Analysis of medium-chain acyl-coenzyme A esters in mouse tissues by liquid chromatography–electrospray ionization mass spectrometry

Kasuya, Fumiyo; Oti, Yusaku; Tatsuki, Takao; Igarashi, Kazuo

doi:10.1016/j.ab.2003.10.043

Cited by 24 publications

(28 citation statements)

References 18 publications

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“…This metabolic phenotype is refl ected in our mapped data: i ) several saturated acyl-CoAs (C 10 -, C 12 -, C 14 -, and C 18 -CoAs) are the highest in heart; ii ) the corresponding unsaturated acyl-CoAs and 3-hydroxyacyl-CoAs, i.e., C 10 -, C 12 -, C 14 -, and C 18 -CoAs, are also relatively high in the heart. Saturated acyl-CoAs, enoyl-CoAs, and 3-hydroxyacyl-CoAs are ␤ oxidation intermediates of fatty acids, the high amounts of these acyl-CoAs refl ect the high activity of fatty acid oxidation in the heart.…”

Section: Discussionmentioning

confidence: 86%

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Novel approach in LC-MS/MS using MRM to generate a full profile of acyl-CoAs: discovery of acyl-dephospho-CoAs

Zhang

Berthiaume

et al. 2014

Journal of Lipid Research

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This article is available online at http://www.jlr.org Acyl-CoAs are a class of important molecules that play essential roles in many physiological processes ( 1 ), such as fatty acid oxidation, lipid synthesis/remodeling, ketone body synthesis, xenobiotic metabolism, and signaling pathways. Classically, acyl-CoAs such as free CoA, acetyl-CoA, and malonyl-CoA are recognized as regulators of metabolic fl ux. The ratio of acetyl-CoA versus free CoA tightly regulates glycolysis and fatty acid oxidation. Malonyl-CoA attenuates fatty acid oxidation by inhibiting acyl-CoA transport into the mitochondrion for oxidation and is utilized in fatty acid synthesis when its concentration is elevated ( 2 ). Many proteins and genes are dynamically regulated by deacylation and acylation via various acyl-CoAs, such as acetyl-CoA, succinyl-CoA, palmitoyl-CoA, etc. ( 3 ). However, acyl-CoAs present in the cell are diverse and may involve molecules beyond fatty acids and their oxidized derivatives. The metabolism of xenobiotics can also lead to the formation of acyl-CoAs, as demonstrated in our previous work on the metabolism of 4-hydroxy acids from C 4 to C 11 in perfused rat liver. The identifi cation of these novel acyl-CoAs extends our understanding of the new catabolic pathways involved in the disposal of 4-hydroxy acids including drugs of abuse and lipid peroxidation products ( 4-8 ).Acyl-CoAs are exclusive to the intracellular metabolites, and the profi le of these biomolecules is indicative of the local metabolic status. Each organ has its specifi c physiological roles with different energetic demands, and therefore, would be expected to exhibit a unique acyl-CoA profi le. The heart preferentially utilizes fatty acids to meet the ATP demand of mechanical contraction. Glucose and/or ketone bodies serve as the primary substrate of the brain for energy

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Section: Discussionmentioning

confidence: 86%

“…However, most methods only assay either short-, medium-, or long-chain acyl-CoAs (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). The best approach for acyl-CoA quantitation, so far, is to measure the target acyl-CoAs from short to long carbon chain length in a single method ( 20,21 ).…”

Section: Lc-ms/ms Is the Most Sensitive Methods To Analyze Acylcoas Anmentioning

confidence: 99%

Novel approach in LC-MS/MS using MRM to generate a full profile of acyl-CoAs: discovery of acyl-dephospho-CoAs

Zhang

Berthiaume

et al. 2014

Journal of Lipid Research

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“…We previously described a method for the determination of acyl-CoAs in the tissues based on selected ion monitoring (SIM) with a positive ionization mode (Kasuya et al, 2004). To improve the selectivity and sensitivity, the medium-chain and long-chain acyl-CoAs were quantified by selective multireaction monitoring (MRM), which is generally known to provide the excellent sensitivity with the femtomole range and specific detection in biomaterials.…”

Section: Lc-esi-ms/ms Analysis Of Acyl-coas and Salicylyl-coamentioning

confidence: 99%

“…The medium-chain acyl-CoAs, long-chain acyl-CoAs, salicylyl-CoA and salicylic acid were extracted from each tissue as described previously (Kasuya et al, 2004). Briefly, the weight of each frozen tissue was determined and 1 ml of 10 mM ammonium acetate buffer (pH 5.3) was added per 0.5 g of wet tissue.…”

Section: Extraction Of Acyl-coa Esters Salicylyl-coa and Salicylic Acidmentioning

confidence: 99%

Effect of salicylic acid and diclofenac on the medium‐chain and long‐chain acyl‐CoA formation in the liver and brain of mouse

Kasuya

Kazumi²,

Tatsuki³

et al. 2009

J of Applied Toxicology

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Medium-chain and long-chain acyl-CoA esters are key metabolites in fatty acid metabolism. Effects of salicylic acid on the in vivo formation of acyl-CoAs in mouse liver and brain were investigated. Further, inhibition of the medium-chain and long-chain acyl-CoA synthetases by salicylic acid and diclofenac was determined in mouse liver and brain mitochondria. Acyl-CoA esters were analyzed by liquid chromatography-tandem mass spectrometry. The amounts of medium-chain acyl-CoAs (C(6), C(8) and C(10)) were less than long-chain acyl-CoAs (C(16:0), C(18:0), C(18:1) and C(20:4)) in both liver and brain. The administration of salicylic acid decreased the levels of both the medium-chain (C(6), C(8) and C(10)) and long-chain acyl-CoAs (C(16:0), C(18:0), C(18:1) and C(20:4)) in liver. In brain, however, only long-chain acyl-CoAs were decreased. The level of salicylyl-CoA detected in brain was about 12% of that in liver. Salicylic acid had a strong inhibitory activity (IC(50) = 0.1 mm) for the liver mitochondrial formation of hexanoyl-CoA from hexanoic acid, whereas diclofenac was weak (IC(50) = 4.4 mm). In contrast, diclofenac (IC(50) = 1.4 mm) inhibited the liver mitochondrial long-chain acyl-CoA synthetases more potently than salicylic acid (IC(50) = 25.5 mm). Similar inhibitory activities for the acyl-CoA synthetases were obtained in the case of the brain and liver mitochondria, except for the weak inhibition of brain medium-chain acyl-CoA synthetases by salicylic acid (IC(50) = 1.8 mm). These findings suggest that salicylic acid and diclofenac exhibit different mechanisms of inhibition of fatty acid metabolism depending on the length of the acyl chain and tissues, and they may contribute to the further understanding of the toxic effects associated with these drugs.

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“…Published methods for the analysis of tissue acyl-coenzyme A content are focused on either short- [1,2], medium- [3] or long-chain acyl-coenzyme A esters [4,5], with the isolation of one acyl-coenzyme A subgroup to the exclusion of others. Recovery of acyl-coenzyme A esters from tissue specimens is often disappointing, with documented recoveries between 30 and 60% [1,5,6].…”

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confidence: 99%

Novel isolation procedure for short-, medium-, and long-chain acyl-coenzyme A esters from tissue

Minkler

Kerner

Ingalls

et al. 2008

Analytical Biochemistry

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A novel procedure for the quantitative isolation and purification of acyl-coenzyme A esters is presented. The procedure involves two steps: 1) tissue extraction using acetonitrile/2-propanol (3+1, v+v) followed by 0.1M potassium phosphate, pH 6.7, and 2) purification using 2-(2-pyridyl)ethyl functionalized silica gel. Recoveries determined by adding radiolabelled acetyl-, malonyl-, octanoyl-, oleoyl-, palmitoyl-or arachidonyl-coenzyme A to powdered rat liver varied from 93% to 104% for tissue extraction and 83% to 90% for solid phase extraction. The procedure described allows for isolation and purification, with high recoveries, of acyl-coenzyme A esters widely differing in chainlength and saturation.Published methods for the analysis of tissue acyl-coenzyme A content are focused on either short-[1,2], medium-[3] or long-chain acyl-coenzyme A esters [4,5], with the isolation of one acyl-coenzyme A subgroup to the exclusion of others. Recovery of acyl-coenzyme A esters from tissue specimens is often disappointing, with documented recoveries between 30 and 60% [1,5,6]. A general procedure for the isolation of a wide range of acyl-coenzyme A esters, with good documented recoveries from tissues, is presently unavailable.Despite their widely different polarities, we have shown that acylcarnitines (short-, medium-, and long-chain) can be isolated, in a single fraction, from biological samples using organic solvent extraction followed by ion-exchange solid phase extraction (SPE) [7]. This is a highly selective approach, since it combines two orthogonal procedures [8] of isolation: organic solvent extraction and ion-exchange. Extraction procedures for short-chain acyl-coenzyme A esters often use acid precipitation [1,2], but these methods would exclude long-chain acylcoenzyme A esters. Therefore, we investigated extraction procedures originally developed for long-chain acyl-coenzyme A esters, using a mixture of acetonitrile, isopropanol, and aqueous buffer [4]. An SPE anion-exchange column is needed that would be uncharged at pH 7, since elution at high pH would cause hydrolysis of acyl-coenzyme A esters. Finding none commercially available, we ordered custom SPE columns from Supelco, (Bellefonte, PA), packed with 100 mg of 2-(2-pyridyl)ethyl functionalized silica gel. The pKa of these SPE *Corresponding author. Fax: +1 216 368 5162. E-mail address: charles.hoppel@case.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. , we analyzed rat heart, skeletal muscle, and liver and we found that the recovery of malonyl-coenzyme A from liver was much worse than for skeletal musc...

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Analysis of medium-chain acyl-coenzyme A esters in mouse tissues by liquid chromatography–electrospray ionization mass spectrometry

Cited by 24 publications

References 18 publications

Novel approach in LC-MS/MS using MRM to generate a full profile of acyl-CoAs: discovery of acyl-dephospho-CoAs

Novel approach in LC-MS/MS using MRM to generate a full profile of acyl-CoAs: discovery of acyl-dephospho-CoAs

Effect of salicylic acid and diclofenac on the medium‐chain and long‐chain acyl‐CoA formation in the liver and brain of mouse

Novel isolation procedure for short-, medium-, and long-chain acyl-coenzyme A esters from tissue

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