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Frederic L. Hoch - One of the best experts on this subject based on the ideXlab platform.
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Minireview: Cardiolipins and Mitochondrial Proton-Selective Leakage
Journal of Bioenergetics and Biomembranes, 1998Co-Authors: Frederic L. HochAbstract:The proton-selective leak (State 4 respiratory rate) but not Δψ, in mitochondria from thyroid-sensitive tissues, responds to in vivo stimuli in unique correlation with changes in Cardiolipins, saturated and mono-unsaturated (extended) fatty acyl contents, Cardiolipins/phospholipids ratios, and/or membrane outer-sidedness. Liver mitochondrial State 4 respiration, basal in fasted rats, contributes little to resting metabolic rate in fed rats, where State 3 depresses Δ_ψ. In a proposed model, an essential inner-membrane outer-surface proton antenna collects protons and donates them, via a water-shuttle, to transmembrane porters: transient water-molecule-chains between extended phospholipid acyls; protonophores, and uncoupling proteins. Only cardiolipin microdomains can donate, from an anomalously-dissociating phosphate group in each headgroup; unadapted Cardiolipins have few conducting water chains. Thyroid states regulate each cardiolipin property, and are permissive, via the proton antenna, for proton leaks, including those through adapted and possibly constitutive BAT and ectopic uncoupling proteins. Slow leakage in liposomes may reflect insufficient cardiolipin proton antennas.
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Cardiolipins and mitochondrial proton-selective leakage.
Journal of bioenergetics and biomembranes, 1998Co-Authors: Frederic L. HochAbstract:The proton-selective leak (State 4 respiratory rate) but not Δψ, in mitochondria from thyroid-sensitive tissues, responds to in vivo stimuli in unique correlation with changes in Cardiolipins, saturated and mono-unsaturated (extended) fatty acyl contents, Cardiolipins/phospholipids ratios, and/or membrane outer-sidedness. Liver mitochondrial State 4 respiration, basal in fasted rats, contributes little to resting metabolic rate in fed rats, where State 3 depresses Δψ. In a proposed model, an essential inner-membrane outer-surface proton antenna collects protons and donates them, via a water-shuttle, to transmembrane porters: transient water-molecule-chains between extended phospholipid acyls; protonophores, and uncoupling proteins. Only cardiolipin microdomains can donate, from an anomalously-dissociating phosphate group in each headgroup; unadapted Cardiolipins have few conducting water chains. Thyroid states regulate each cardiolipin property, and are permissive, via the proton antenna, for proton leaks, including those through adapted and possibly constitutive BAT and ectopic uncoupling proteins. Slow leakage in liposomes may reflect insufficient cardiolipin proton antennas.
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Cardiolipins and biomembrane function
Biochimica et biophysica acta, 1992Co-Authors: Frederic L. HochAbstract:Evidence is discussed for roles of Cardiolipins in oxidative phosphorylation mechanisms that regulate State 4 respiration by returning ejected protons across and over bacterial and mitochondrial membrane phospholipids, and that regulate State 3 respiration through the relative contributions of proteins that transport protons, electrons and/or metabolites. The barrier properties of phospholipid bilayers support and regulate the slow proton leak that is the basis for State 4 respiration. Proton permeability is in the range 10(-3)-10(-4) cm s-1 in mitochondria and in protein-free membranes formed from extracted mitochondrial phospholipids or from stable synthetic phosphatidylcholines or phosphatidylethanolamines. The roles of Cardiolipins in proton conductance in model phospholipid membrane systems need to be assessed in view of new findings by Hubner et al. [313]: saturated Cardiolipins form bilayers whilst natural highly unsaturated Cardiolipins form nonlamellar phases. Mitochondrial Cardiolipins apparently participate in bilayers formed by phosphatidylcholines and phosphatidylethanolamines. It is not yet clear if Cardiolipins themselves conduct protons back across the membrane according to their degree of fatty acyl saturation, and/or modulate proton conductance by phosphatidylcholines and phosphatidylethanolamines. Mitochondrial Cardiolipins, especially those with high 18:2 acyl contents, strongly bind many carrier and enzyme proteins that are involved in oxidative phosphorylation, some of which contribute to regulation of State 3 respiration. The role of Cardiolipins in biomembrane protein function has been examined by measuring retained phospholipids and phospholipid binding in purified proteins, and by reconstituting delipidated proteins. The reconstitution criterion for the significance of cardiolipin-protein interactions has been catalytical activity; proton-pumping and multiprotein interactions have yet to be correlated. Some proteins, e.g., cytochrome c oxidase are catalytically active when dimyristoylphosphatidylcholine replaces retained Cardiolipins. Cardiolipin-protein interactions orient membrane proteins, matrix proteins, and on the outerface receptors, enzymes, and some leader peptides for import; activate enzymes or keep them inactive unless the inner membrane is disrupted; and modulate formation of nonbilayer HII-phases. The capacity of the proton-exchanging uncoupling protein to accelerate thermogenic respiration in brown adipose tissue mitochondria of cold-adapted animals is not apparently affected by the increased cardiolipin unsaturation; this protein seems to take over the protonophoric role of Cardiolipins in other mitochondria. Many in vivo influences that affect proton leakage and carrier rates selectively alter Cardiolipins in amount per mitochondrial phospholipids, in fatty acyl composition and perhaps in sidedness; other mitochondrial membrane phospholipids respond less or not at all.(ABSTRACT TRUNCATED AT 400 WORDS)
Grant M. Hatch - One of the best experts on this subject based on the ideXlab platform.
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Cardiolipin Metabolism in Experimental and Human Heart Failure
Molecular Defects in Cardiovascular Disease, 2011Co-Authors: Grant M. HatchAbstract:Heart failure accounts for approximately 5% of all medical admissions and is the single most common cause of hospital admissions in individuals aged 65 years and over. The biochemical mechanisms for the development of heart failure are beginning to emerge. Cardiolipin is a major mitochondrial membrane phospholipid required for the activity of key mitochondrial enzymes involved in cellular energy production. Loss of cardiolipin results in the inability of mitochondria to sustain oxidative phosphorylation. Cardiolipin metabolism is altered leading to reduction in tetralinoleoyl-cardiolipin levels in experimental animal models of heart failure and in humans. This loss in tetralinoleoyl-cardiolipin results in reduced mitochondrial function which may contribute to the development of heart failure. Thus, cardiolipin biosynthetic and remodeling enzymes may represent targets for pharmacotherapeutic modulation in both left ventricular- as well as right ventricular-mediated heart failure.
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Status of cardiolipin synthesis in heart failure
Future Lipidology, 2008Co-Authors: Grant M. HatchAbstract:Phospholipids are important structural and functional components of all biological membranes. The mitochondrial phospholipid, cardiolipin, comprises approximately 15% of the entire phospholipid mass of the heart. Cardiolipin plays an important role in the regulation of various mitochondrial processes, including ATP generation, apoptosis, electron transport and mitochondrial lipid and protein import. Alterations in the content and fatty acid composition of phospholipids within the heart are linked to sustained differences in myocardial electrical activity. Reduced levels of cardiolipin are an underlying biochemical cause of the Barth syndrome, a rare X-linked genetic disease that is associated with cardiomyopathy and heart failure. This article focuses on the synthesis of cardiolipin, the regulation of cardiolipin synthesis and the implications of heart failure on cardiac cardiolipin and its synthesis.
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Cardiolipin metabolism and Barth Syndrome
Progress in Lipid Research, 2006Co-Authors: Kristin Hauff, Grant M. HatchAbstract:Many advances have occurred in the field of Barth Syndrome biology in the 26 years since it was first described as an X-linked cardiomyopathy. Barth Syndrome is the first human disease recognized in which the primary causative factor is an alteration in cardiolipin remodeling. Cardiolipin is required for the optimal function of many proteins within the mitochondria, particularly in the respiratory chain and is involved in the mitochondrial-mediated apoptotic process. The appropriate content of cardiolipin appears to be critical for these functions. Cardiolipin is synthesized de novo in mitochondria and is rapidly remodeled to produce CL enriched in linoleic acid. The Barth Syndrome gene TAZ has been identified and expression of the gene yields proteins known as tafazzins. Mutations in TAZ result in a decrease in tetra-linoleoyl species of cardiolipin and an accumulation of monolysocardiolipin within cells from Barth Syndrome patients. Although the protein product of the TAZ gene shows sequence homology to the glycerolipid acyltransferase family of enzymes, its precise biochemical function remains to be elucidated. In this review we highlight some of the recent literature on cardiolipin metabolism and Barth Syndrome.
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Expression of monolysocardiolipin acyltransferase activity is regulated in concert with the level of cardiolipin and cardiolipin biosynthesis in the mammalian heart
BMC biochemistry, 2002Co-Authors: William A. Taylor, Brian J., Thomas C. Mutter, Vernon W. Dolinsky, Grant M. HatchAbstract:Background Monolysocardiolipin acyltransferase (MLCL AT) catalyzes the acylation of monolysocardiolipin to cardiolipin in mammalian tissues. We previously reported that cardiac cardiolipin levels, MLCL AT and cardiolipin synthase activities were all elevated in rats made hyperthyroid by thyroxine treatment. In this study, we examined if cardiac mitochondrial MLCL AT activity was dependent upon the biosynthesis and level of cardiolipin in the heart. Rat heart mitochondrial MLCL AT activity was determined under conditions in which the levels of cardiac cardiolipin and cardiolipin synthase activity were either reduced or unaltered using four different disease models in the rat. In addition, these parameters were examined in a murine model of cardiac cell differentiation.
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Regulation of cardiolipin biosynthesis in the heart
Molecular and cellular biochemistry, 1996Co-Authors: Grant M. HatchAbstract:Cardiolipin is one of the principle phospholipids in the mammalian heart comprising as much as 15-20% of the entire phospholipid phosphorus mass of that organ. Cardiolipin is localized primarily in the mitochondria and appears to be essential for the function of several enzymes of oxidative phosphorylation. Thus, cardiolipin is essential for production of energy for the heart to beat. Cardiac cardiolipin is synthesized via the cytidine-5'-diphosphate-1,2-diacyl-sn-glycerol pathway. The properties of the four enzymes of the cytidine-5'-diphosphate-1,2-diacyl-sn-glycerol pathway have been characterized in the heart. The rate-limiting step of this pathway is catalyzed by the phosphatidic acid: cytidine-5'-triphosphate cytidylyltransferase. Several regulatory mechanisms that govern cardiolipin biosynthesis in the heart have been uncovered. Current evidence suggests that cardiolipin biosynthesis is regulated by the energy status (adenosine-5'-triphosphate and cytidine-5'-triphosphate level) of the heart. Thyroid hormone and unsaturated fatty acids may regulate cardiolipin biosynthesis at the level of three key enzymes of the cytidine-5'-diphosphate-1,2-diacyl-sn-glycerol pathway, phosphatidylglycerol phosphate synthase, phosphatidyl-glycerolphosphate phosphatase and cardiolipin synthase. Newly synthesized phosphatidic acid and phosphatidylglycerol may be preferentially utilized for cardiolipin biosynthesis in the heart. In addition, separate pools of phosphatidylglycerol, including an exogenous (extra-mitochondrial) pool not derived from de novo phosphatidylglycerol biosynthesis, may be utilized for cardiac cardiolipin biosynthesis. In several mammalian tissues a significant number of studies on polyglycerophospholipid biosynthesis have been documented, including detailed studies in the lung and liver. However, in spite of the important role of cardiolipin in the maintenance of mitochondrial function and membrane integrity, studies on the control of cardiolipin biosynthesis in the mammalian heart have been largely neglected. The purpose of this review will be to briefly discuss cardiolipin and cardiolipin biosynthesis in some selected model systems and focus primarily on current studies involving the regulation of cardiolipin biosynthesis in the heart.
Michael Schlame - One of the best experts on this subject based on the ideXlab platform.
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Metabolism and function of mitochondrial cardiolipin.
Progress in lipid research, 2014Co-Authors: Mindong Ren, Colin K L Phoon, Michael SchlameAbstract:Since it has been recognized that mitochondria are crucial not only for energy metabolism but also for other cellular functions, there has been a growing interest in cardiolipin, the specific phospholipid of mitochondrial membranes. Indeed, cardiolipin is a universal component of mitochondria in all eukaryotes. It has a unique dimeric structure comprised of two phosphatidic acid residues linked by a glycerol bridge, which gives rise to unique physicochemical properties. Cardiolipin plays an important role in the structural organization and the function of mitochondrial membranes. In this article, we review the literature on cardiolipin biology, focusing on the most important discoveries of the past decade. Specifically, we describe the formation, the migration, and the degradation of cardiolipin and we discuss how cardiolipin affects mitochondrial function. We also give an overview of the various phenotypes of cardiolipin deficiency in different organisms.
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comparison of Cardiolipins from drosophila strains with mutations in putative remodeling enzymes
Chemistry and Physics of Lipids, 2012Co-Authors: Michael Schlame, Mindong Ren, Steven Blais, Irit Edelmannovemsky, Fleurise Montecillo, Colin K L Phoon, Thomas A NeubertAbstract:Abstract Cardiolipin is a dimeric phospholipid with a characteristic acyl composition that is generated by fatty acid remodeling after de novo synthesis. Several enzymes have been proposed to participate in acyl remodeling of cardiolipin. In order to compare the effect of these enzymes, we determined the pattern of cardiolipin molecular species in Drosophila strains with specific enzyme deletions, using MALDI-TOF mass spectrometry with internal standards. We established the linear range of the method for cardiolipin quantification, determined the relative signal intensities of several cardiolipin standards, and demonstrated satisfying signal-to-noise ratios in cardiolipin spectra from a single fly. Our data demonstrate changes in the cardiolipin composition during the Drosophila life cycle. Comparison of cardiolipin spectra, using vector algebra, showed that inactivation of tafazzin had a large effect on the molecular composition of cardiolipin, inactivation of calcium-independent phospholipase A2 had a small effect, whereas inactivation of acyl-CoA:lysocardiolipin-acyltransferase and of the trifunctional enzyme did not affect the cardiolipin composition.
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The role of cardiolipin in the structural organization of mitochondrial membranes
Biochimica et biophysica acta, 2009Co-Authors: Michael Schlame, Mindong RenAbstract:Considerable progress has recently been made in understanding the role of cardiolipin in mitochondria. In this brief review, we discuss new data that show how cardiolipin specifically contributes to the lateral organization of mitochondrial membranes. We argue that the function of cardiolipin has to be understood in the context of dynamic membrane assembly rather than static membrane structure, and we propose that remodeling of cardiolipin, i.e. the formation of uniformly substituted molecular species, may reduce the energy barrier of the assembly process.
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Molecular symmetry in mitochondrial Cardiolipins.
Chemistry and physics of lipids, 2005Co-Authors: Michael Schlame, Mindong Ren, Miriam L Greenberg, Ivan HallerAbstract:Cardiolipin is a unique mitochondrial phospholipid with an atypical fatty acid profile, but the significance of its acyl specificity has not been understood. We explored the enormous combinatorial diversity among cardiolipin species, which results from the presence of four fatty acids in each molecule, by integrated use of high-performance liquid chromatography, mass spectrometry, diacylglycerol species analysis, fatty acid analysis, and selective cleavage of fatty acids by phospholipase A2. The most abundant cardiolipin species from various organisms and tissues (human heart, human lymphoblasts, rat liver, Drosophila, sea urchin sperm, yeast, mung bean hypocotyls) contained only one or two types of fatty acids, which generated a high degree of structural uniformity and molecular symmetry. However, an exception was found in patients with Barth syndrome, in whom an acyltransferase deficiency led to loss of acyl selectivity and formation of multiple molecular species. These results suggest that restriction of the number of fatty acid species, rather than the selection of a particular kind of fatty acid, is the common theme of eukaryotic Cardiolipins. This limits the structural diversity of the cardiolipin species and creates molecular symmetry with implications for the stereochemistry of cardiolipin.
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Effect of Cardiolipin Oxidation on Solid-Phase Immunoassay for Antiphospholipid Antibodies
Thrombosis and Haemostasis, 2001Co-Authors: Michael Schlame, Ivan Haller, Lisa Sammaritano, Thomas BlanckAbstract:SummaryDiagnostic assays for antiphospholipid antibodies are routinely performed on microtitre plates coated with cardiolipin. Here we show that contact between cardiolipin and NUNC-Immuno® plates leads to extensive oxidation, generating a series of peroxy-Cardiolipins which were identified by electrospray ionization mass spectrometry. To investigate the impact of oxidation on the antibody assay, cardiolipin was resolved into 12 molecular species, including oxidized species and non-oxidized species with different degrees of unsaturation. All 12 species reacted under anaerobic conditions with serum from patients with primary antiphospholipid syndrome. Immune reactivity was similar for tetralinoleoyl-cardiolipin, trilinoleoyl-oleoyl-cardiolipin, and peroxyCardiolipins, but somewhat lower for tristearoyl-oleoyl-cardiolipin. Oxidative treatment of cardiolipin with air, cytochrome c, or Cu2+/tert-butylhydroperoxide, either before or during the assay, did not enhance immune reactivity. Similar results were obtained with a monoclonal IgM from lupus-prone mice, that binds cardiolipin in the absence of protein cofactors. We conclude that the solid-phase assay for antiphospholipid antibodies can be supported by various oxidized and nonoxididized molecular species of cardiolipin.
Frédéric M. Vaz - One of the best experts on this subject based on the ideXlab platform.
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The enigmatic role of tafazzin in cardiolipin metabolism.
Biochimica et biophysica acta, 2009Co-Authors: Riekelt H. Houtkooper, Ronald J.a. Wanders, Willem Kulik, Marjolein Turkenburg, Bwee Tien Poll-the, Daniela Karall, Celia Pérez-cerdá, Amelia Morrone, Sabrina Malvagia, Frédéric M. VazAbstract:The mitochondrial phospholipid cardiolipin plays an important role in cellular metabolism as exemplified by its involvement in mitochondrial energy production and apoptosis. Following its biosynthesis, cardiolipin is actively remodeled to achieve its final acyl composition. An important cardiolipin remodeling enzyme is tafazzin, of which several mRNA splice variants exist. Mutations in the tafazzin gene cause the X-linked recessive disorder Barth syndrome. In addition to providing an overview of the current knowledge in literature about tafazzin, we present novel experimental data and use this to discuss the functional role of the different tafazzin variants in cardiolipin metabolism in relation to Barth syndrome. We developed and performed specific quantitative PCR analyses of different tafazzin mRNA splice variants in 16 human tissues and correlated this with the tissue cardiolipin profile. In BTHS fibroblasts we showed that mutations in the tafazzin gene affected both the level and distribution of tafazzin mRNA variants. Transient expression of selected human tafazzin variants in BTHS fibroblasts showed for the first time in a human cell system that tafazzin lacking exon5 indeed functions in cardiolipin remodeling.
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Cardiolipin, the heart of mitochondrial metabolism.
Cellular and molecular life sciences : CMLS, 2008Co-Authors: Riekelt H. Houtkooper, Frédéric M. VazAbstract:Cardiolipin is a unique phospholipid, which is almost exclusively localized in the mitochondrial inner membrane where it is synthesized from phosphatidylglycerol and cytidinediphosphate-diacylglycerol. After primary synthesis, the mature acyl chain composition of cardiolipin is achieved by at least two remodeling mechanisms. In the mitochondrial membrane cardiolipin plays an important role in energy metabolism, mainly by providing stability for the individual enzymes and enzyme complexes involved in energy production. Moreover, cardiolipin is involved in different stages of the mitochondrial apoptotic process and in mitochondrial membrane dynamics. Cardiolipin alterations have been described in various pathological conditions. Patients suffering from Barth syndrome have an altered cardiolipin homeostasis caused by a primary deficiency in cardiolipin remodeling. Alterations in cardiolipin content or composition have also been reported in more frequent diseases such as diabetes and heart failure. In this review we provide an overview of cardiolipin metabolism, function and its role in different pathological states.
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Identification and characterization of human cardiolipin synthase
FEBS letters, 2006Co-Authors: Riekelt H. Houtkooper, Ronald J.a. Wanders, Hana Akbari, Henk Van Lenthe, Willem Kulik, Margrit Frentzen, Frédéric M. VazAbstract:Abstract The mitochondrial phospholipid cardiolipin is synthesized from cytidinediphosphate-diacylglycerol and phosphatidylglycerol, a process catalyzed by the enzyme cardiolipin synthase. In this study, we identified a human candidate gene/cDNA for cardiolipin synthase, C20orf155. Expression of this candidate cDNA in the (cardiolipin synthase-deficient) crd1Δ yeast confirmed that it indeed encodes human cardiolipin synthase. Purified mitochondria of the crd1Δ expressing human cardiolipin synthase were used to characterize the enzyme. It has an alkaline pH optimum, requires divalent cations for activity and appears to have a different substrate preference for cytidinediphosphate-diacylglycerol species when compared to phosphatidylglycerol species. The possible implications for CL synthesis and remodeling are discussed.
Valerian E. Kagan - One of the best experts on this subject based on the ideXlab platform.
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lipidomics detection of brain Cardiolipins in plasma is associated with outcome after cardiac arrest
Critical Care Medicine, 2019Co-Authors: Tamil S. Anthonymuthu, Andrew A. Amoscato, Elizabeth M Kenny, Andrew M Lamade, Hitesh Gidwani, Nicholas Krehel, Amalea Misse, Xiaotian Gao, Adam C Straub, Valerian E. KaganAbstract:OBJECTIVES Brain mitochondrial dysfunction limits neurologic recovery after cardiac arrest. Brain polyunsaturated Cardiolipins, mitochondria-unique and functionally essential phospholipids, have unprecedented diversification. Since brain Cardiolipins are not present in plasma normally, we hypothesized their appearance would correlate with brain injury severity early after cardiac arrest and return of spontaneous circulation. DESIGN Observational case-control study. SETTING Two medical centers within one city. PARTICIPANTS (SUBJECTS) We enrolled 41 adult cardiac arrest patients in whom blood could be obtained within 6 hours of resuscitation. Two subjects were excluded following outlier analysis. Ten healthy subjects were controls. Sprague-Dawley rats were used in asphyxial cardiac arrest studies. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS We developed a high-resolution liquid chromatography/mass spectrometry method and determined Cardiolipins speciation in human brain, heart, and plasma within 6 hours of (return of spontaneous circulation) from 39 patients with cardiac arrest, 5 with myocardial infarction, and 10 healthy controls. Cerebral score was derived from brain-specific Cardiolipins identified in plasma of patients with varying neurologic injury and outcome. Using a rat model of cardiac arrest, Cardiolipins were quantified in plasma, brain, and heart. Human brain exhibited a highly diverse cardiolipinome compared with heart that allowed the identification of brain-specific Cardiolipins. Nine of 26 brain-specific Cardiolipins were detected in plasma and correlated with brain injury. The cerebral score correlated with early neurologic injury and predicted discharge neurologic/functional outcome. Cardiolipin (70:5) emerged as a potential point-of-care marker predicting injury severity and outcome. In rat cardiac arrest, a significant reduction in hippocampal Cardiolipins corresponded to their release from the brain into systemic circulation. Cerebral score was significantly increased in 10 minutes versus 5 minutes no-flow cardiac arrest and naive controls. CONCLUSIONS Brain-specific Cardiolipins accumulate in plasma early after return of spontaneous circulation and proportional to neurologic injury representing a promising novel biomarker.
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characterization of Cardiolipins and their oxidation products by lc ms analysis
Chemistry and Physics of Lipids, 2014Co-Authors: Yulia Y. Tyurina, Vladimir A. Tyurin, Hülya Bayır, Andrew A. Amoscato, Rosario Domingues, Elisabete Maciel, Pedro Domingues, Valerian E. KaganAbstract:Cardiolipins, a class of mitochondria-specific lipid molecules, is one of the most unusual and ancient phospholipids found in essentially all living species. Typical of mammalian cells is the presence of vulnerable to oxidation polyunsaturated fatty acid resides in CL molecules. The overall role and involvement of cardiolipin oxidation (CLox) products in major intracellular signaling as well as extracellular inflammatory and immune responses have been established. However, identification of individual peroxidized molecular species in the context of their ability to induce specific biological responses has not been yet achieved. This is due, at least in part, to technological difficulties in detection, identification, structural characterization and quantitation of CLox associated with their very low abundance and exquisite diversification. This dictates the need for the development of new methodologies for reliable, sensitive and selective analysis of both CLox. LC-MS-based oxidative lipidomics with high mass accuracy instrumentation as well as new software packages are promising in achieving the goals of expedited and reliable analysis of cardiolipin oxygenated species in biosamples.
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Interactions of cardiolipin and lyso-Cardiolipins with cytochrome c and tBid: conflict or assistance in apoptosis
Cell death and differentiation, 2006Co-Authors: Vladimir A. Tyurin, Y.y. Tyurina, A. N. Osipov, Natalia A. Belikova, Liana V. Basova, Alexander A. Kapralov, Hülya Bayır, Valerian E. KaganAbstract:Interactions of cardiolipin and lyso-Cardiolipins with cytochrome c and tBid: conflict or assistance in apoptosis