Simultaneous quantitation of folates, flavins and B6 metabolites in human plasma by LC–MS/MS assay: Applications in colorectal cancer

Asante, Isaac; Peng, Hua; Zhou, Eugene; Liu, Siyu; Chui, Darryl; Yoo, Eunjeong; Louie, Stan G.

doi:10.1016/j.jpba.2018.05.030

Cited by 18 publications

(23 citation statements)

References 33 publications

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“…Furthermore, we (Louie and Asante) have developed a validated and more sensitive and precise assay to quantify blood B vitamins. This validated multianalyte LC‐MS method can simultaneously measure the endogenous plasma levels of metabolites involved in FOCM (Asante et al, ). However, our study also has several limitations.…”

Section: Discussionmentioning

confidence: 99%

Genome‐wide association study of circulating folate one‐carbon metabolites

Wang

Asante

Baron

et al. 2019

Genetic Epidemiology

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Experimental, observational, and clinical trials support a critical role of folate one-carbon metabolism (FOCM) in colorectal cancer (CRC) development. In this report, we focus on understanding the relationship between common genetic variants and metabolites of FOCM. We conducted a genome-wide association study of FOCM biomarkers among 1,788 unaffected (without CRC) individuals of European ancestry from the Colon Cancer Family Registry.Twelve metabolites, including 5-methyltetrahydrofolate, vitamin B 2 (flavin mononucleotide and riboflavin), vitamin B 6 (4-pyridoxic acid, pyridoxal, and pyridoxamine), total homocysteine, methionine, S-adenosylmethionine, Sadenosylhomocysteine, cystathionine, and creatinine were measured from plasma using liquid chromatography-mass spectrometry (LC-MS) or LC-MS/ MS. For each individual biomarker, we estimated genotype array-specific associations followed by a fixed-effect meta-analysis. We identified the variant rs35976024 (at 2p11.2 and intronic of ATOH8) associated with total homocysteine (p = 4.9 × 10 −8 ). We found a group of six highly correlated variants on chromosome 15q14 associated with cystathionine (all p < 5 × 10 −8 ), with the most significant variant rs28391580 (p = 2.8 × 10 −8 ). Two variants (rs139435405 and rs149119426) on chromosome 14q13 showed significant (p < 5 × 10 −8 ) associations with S-adenosylhomocysteine. These three

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Section: Discussionmentioning

confidence: 99%

Genome‐wide association study of circulating folate one‐carbon metabolites

Wang

Asante

Baron

et al. 2019

Genetic Epidemiology

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“…Methods have been described for the measurement of individual folate species in serum, red cells and CSF, typically using liquid chromatography-mass spectrometry (LC-MS). [24][25][26][27][28][29] Such methods are not generally available in a diagnostic setting. For the diagnosis of CFD, the most frequently used method is high performance liquid chromatography (HPLC) with fluorescence detection or electrochemical detection (ECD) of 5-MTHF in CSF.…”

Section: Analytical Methods For Assessment Of Folate Statusmentioning

confidence: 99%

Cerebral folate deficiency: Analytical tests and differential diagnosis

Pope

Artuch

Heales

et al. 2019

J of Inher Metab Disea

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Cerebral folate deficiency is typically defined as a deficiency of the major folate species 5‐methyltetrahydrofolate in the cerebrospinal fluid (CSF) in the presence of normal peripheral total folate levels. However, it should be noted that cerebral folate deficiency is also often used to describe conditions where CSF 5‐MTHF is low, in the presence of low or undefined peripheral folate levels. Known defects of folate transport are deficiency of the proton coupled folate transporter, associated with systemic as well as cerebral folate deficiency, and deficiency of the folate receptor alpha, leading to an isolated cerebral folate deficiency associated with intractable seizures, developmental delay and/or regression, progressive ataxia and choreoathetoid movement disorders. Inborn errors of folate metabolism include deficiencies of the enzymes methylenetetrahydrofolate reductase, dihydrofolate reductase and 5,10‐methenyltetrahydrofolate synthetase. Cerebral folate deficiency is potentially a treatable condition and so prompt recognition of these inborn errors and initiation of appropriate therapy is of paramount importance. Secondary cerebral folate deficiency may be observed in other inherited metabolic diseases, including disorders of the mitochondrial oxidative phosphorylation system, serine deficiency, and pyridoxine dependent epilepsy. Other secondary causes of cerebral folate deficiency include the effects of drugs, immune response activation, toxic insults and oxidative stress. This review describes the absorption, transport and metabolism of folate within the body; analytical methods to measure folate species in blood, plasma and CSF; inherited and acquired causes of cerebral folate deficiency; and possible treatment options in those patients found to have cerebral folate deficiency.

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“…Analytes of the FOCM (including their metabolites) -B 2 , FMN, B 6 , 4PA, PL, PM, FA, DHF, THF, and 5MTHF were targeted during this scan. The samples were analyzed with the targeted approach using a published assay 16 .…”

Section: Lcms Data Acquisition For Targeted and Untargeted Scanmentioning

confidence: 99%

“…The untargeted analysis was conducted with a modification of the targeted assay 16 , but separation was achieved with a longer reverse phase Kinetex PFP 100A (75 X 3.0 mm, 2.6 μm) column (Phenomenex Technologies Inc., Torrance, CA) at an extended 33-min gradient.…”

Section: Lcms Data Acquisition For Targeted and Untargeted Scanmentioning

confidence: 99%