ammonia + dihydrolipoylprotein
- Betaine Metabolism:
S-Adenosylhomocysteine + Water ⟶ Adenosine + Homocysteine
- Methionine Metabolism:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Folate Metabolism:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Cystathionine beta-Synthase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Hypermethioninemia:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- S-Adenosylhomocysteine (SAH) Hydrolase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Glycine N-Methyltransferase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Methylenetetrahydrofolate Reductase Deficiency (MTHFRD):
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Methionine Adenosyltransferase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Methylenetetrahydrofolate Reductase Deficiency (MTHFRD):
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Homocystinuria-Megaloblastic Anemia Due to Defect in Cobalamin Metabolism, cblG Complementation Type:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Folate Malabsorption, Hereditary:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Folate Metabolism:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- One Carbon Pool by Folate:
S-Aminomethyldihydrolipoylprotein; + Tetrahydrofolic acid ⟶ 5,10-Methylene-THF + Ammonia + dihydrolipoylprotein
- S-Adenosyl-L-Methionine Cycle:
S-Adenosylhomocysteine + Water ⟶ Adenine + S-ribosyl-L-homocysteine
- Folate Metabolism:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Sarcosine Oncometabolite Pathway:
L-Serine + Tetrahydrofolic acid ⟶ 5,10-Methylene-THF + Glycine + Water
- One Carbon Pool by Folate I:
S-Aminomethyldihydrolipoylprotein; + Tetrahydrofolic acid ⟶ 5,10-Methylene-THF + Ammonia + dihydrolipoylprotein
- Betaine Metabolism:
S-Adenosylhomocysteine + Water ⟶ Adenosine + Homocysteine
- Methionine Metabolism:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Folate Malabsorption, Hereditary:
5-Formiminotetrahydrofolic acid ⟶ 5,10-Methenyltetrahydrofolic acid + Ammonia
- Cystathionine beta-Synthase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Glycine N-Methyltransferase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Hypermethioninemia:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
- Methionine Adenosyltransferase Deficiency:
L-Cystathionine + Water ⟶ 2-Ketobutyric acid + L-Cysteine
PharmGKB(0)
2 个相关的物种来源信息
在这里通过桑基图来展示出与当前的这个代谢物在我们的BioDeep知识库中具有相关联信息的其他代谢物。在这里进行关联的信息来源主要有:
- PubMed: 来源于PubMed文献库中的文献信息,我们通过自然语言数据挖掘得到的在同一篇文献中被同时提及的相关代谢物列表,这个列表按照代谢物同时出现的文献数量降序排序,取前10个代谢物作为相关研究中关联性很高的代谢物集合展示在桑基图中。
- NCBI Taxonomy: 通过文献数据挖掘,得到的代谢物物种来源信息关联。这个关联信息同样按照出现的次数降序排序,取前10个代谢物作为高关联度的代谢物集合展示在桑吉图上。
- Chemical Taxonomy: 在物质分类上处于同一个分类集合中的其他代谢物
- Chemical Reaction: 在化学反应过程中,存在为当前代谢物相关联的生化反应过程中的反应底物或者反应产物的关联代谢物信息。
点击图上的相关代谢物的名称,可以跳转到相关代谢物的信息页面。
文献列表
- Han Yang, Jinning Yang, Cheng Liu, Xueqin Lv, Long Liu, Jianghua Li, Guocheng Du, Jian Chen, Yanfeng Liu. High-Level 5-Methyltetrahydrofolate Bioproduction in Bacillus subtilis by Combining Modular Engineering and Transcriptomics-Guided Global Metabolic Regulation.
Journal of agricultural and food chemistry.
2022 May; 70(19):5849-5859. doi:
10.1021/acs.jafc.2c01252
. [PMID: 35521920] - Yu Cheng, Shuai Liu, Duo Chen, Yiman Yang, Qiongyue Liang, Ya Huo, Ziyi Zhou, Nan Zhang, Zhuo Wang, Lishun Liu, Yun Song, Xiangyi Liu, Yong Duan, Xiuwen Liang, Bingjie Hou, Binyan Wang, Genfu Tang, Xianhui Qin, Fangrong Yan. Association between serum 5-methyltetrahydrofolate and homocysteine in Chinese hypertensive participants with different MTHFR C677T polymorphisms: a cross-sectional study.
Nutrition journal.
2022 05; 21(1):29. doi:
10.1186/s12937-022-00786-w
. [PMID: 35562805] - Ajana Pathikkal, Bijesh Puthusseri, Peethambaran Divya, Sudha Rudrappa, Vikas Singh Chauhan. Folate derivatives, 5-methyltetrahydrofolate and 10-formyltetrahydrofolate, protect BEAS-2B cells from high glucose-induced oxidative stress and inflammation.
In vitro cellular & developmental biology. Animal.
2022 May; 58(5):419-428. doi:
10.1007/s11626-022-00691-w
. [PMID: 35678985] - Hong Wu, Zhengduo Zhang, Yuxin Wang, Tianran Zhang, Shaojun Qi, Yanjin Tang, Xibao Gao. Investigation into the Properties of L-5-Methyltetrahydrofolate and Seal Oil as a Potential Atherosclerosis Intervention in Rats.
Journal of nutritional science and vitaminology.
2022; 68(2):87-96. doi:
10.3177/jnsv.68.87
. [PMID: 35491209] - Shaimaa M Sallam, Eman Shawky, Samah M El Sohafy. Determination of the effect of germination on the folate content of the seeds of some legumes using HPTLC-mass spectrometry-multivariate image analysis.
Food chemistry.
2021 Nov; 362(?):130206. doi:
10.1016/j.foodchem.2021.130206
. [PMID: 34082289] - Zenglin Lian, Hong Chen, Kang Liu, Qianghua Jia, Feng Qiu, Yongzhi Cheng. Improved Stability of a Stable Crystal Form C of 6S-5-Methyltetrahydrofolate Calcium Salt, Method Development and Validation of an LC-MS/MS Method for Rat Pharmacokinetic Comparison.
Molecules (Basel, Switzerland).
2021 Oct; 26(19):. doi:
10.3390/molecules26196011
. [PMID: 34641555] - Seok-Won Hyung, Sunyoung Lee, Jeesoo Han, Joonhee Lee, Song-Yee Beak, Byungjoo Kim, Kiwhan Choi, Seonghee Ahn. Highly sensitive analytical method for the accurate determination of 5-methyltetrahydrofolic acid monoglutamate in various volumes of human plasma using isotope dilution ultra-high performance liquid chromatography-mass spectrometry.
Journal of chromatography. B, Analytical technologies in the biomedical and life sciences.
2021 Aug; 1179(?):122725. doi:
10.1016/j.jchromb.2021.122725
. [PMID: 34311437] - Xuanye Cao, Annika Wolf, Sung-Eun Kim, Robert M Cabrera, Bogdan J Wlodarczyk, Huiping Zhu, Margaret Parker, Ying Lin, John W Steele, Xiao Han, Vincent Th Ramaekers, Robert Steinfeld, Richard H Finnell, Yunping Lei. CIC de novo loss of function variants contribute to cerebral folate deficiency by downregulating FOLR1 expression.
Journal of medical genetics.
2021 07; 58(7):484-494. doi:
10.1136/jmedgenet-2020-106987
. [PMID: 32820034] - Mengyi Liu, Zhuxian Zhang, Chun Zhou, Qinqin Li, Panpan He, Yuanyuan Zhang, Huan Li, Chengzhang Liu, Min Liang, Xiaobin Wang, Xiping Xu, Fan Fan Hou, Xianhui Qin. Relationship of several serum folate forms with the risk of mortality: A prospective cohort study.
Clinical nutrition (Edinburgh, Scotland).
2021 06; 40(6):4255-4262. doi:
10.1016/j.clnu.2021.01.025
. [PMID: 33551219] - Emanuela Pannia, Rola Hammoud, Ruslan Kubant, Jong Yup Sa, Rebecca Simonian, Brandi Wasek, Paula Ashcraft, Teodoro Bottiglieri, Zdenka Pausova, G Harvey Anderson. High Intakes of [6S]-5-Methyltetrahydrofolic Acid Compared with Folic Acid during Pregnancy Programs Central and Peripheral Mechanisms Favouring Increased Food Intake and Body Weight of Mature Female Offspring.
Nutrients.
2021 Apr; 13(5):. doi:
10.3390/nu13051477
. [PMID: 33925570] - Patrycja Guzik, Martina Benešová, Magdalena Ratz, Josep M Monné Rodríguez, Luisa M Deberle, Roger Schibli, Cristina Müller. Preclinical evaluation of 5-methyltetrahydrofolate-based radioconjugates-new perspectives for folate receptor-targeted radionuclide therapy.
European journal of nuclear medicine and molecular imaging.
2021 04; 48(4):972-983. doi:
10.1007/s00259-020-04980-y
. [PMID: 33063250] - Pooja Dhiman, Raji Ramachandran Pillai, Anand Babu Wilson, Nancy Premkumar, Balaji Bharadwaj, Veena P Ranjan, Soundravally Rajendiran. Cross-sectional association between vitamin B12 status and probable postpartum depression in Indian women.
BMC pregnancy and childbirth.
2021 Feb; 21(1):146. doi:
10.1186/s12884-021-03622-x
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Food chemistry.
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The American journal of clinical nutrition.
2012 Oct; 96(4):789-800. doi:
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Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation.
2012 Sep; 22(5):507-514.e1. doi:
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Rapid communications in mass spectrometry : RCM.
2012 Jul; 26(14):1617-30. doi:
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2012 Jun; 344(?):e3533. doi:
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2012 Jun; 73(6):843-8. doi:
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2012 Jun; 69(6):778-9. doi:
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Pharmacogenetics and genomics.
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Clinical chemistry and laboratory medicine.
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The British journal of nutrition.
2012 Mar; 107(6):800-8. doi:
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2012 Feb; 142(2):389-95. doi:
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2012 Jan; 11(?):6. doi:
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Journal of nutrigenetics and nutrigenomics.
2012; 5(3):132-57. doi:
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Journal of nutritional science and vitaminology.
2012; 58(1):20-8. doi:
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