Determination of Coenzyme A and Acetyl-Coenzyme A in Biological Samples Using HPLC with UV Detection

Shurubor, Yevgeniya I.; D'Aurelio, Marilena; Clark-Matott, Joanne; Исакова, Е. П.; Deryabina, Yulia I.; Beal, M. Flint; Cooper, Arthur J. L.; Krasnikov, Boris F.

doi:10.3390/molecules22091388

Cited by 55 publications

(46 citation statements)

References 37 publications

(83 reference statements)

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“…This further supports our above speculation about the anti-influenza effect of B. animalis. Although valine and CoA have been known to improve host health status or modulate immune responses [28][29][30], this is the first report about their anti-influenza effect, and further studies are still needed to explain their anti-influenza molecular mechanisms.…”

Section: Discussionmentioning

confidence: 92%

Influenza infection elicits an expansion of gut population of endogenous Bifidobacterium animalis which protects mice against infection

Zhang

Feng

et al. 2020

Genome Biol

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Background: Influenza is a severe respiratory illness that continually threatens global health. It has been widely known that gut microbiota modulates the host response to protect against influenza infection, but mechanistic details remain largely unknown. Here, we took advantage of the phenomenon of lethal dose 50 (LD 50) and metagenomic sequencing analysis to identify specific anti-influenza gut microbes and analyze the underlying mechanism. Results: Transferring fecal microbes from mice that survive virulent influenza H7N9 infection into antibiotic-treated mice confers resistance to infection. Some gut microbes exhibit differential features to lethal influenza infection depending on the infection outcome. Bifidobacterium pseudolongum and Bifidobacterium animalis levels are significantly elevated in surviving mice when compared to dead or mockinfected mice. Oral administration of B. animalis alone or the combination of both significantly reduces the severity of H7N9 infection in both antibiotic-treated and germ-free mice. Functional metagenomic analysis suggests that B. animalis mediates the anti-influenza effect via several specific metabolic molecules. In vivo tests confirm valine and coenzyme A produce an anti-influenza effect. Conclusions: These findings show that the severity of influenza infection is closely related to the heterogeneous responses of the gut microbiota. We demonstrate the anti-influenza effect of B. animalis, and also find that the gut population of endogenous B. animalis can expand to enhance host influenza resistance when lethal influenza infection occurs, representing a novel interaction between host and gut microbiota. Further, our data suggest the potential utility of Bifidobacterium in the prevention and as a prognostic predictor of influenza.

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Section: Discussionmentioning

confidence: 92%

Influenza infection elicits an expansion of gut population of endogenous Bifidobacterium animalis which protects mice against infection

Zhang

Feng

et al. 2020

Genome Biol

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“…Here, our correlational analysis of data from 296 brain-tissue samples found no relationship between CAG repeat number and vitamin B5 levels in cases or controls. Further studies, including measurements of tissue levels of CoA and acetyl-CoA by published methods [62], and of the five linked enzymes in the CoA biosynthetic pathway [28], are required to investigate the potential role of altered regulation of this pathway in HD.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease

Patassini

Begley

et al. 2019

Metabolites

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Huntington’s disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in exon 1 of the HTT gene. HD usually manifests in mid-life with loss of GABAergic projection neurons from the striatum accompanied by progressive atrophy of the putamen followed by other brain regions, but linkages between the genetics and neurodegeneration are not understood. We measured metabolic perturbations in HD-human brain in a case-control study, identifying pervasive lowering of vitamin B5, the obligatory precursor of coenzyme A (CoA) that is essential for normal intermediary metabolism. Cerebral pantothenate deficiency is a newly-identified metabolic defect in human HD that could potentially: (i) impair neuronal CoA biosynthesis; (ii) stimulate polyol-pathway activity; (iii) impair glycolysis and tricarboxylic acid cycle activity; and (iv) modify brain-urea metabolism. Pantothenate deficiency could lead to neurodegeneration/dementia in HD that might be preventable by treatment with vitamin B5.

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“…One may suspect that neurons of different neurotransmitter systems might contain variable profiles of intraneuronal compartmentation acetyl-CoA. Therefore, estimations of acetyl-CoA level in whole brain tissue may not adequately reflect the distribution of this metabolite between subcellular compartments in specific cell groups ( Table 2 ) ( Rícný and Tucek, 1982 ; Szutowicz et al, 1996 , 2013 ; Pietrocola et al, 2015 ; Shurubor et al, 2017 ).…”

Section: Acetyl-coa Levels In the Brainmentioning

confidence: 99%

The Regulatory Effects of Acetyl-CoA Distribution in the Healthy and Diseased Brain

Ronowska

Szutowicz

Bielarczyk

et al. 2018

Front. Cell. Neurosci.

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Brain neurons, to support their neurotransmitter functions, require a several times higher supply of glucose than non-excitable cells. Pyruvate, the end product of glycolysis, through pyruvate dehydrogenase complex reaction, is a principal source of acetyl-CoA, which is a direct energy substrate in all brain cells. Several neurodegenerative conditions result in the inhibition of pyruvate dehydrogenase and decrease of acetyl-CoA synthesis in mitochondria. This attenuates metabolic flux through TCA in the mitochondria, yielding energy deficits and inhibition of diverse synthetic acetylation reactions in all neuronal sub-compartments. The acetyl-CoA concentrations in neuronal mitochondrial and cytoplasmic compartments are in the range of 10 and 7 μmol/L, respectively. They appear to be from 2 to 20 times lower than acetyl-CoA Km values for carnitine acetyltransferase, acetyl-CoA carboxylase, aspartate acetyltransferase, choline acetyltransferase, sphingosine kinase 1 acetyltransferase, acetyl-CoA hydrolase, and acetyl-CoA acetyltransferase, respectively. Therefore, alterations in acetyl-CoA levels alone may significantly change the rates of metabolic fluxes through multiple acetylation reactions in brain cells in different physiologic and pathologic conditions. Such substrate-dependent alterations in cytoplasmic, endoplasmic reticulum or nuclear acetylations may directly affect ACh synthesis, protein acetylations, and gene expression. Thereby, acetyl-CoA may regulate the functional and adaptative properties of neuronal and non-neuronal brain cells. The excitotoxicity-evoked intracellular zinc excess hits several intracellular targets, yielding the collapse of energy balance and impairment of the functional and structural integrity of postsynaptic cholinergic neurons. Acute disruption of brain energy homeostasis activates slow accumulation of amyloid-β1-42 (Aβ). Extra and intracellular oligomeric deposits of Aβ affect diverse transporting and signaling pathways in neuronal cells. It may combine with multiple neurotoxic signals, aggravating their detrimental effects on neuronal cells. This review presents evidences that changes of intraneuronal levels and compartmentation of acetyl-CoA may contribute significantly to neurotoxic pathomechanisms of different neurodegenerative brain disorders.

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Determination of Coenzyme A and Acetyl-Coenzyme A in Biological Samples Using HPLC with UV Detection

Cited by 55 publications

References 37 publications

Influenza infection elicits an expansion of gut population of endogenous Bifidobacterium animalis which protects mice against infection

Influenza infection elicits an expansion of gut population of endogenous Bifidobacterium animalis which protects mice against infection

Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease

The Regulatory Effects of Acetyl-CoA Distribution in the Healthy and Diseased Brain

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