Acetylcarnitine increases membrane cytoskeletal protein-protein interactions

Butterfield, D. Allan; Rangachari, Anuradha

doi:10.1016/0024-3205(93)90221-n

Cited by 17 publications

(8 citation statements)

References 26 publications

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“…It would appear that carnitine is able to strengthen the bonds among the proteins that form the cytoskeleton, and that such action is responsible for increasing membrane elasticity, which in turn improves RBC rheology. In support of these experimental findings, it has also been observed that carnitine significantly enhances interaction among membrane-skeleton proteins within the cell membrane (16).…”

Section: Altered Composition Of the Erythrocyte Cell Membranesupporting

confidence: 68%

Erythrocyte Alterations and Increased Cardiovascular Risk in Chronic Renal Failure

et al. 2017

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Patients suffering from chronic renal failure have a higher burden of cardiovascular events, which increases in a dose-dependent fashion as renal function worsens. Increased cardiovascular risk in these patients is thought to be mediated by the simultaneous presence of both traditional and non-traditional cardiovascular risk factors, the latter being associated with renal impairment. Red blood cells are usually considered as carries of nutrients for tissues and respiratory gases, less so as compartments essential to vascular integrity. However, erythrocyte number, size, and integrity seem to severely affect cardiovascular morbidity and mortality as established in recent clinical studies with large patient cohorts. In particular, the role of red blood cells in chronic renal failure tends only to be considered exclusively in relation to a change in their number. However, these cells in the uremic milieu are prone to many alterations, which may adversely affect the cardiovascular system. In this review, we highlight the main qualitative erythrocyte alterations that may have a pathophysiologic role in the elevated cardiovascular risk of chronic renal failure.

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Section: Altered Composition Of the Erythrocyte Cell Membranesupporting

confidence: 68%

Erythrocyte Alterations and Increased Cardiovascular Risk in Chronic Renal Failure

et al. 2017

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“…26 ALCAR also increases the membrane molecular dynamics of brain microsomes and liposomes produced from rat brain microsomal lipid extracts 27 and carnitine partially shares this effect with ALCAR. Butterfield and Rangachari 28 showed that ALCAR increases membrane cytoskeletal protein-protein interactions, but no change in lipid order or molecular dynamics could be demonstrated. Since carnitine was reported to exert the same effect, these authors suggested that the acetyl group of ALCAR is not hydrophobic enough to direct ALCAR to the bilayer phase of the membrane.…”

Section: Alcar's Modulation Of Membranesmentioning

confidence: 99%

“…94 However, ALCAR did not have any normalizing effect on catecholamine concentrations, tyrosine hydroxylase, neurofilament or glial fibrillary acid protein, suggesting the ALCAR protective action could be related to energy metabolism and not to effects on dopaminergic systems. Forloni et al 95 reported that ALCAR reduces the mortality in rat brain cell cultures after exposure to neurotoxic stimuli including NMDA and A␤ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) peptide and ALCAR can inhibit cell apoptosis and retard DNA fragmentation and nuclear condensation in a teratocarcinoma cell line in which apoptosis was induced by serum deprivation. 96 Although this last study was done in a non-brain tissue, it may indicate that ALCAR could have similar effects in CNS tissue.…”

Section: Alcar's Protection Of Brain Tissue Against Neurotoxinsmentioning

confidence: 99%

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

2000

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Acetyl-L-carnitine (ALCAR) contains carnitine and acetyl moieties, both of which have neurobiological properties. Carnitine is important in the ␤-oxidation of fatty acids and the acetyl moiety can be used to maintain acetyl-CoA levels. Other reported neurobiological effects of ALCAR include modulation of: (1) brain energy and phospholipid metabolism; (2) cellular macromolecules, including neurotrophic factors and neurohormones; (3) synaptic morphology; and (4) synaptic transmission of multiple neurotransmitters. Potential molecular mechanisms of ALCAR activity include: (1) acetylation of -NH 2 and -OH functional groups in amino acids and N terminal amino acids in peptides and proteins resulting in modification of their structure, dynamics, function and turnover; and (2) acting as a molecular chaperone to larger molecules resulting in a change in the structure, molecular dynamics, and function of the larger molecule. ALCAR is reported in double-blind controlled studies to have beneficial effects in major depressive disorders and Alzheimer's disease (AD), both of which are highly prevalent in the geriatric population. Molecular Psychiatry (2000) 5, 616-632.

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“…Despite the lack of mitochondria, evidence for a role of LC in red cell metabolism is suggested by the presence of LC and carnitine palmitoyl-transferase in the red cell, and their involvement in membrane phospholipid fatty acid turnover [17][18][19]. Furthermore, LC and its short chain esters were found to favorably affect the biophysical status and rheological properties of erythrocyte membrane under normal and adverse conditions [20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Cellular properties of human erythrocytes preserved in saline–adenine–glucose–mannitol in the presence of L‐carnitine

Arduini¹,

Minetti

Ciana

et al. 2006

American J Hematol

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L-Carnitine (LC) in the preservation medium during storage of red blood cells (RBC) can improve the mean 24-hr percent recovery in vivo and increase RBC life-span after reinfusion. The purpose of the study was to investigate the differences in the biochemical properties of RBCs stored in the presence or absence of LC, and the cell-age related responses to storage conditions and to LC. RBC concentrates in saline-adenine-glucose-mannitol (SAG-M) were stored in the presence or absence of 5 mM LC at 48C for up to 8 weeks. RBC subpopulations of different densities were prepared by centrifugation on Stractan density gradient. Cells were sampled at 0, 3, 6, and 8 weeks, and hematological and cellular properties analyzed (MCV, MCHC, 4.1a/4.1b ratio as a cell age parameter, intracellular Na + and K + ). After 6 weeks, MCV of RBC stored in the presence of LC was lower than that of controls (6 weeks MCV: controls 95.4 ± 1.8 fl; LC 91.5 ± 2.0 fl; n = 6; P < 0.005). This was due to swelling of control cells, and affected mainly older RBCs. LC appeared to reduce or retard cell swelling. Among the osmotically active substances whose changes during storage could contribute to cell swelling, only intracellular Na

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Acetylcarnitine increases membrane cytoskeletal protein-protein interactions

Cited by 17 publications

References 26 publications

Erythrocyte Alterations and Increased Cardiovascular Risk in Chronic Renal Failure

Erythrocyte Alterations and Increased Cardiovascular Risk in Chronic Renal Failure

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

Cellular properties of human erythrocytes preserved in saline–adenine–glucose–mannitol in the presence of L‐carnitine

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