Quantitative determination of cholesterol sulphate in plasma by stable isotope dilution fast atom bombardment mass spectrometry

Veares, Martin P.; Evershed, R. P.; Prescott, Mark; Goad, L. John

doi:10.1002/bms.1200191002

Cited by 20 publications

(4 citation statements)

References 24 publications

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“…Indeed, different methods were used to detect and determine cholesterol such as MS spectroscopic [11,12], chromatographic [13,14], electrochemical [15][16][17][18], spectrophotometric [7,19] and fluorometric methods [20][21][22][23].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Synthesis, spectral characterization, molecular modeling, antibacterial and antioxidant activities and stability study of binuclear Pd(II) and Ru(III) complexes with novel bis-[1-(2-[(2-hydroxynaphthalen-1-yl)methylidene]amino}ethyl)-1-ethyl-3-phenylthiourea] ligand: Application to detection of cholesterol

Terbouche

Ait‐Ramdane‐Terbouche

Bendjilali

et al. 2018

Spectrochimica Acta Part A: Molecular and Biomolecular Spectros

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A novel bis-[1-(2-[(2-hydroxynaphthalen-1-yl) methylidene]amino}ethyl)-1-ethyl-3-phenylthiourea] Schiff base (L) and its binuclear palladium and ruthenium complexes have been prepared and characterized by ESI-MS, elemental analysis, NMR (H NMR, C NMR, COSY, NEOSY and HSQC), FT-IR, ATR, UV-Visible spectra, TGA measurements, conductivity and cyclic voltammetry. The experimental results and the molecular parameters calculated using DFT method revealed a square planar geometry around Pd and octahedral geometry around ruthenium metal. The antibacterial activity of the ligand L and its complexes was evaluated against different human bacteria. In addition, the formation constants of the synthesized Schiff base-metal complexes and the systems formed with these chelates and cholesterol were estimated using spectrophotometric technique. The detection of cholesterol using novel Pd and Ru Schiff base complexes was studied using fluorometric method, and the measurements showed that the sensitive fluorometric response towards cholesterol analysis was determined using palladium complex. The limit of detection (LOD) of cholesterol calculated using this complex (4.6 μM) is lower (better) than LOD found using ruthenium complex (19.1 μM) and different compounds previously published around linear range of 0-5 mM.

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Section: Accepted Manuscriptmentioning

confidence: 99%

Synthesis, spectral characterization, molecular modeling, antibacterial and antioxidant activities and stability study of binuclear Pd(II) and Ru(III) complexes with novel bis-[1-(2-[(2-hydroxynaphthalen-1-yl)methylidene]amino}ethyl)-1-ethyl-3-phenylthiourea] ligand: Application to detection of cholesterol

Terbouche

Ait‐Ramdane‐Terbouche

Bendjilali

et al. 2018

Spectrochimica Acta Part A: Molecular and Biomolecular Spectros

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“…The apparent validity of this initial value was soon confirmed by reports of plasma cholesterol sulfate levels involving a limited number of subjects that ranged from 174 to 328 g/100 ml (31)(32)(33). Studies involving larger groups of subjects but utilizing different methodologies revealed plasma cholesterol sulfate levels in normal subjects of 150-250 g/ml (34,35), 178 Ϯ 31 g/100 ml (men and women) (36), 134-322 g/ml (men) and 117-214 g/ ml (women) (37), 118-138 g/ml (men) (38), 272 Ϯ 64 g/ml (men) and 175 Ϯ 70 g/ml (women) (39), 134 Ϯ 29 g/ml (men) (40), and 253 Ϯ 25 g/ml (women) (41). Plasma cholesterol sulfate, which is carried in part by LDLs (35,42,43), can be significantly elevated in certain pathologic conditions, such as cirrhosis of the liver (41), hypercholesterolemia (36,41), and hypothyroidism (44).…”

Section: Plasma Levelsmentioning

confidence: 99%

Cholesterol sulfate in human physiology: what's it all about?

Strott

Higashi

2003

Journal of Lipid Research

202

184

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Cholesterol sulfate is quantitatively the most important known sterol sulfate in human plasma, where it is present in a concentration that overlaps that of the other abundant circulating steroid sulfate, dehydroepiandrosterone (DHEA) sulfate. Although these sulfolipids have similar production and metabolic clearance rates, they arise from distinct sources and are metabolized by different pathways. While the function of DHEA sulfate remains an enigma, cholesterol sulfate has emerged as an important regulatory molecule. Cholesterol sulfate is a component of cell membranes where it has a stabilizing role, e.g., protecting erythrocytes from osmotic lysis and regulating sperm capacitation. It is present in platelet membranes where it supports platelet adhesion. Cholesterol sulfate can regulate the activity of serine proteases, e.g., those involved in blood clotting, fibrinolysis, and epidermal cell adhesion. As a result of its ability to regulate the activity of selective protein kinase C isoforms and modulate the specificity of phosphatidylinositol 3-kinase, cholesterol sulfate is involved in signal transduction. Cholesterol sulfate functions in keratinocyte differentiation, inducing genes that encode for key components involved in development of the barrier. The accumulating evidence demonstrating a regulatory function for cholesterol sulfate appears solid; the challenge now is to work out the molecular mechanisms whereby this interesting molecule carries out its various roles. -Strott, C. A., and Y. Higashi. Cholesterol sulfate in human physiology: what's it all about? J.

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“…The concentrations of cholesterol sulfate in human plasma range from 134 to 254 g/ml (12,14,15). Cholesterol sulfate is also present in various body fluids and tissues, including urine, bile, seminal plasma, skin, adrenal glands, kidney, and liver (12,16).…”

mentioning

confidence: 99%

Cholesterol Sulfate and Cholesterol Sulfotransferase Inhibit Gluconeogenesis by Targeting Hepatocyte Nuclear Factor 4α

Shi

Cheng

et al. 2014

Molecular and Cellular Biology

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e Sulfotransferase (SULT)-mediated sulfation represents a critical mechanism in regulating the chemical and functional homeostasis of endogenous and exogenous molecules. The cholesterol sulfotransferase SULT2B1b catalyzes the sulfoconjugation of cholesterol to synthesize cholesterol sulfate (CS). In this study, we showed that the expression of SULT2B1b in the liver was induced in obese mice and during the transition from the fasted to the fed state, suggesting that the regulation of SULT2B1b is physiologically relevant. CS and SULT2B1b inhibited gluconeogenesis by targeting the gluconeogenic factor hepatocyte nuclear factor 4␣ (HNF4␣) in both cell cultures and transgenic mice. Treatment of mice with CS or transgenic overexpression of the CSgenerating enzyme SULT2B1b in the liver inhibited hepatic gluconeogenesis and alleviated metabolic abnormalities both in mice with diet-induced obesity (DIO) and in leptin-deficient (ob/ob) mice. Mechanistically, CS and SULT2B1b inhibited gluconeogenesis by suppressing the expression of acetyl coenzyme A (acetyl-CoA) synthetase (Acss), leading to decreased acetylation and nuclear exclusion of HNF4␣. Our results also suggested that leptin is a potential effector of SULT2B1b in improving metabolic function. We conclude that SULT2B1b and its enzymatic by-product CS are important metabolic regulators that control glucose metabolism, suggesting CS as a potential therapeutic agent and SULT2B1b as a potential therapeutic target for metabolic disorders.

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Quantitative determination of cholesterol sulphate in plasma by stable isotope dilution fast atom bombardment mass spectrometry

Cited by 20 publications

References 24 publications

Cholesterol sulfate in human physiology: what's it all about?

Cholesterol Sulfate and Cholesterol Sulfotransferase Inhibit Gluconeogenesis by Targeting Hepatocyte Nuclear Factor 4α

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