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PubMed1987

Phosphatidylcholine as the choline donor in sphingomyelin synthesis.

Sphingomyelin synthesis was studied in cultured Novikoff rat hepatoma cells by following transfer of [14C]choline label into sphingomyelin (SPH). The study was facilitated by the fact that prelabeling of the cells with [methyl-14C]choline resulted in rapid accumulation of essentially all the label (approximately 95%) in phosphatidylcholine (PC). The redistribution of PC label during a 15-hr chase was dependent upon the extracellular choline concentration. Under conditions of free choline diffusion (500 microM choline), loss of label from PC was most pronounced, and the percentage of total radioactivity that became trapped in the extracellular water-soluble choline pool was an order of magnitude greater than in low choline medium (27 microM choline). Despite the significant loss of water-soluble label from the cells in high choline medium, SPH labeling proceeded at essentially the same rate at either choline concentration. During the label chase in 500 microM choline, the specific radioactivity of PC decreased, but the specific radioactivity of SPH continued to increase for 9-12 hr until it reached the specific radioactivity of PC. In the presence of 300 microM neophenoxine (NPO), transfer of label from PC into SPH was stimulated. NPO also decreased the specific radioactivity of PC to about the same extent as that of SPH was increased. Because transfer of choline label from PC to SPH was not affected by loss or dilution of water-soluble precursors, and because the specific radioactivity of PC and SPH, in the absence or presence of NPO, responded in a characteristic precursor product fashion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

[methyl-3H]Choline incorporation into MCF7 tumour cells: correlation with proliferation.

PURPOSE: The aim of the study was to investigate the intracellular location of [methyl-(3)H]choline in MCF7 tumour cells and to determine the relationship between [methyl-(3)H]choline incorporation and proliferation. METHODS: Tumour cells were incubated with [methyl-(3)H]choline for 10 min, and then in cold medium to simulate the rapid blood clearance of [methyl-(11)C]choline. Labelled metabolites were then extracted from cells by treating them with organic and aqueous solvents to determine the distribution of tracer between phospholipid and water-soluble metabolite pools. Aqueous extracts were subjected to thin-layer chromatography, ion exchange chromatography and a choline extraction procedure to identify (3)H-containing metabolites. Procedures were carried out on fast- and slow-growing populations of MCF7 cells to determine the relationship between choline incorporation and proliferation. RESULTS: Only about 5% of [methyl-(3)H]choline was present as phospholipid. [methyl-(3)H]choline incorporation was found to be related to S-phase fraction. In another experiment, [methyl-(14)C]choline incorporation was found to be correlated with [methyl-(3)H]thymidine incorporation. The V(max) of choline uptake was found to be increased whilst K(m) was decreased in populations of MCF7 cells with higher proliferative fractions, compared with populations having lower proliferative fractions. CONCLUSION: Choline incorporation into tumour cells under conditions that simulate rapid blood clearance of [methyl-(11)C]choline is correlated with proliferation. Most of the activity (about 95%) was in the non-lipid fraction of the cell.

Breast Neoplasms↗
PubMed1984

Determination of picomole quantities of acetylcholine and choline in physiologic salt solutions.

An assay capable of detecting tens-of-picomole quantities of choline and acetylcholine in milliliter volumes of a physiological salt solution has been developed. Silica column chromatography was used to bind and separate 10-3000 pmol [14C]choline and [14C]acetylcholine standards made up in 3 ml of a bicarbonate-buffered Krebs-Ringer solution. The silica columns bound 95-98% of both choline and acetylcholine. Of the bound choline 84-87% was eluted in 1.5 ml of 0.075 N HCl, whereas 95-98% of the bound acetylcholine was eluted in a subsequent wash with 1.5 ml of 0.030 N HCl in 10% 2-butanone. Vacuum centrifugation of the eluants yielded small white pellets with losses of choline and acetylcholine of only 1%. Dried pellets of unlabeled choline and acetylcholine standards were assayed radioenzymatically using [gamma-32P]ATP, choline kinase, and acetylcholinesterase. The net disintegrations per minute of choline[32P]phosphate product was proportional to both the acetylcholine (10-3000 pmol) and choline (30-3000 pmol) standards. The "limit sensitivity" was 8.5 pmol for acetylcholine and 11.4 pmol for choline. Cross-contamination of the choline assay by acetylcholine averaged 1.3%, whereas contamination of the acetylcholine assay by choline averaged 3.1%.

Acetylcholine↗
PubMed1979

A possible mechanism for the increased oxidation of choline after chronic ethanol ingestion.

An attempt has been made to determine the location of the site at which the metabolism of ethanol interacts with that of choline to produce an increase in the oxidation of choline. The first enzyme in the oxidation pathway for choline, choline dehydrogenase, was assayed using a newly developed spectrophotometric assay and freshly isolated intact rat liver mitochondria. No changes were observed in either 'apparent' V or the 'apparent' Km values of choline dehydrogenase for choline after ethanol ingestion. However, when the choline oxidase system was assayed, a 28% decrease in 'apparent' Km for choline and a 53% increase in 'apparent' V was observed. The effects of ATP on choline oxidase were studied further, and a 29.4% decrease was observed in mitochondrial ATP levels from freshly isolated mitochondria from the ethanol-treated rats. In vitro aging of mitochondria further decreased the level of ATP, and the rate of decrease was considerably faster during the first hour in the mitochondria from the ethanol-treated animals. The decreases in ATP from both control and experimental mitochondria were accompanied by increases in choline oxidase activity. The initial decrease in ATP was correlated with an increase in mitochondrial ATPase activity which may be related to an increase in mitochondria Mg2+. Because chronic ethanol ingestion has resulted in decreased oxidation rates of succinate and beta-hydroxybutyrate while at the same time increasing the oxidation rates of choline, the studies reported here suggest that the effect of chronic ethanol ingestion is primarily on a step that is unique to choline and which probably exists prior to the electron transport chain.

Adenosine Triphosphatases↗
PubMed1988

Red blood cell/plasma choline ratio in elderly depressed and demented patients.

In further study of red blood cell (RBC) and plasma choline concentrations in 160 elderly subjects, we found no significant differences in RBC/plasma choline ratios among depressed, demented, and healthy subjects. On the basis of a smaller sample, we had earlier reported that a significantly higher proportion of Alzheimer patients had RBC/plasma choline ratios greater than 1.9. Thus, it now appears that static RBC choline levels cannot be recommended as a specific marker of Alzheimer's dementia. However, within subgroups of these diagnostic categories, determined by RBC/plasma choline ratios less than or equal to 1.9 or greater than 1.9, consistent differences in electroencephalographic (EEG) sleep measures were found. The subgroup of demented patients with a RBC/plasma choline ratio greater than 1.9 was more impaired on the Blessed Dementia Rating Scale and had less rapid eye movement (REM) sleep than the subgroup with a choline ratio less than or equal to 1.9. Similarly, depressives with a choline ratio less than or equal to 1.9 had a lower REM latency than depressives with a choline ratio greater than 1.9. Finally, depressed-demented (i.e., mixed-symptom) patients with a choline ratio greater than 1.9 showed less sleep continuity disturbance but more indeterminate non-REM sleep (reflecting loss of spindles and K-complexes) than those with lower choline ratios. These differences parallel those previously reported for diagnostically "pure" depressed and demented patients, and they suggest a possible link between peripheral RBC/plasma choline measures and central nervous system function as reflected in sleep physiological alterations.

Aged↗
PubMed2005

Molecular cloning and functional characterization of a neuronal choline transporter from Trichoplusia ni.

A cDNA encoding a high-affinity Na(+)-dependent choline transporter (TrnCHT) was isolated from the CNS of the cabbage looper Trichoplusia ni using an RT-PCR-based approach. The deduced amino acid sequence of the CHT cDNA predicts a 594 amino acid protein of 64.74 kDa prior to glycosylation. TrnCHT has 80%, 79%, 76%, and 58% amino acid identity to putative CHTs from Anopheles gambiae, Drosophila melanogaster and Apis mellifera, and a cloned CHT from Limulus polyphemus, respectively. In situ hybridization of TrnCHT cRNA in whole-mount preparations of caterpillar CNS revealed that TrnCHT mRNA is expressed by hundreds of presumably cholinergic neurons present in both the brain and cortex of all segmental ganglia. Na(+)-dependent [(3)H]-choline uptake was induced in Sf9 cells in vitro following infection with a TrnCHT-expressing recombinant baculovirus. Virally induced [(3)H]-choline uptake was found to approximately equal the endogenous rate of choline uptake in insect cells, seen either after infection with a control virus or in TrnCHT-infected cells exposed to [(3)H]-choline in the absence of Na(+). The Na(+)-dependent component of [(3)H]-choline uptake by TrnCHT-infected cells was saturable with a K(m) for choline transport of 8.4 microM. Several compounds reported to be potent blockers of [(3)H]-choline uptake by cloned vertebrate choline transporters proved to be relatively weak inhibitors of choline uptake by Sf9 cells expressing TrnCHT. Hemicholinium-3 (K(i)=4.1 microM) and two oxoquinuclidium analogues of choline, quireston-A (K(i) approximately 10 microM) and quireston (K(i) approximately 100 microM) inhibited 50% of control uptake only at micromolar concentrations. The endogenous low-affinity Na(+)-independent uptake of [(3)H]-choline was also inhibited by high micromolar concentrations of hemicholinium-3.

Amino Acid Sequence↗
PubMed1999

Choline availability to the developing rat fetus alters adult hippocampal long-term potentiation.

Supplementation with choline during pregnancy in rats causes a long-lasting improvement of visuospatial memory of the offspring. To determine if the behavioral effects of choline are related to physiological changes in hippocampus, the effect of perinatal choline supplementation or deficiency on long-term potentiation (LTP) was examined in hippocampal slices of 6-8 and 12-14 month old rats born to dams consuming a control, choline-supplemented, or a choline-free diet during pregnancy. Stimulating and recording electrodes were placed in stratum radiatum of area CA1 to record extracellular population excitatory postsynaptic potentials (pEPSPs). To induce LTP, a theta-like stimulus train was generated. The amplitude of the stimulus pulses was set at either 10% or 50% of the stimulus intensity which had induced the maximal pEPSP slope on the input/output curve. We found that at both ages, a significantly smaller percentage of slices from perinatally choline-deficient rats displayed LTP after 10% stimulus intensity (compared with control and choline-supplemented rats), and a significantly larger percentage of slices from choline-supplemented rats displayed LTP at 50% stimulus intensity (compared with control and choline-deficient rats). Results reveal that alterations in the availability of dietary choline during discrete periods of development lead to changes in hippocampal electrophysiology that last well into adulthood. These changes in LTP threshold may underlie the observed enhancement of visuospatial memory seen after prenatal choline supplementation and point to the importance of choline intake during pregnancy for development of brain and memory function.

Aging↗
PubMed2000

In vivo changes in free choline level induced by autonomic agonists in mouse organs, including three major salivary glands.

Whether free choline levels are changeable in vivo in response to different types of autonomic agonists was examined in several mouse organs. Upon one subcutaneous injection of isoproterenol, phenylephrine and pilocarpine, choline levels in whole organ decreased, increased and decreased, respectively, in various organs within 30 min and returned to initial levels in a day. In the three major salivary glands, a delayed choline elevation also appeared on day 2 after one isoproterenol injection and subsided by day 6. Only in the three salivary glands more choline was accumulated after 10 once-a-day injections of isoproterenol than after one isoproterenol injection. Neither phenylephrine nor pilocarpine induced comparable choline accumulation in any organs examined. Isoproterenol injection repeated at a 2-day interval augmented the subsequent, delayed choline elevation. Examination with dobutamine and the adenylyl cyclase activator 6-(3-dimethylaminopropionyl)forskolin suggested that isoproterenol-induced immediate choline lowering was down-stream of cAMP synthesis and linked to cAMP more tightly than the choline accumulation, though both choline changes occurred via beta1-adrenergic receptors. Choline levels in the salivary glands also changed depending on the form of diet given and particularly in the parotid gland in parallel with gland weights. These results provide the first evidence for the autonomic control of intracellular choline levels; intracellular choline levels might be an integral part of the autonomic signalling pathway.

Adrenergic alpha-Agonists↗
PubMed1998

A novel Na+/HCO3--codependent choline transporter in the syncytial epithelium of the cestode Hymenolepis diminuta.

Absorption of exogenous choline by the cestode Hymenolepis diminuta was found to be both Na+- and HCO3--dependent and, at pH 6 to 7, accounted for up to 65% of the total choline uptake. Na+/HCO3- dependent choline uptake was activated at approximately 6 mM HCO3- (EC50 approximately 9 mM), and, above 100 mM Na+, the rate of uptake was directly proportional to the Na+ concentration. Atempts to uncouple Na+-dependent uptake from HCO3--dependent uptake were not successful: K+-depolarization was without effect on HCO3--dependent choline uptake, and use of valinoomycin to hyperpolarize the brush-border membrane resulted in inhibition of uptake. Na-/HCO3--dependent choline uptake was not associated with solvent drag. The Na+/HCO3--dependent choline uptake displayed a Q10 of 6.4 (27 degrees to 37 degrees) and a relatively high activation energy of 126 kJ x mol(-1). At pH 6.0 and 7.0, Na-/HCO3--dependent choline uptake rates were similar, but Na+/HCO3--dependent choline uptake was reduced at pH 5.0. The Na+/HCO3--dependent choline uptake, at pH 7.0, displayed a Kt of approximately 500 microM and a Vmax of 4.01 pmol x mg wet weight(-1) x min(-1). The Na+/HCO3--dependent choline uptake was hemicholinium-3 sensitive, but not significantly inhibited by 200 microM bumetanide, 100 microM amiloride, benzamil, or EIPA or by 1 mM 4,4'-diisothiocyano-2,2'-stilbene disulfonate (DIDS) or 4-acetamido-4'-isothiocvanostilbene-2,2'-disulfonic acid (SITS). Although it remains to be shown that HCO3- uptake is coupled directly to both choline and Na+ uptake, the data suggest that choline up take occurs via choline/Na+/HCO3--co-trans porter.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Formation of free choline in brain tissue during in vitro energy deprivation.

Free choline and ATP contents were measured in Mongolian gerbil hippocampal slices (tissue) and incubation media (media) during exposure to 30 min of aglycemia, high potassium, anoxia, or ischemia. Changes in choline levels reflected the degree of energy reduction, lower ATP levels being associated with high choline (4-fold increase during exposure to high potassium and anoxia, and 11-fold increase during ischemia). Media (extracellular) choline was particularly affected and increased about twofold during relatively mild energy depletion (e.g., aglycemia), but tissue choline content was less sensitive to energy reduction. A plot of choline vs. ATP levels indicated a nonlinear correlation, and the sharp increase in choline occurred when ATP values fell to about 2.5 nmol/mg of protein. Inhibition of acetylcholine sterase by 10 microM physostigmine during ischemia did not prevent an increase in choline contents but rather enhanced them, indicating that acetylcholine hydrolysis was not the source of free choline. Formation of free choline was Ca2+ independent. These findings suggest the involvement of phospholipase D and phosphatidylcholine hydrolysis in free choline formation during energy stress. The extent of choline formation may be an indicator of the degree of membranal damage, which in turn reflects damage to the metabolic machinery of the cell.

Acetylcholinesterase↗
PubMed1984

Uptake and output of various forms of choline by organs of the conscious chronically catheterized sheep.

The net uptake and output of plasma unesterified choline, glycerophosphocholine, phosphocholine and lipid choline by organs of the conscious chronically catheterized sheep were measured. There was significant production of plasma unesterified choline by the upper- and lower-body regions and the alimentary tract and uptake by the liver, lungs and kidneys. The upper- and lower-body regions drained by the venae cavae provided the bulk (about 82%) of the total body venous return of plasma unesterified choline. Production of plasma unesterified choline by the alimentary tract was approximately balanced by the plasma unesterified choline taken up by the liver, and was almost equal to the amount of choline secreted in the bile. There was a considerable amount of glycerophosphocholine in the liver and there was production of plasma glycerophosphocholine by the liver and uptake by the lungs and kidneys. Glycerophosphocholine was higher in the plasma of sheep than in that of rats. Plasma phosphocholine was produced by the alimentary tract and kidneys. There was production of plasma lipid choline by the upper- and lower-body regions drained by the venae cavae. The results suggest that the sheep synthesizes substantial amounts of choline in ectrahepatic tissues and has the capacity for extensive retention and recycling of bile choline. These observations, coupled with a slow turnover of the endogenous choline body pool, explain the low requirement of sheep for dietary choline in contrast with non-ruminant species.

Animals↗
PubMed2002

Disruption of choline methyl group donation for phosphatidylethanolamine methylation in hepatocarcinoma cells.

Despite being widely hypothesized, the actual contribution of choline as a methyl source for phosphatidylethanolamine (PE) methylation has never been demonstrated, mainly due to the inability of conventional methods to distinguish the products from that of the CDP-choline pathway. Using a novel combination of stable-isotope labeling and tandem mass spectrometry, we demonstrated for the first time that choline contributed to phosphatidylcholine (PC) synthesis both as an intact choline moiety via the CDP-choline pathway and as a methyl donor via PE methylation pathway. When hepatocytes were labeled with d(9)-choline containing three deuterium atoms on each of the three methyl groups, d(3)-PC and d(6)-PC were detected, indicating that newly synthesized PC contained one or more individually mobilized methyl groups from d(9)-choline. The synthesis of d(3)-PC and d(6)-PC was sensitive to the general methylation inhibitor 3-deazaadenosine and were specific products of PE methylation using choline as a one-carbon donor. While the contribution to the CDP-choline pathway remained intact in hepatocarcinoma cells, contribution of choline to PE methylation was completely disrupted. In addition to a previously identified lack of PE methyltransferase, hepatocarcinoma cells were found to lack the abilities to oxidize choline to betaine and to donate the methyl group from betaine to homocysteine, whereas the usage of exogenous methionine as a methyl group donor was normal. The failure to use choline as a methyl source in hepatocarcinoma cells may contribute to methionine dependence, a widely observed aberration of one-carbon metabolism in malignancy.

Animals↗
PubMed2005

Ad libitum choline intake in healthy individuals meets or exceeds the proposed adequate intake level.

Choline is an essential nutrient for humans that is used to synthesize membrane phospholipids and the neurotransmitter acetylcholine. Betaine, a metabolite of choline, functions as a methyl-group donor in the conversion of homocysteine to methionine, and is important for renal function. Accurate analysis of choline intake was previously not possible because the choline content of most foods was not known. Using new and recently published data on the concentrations of choline in common foods, we measured the choline content of diets consumed ad libitum by healthy adult volunteers housed in a clinical research center and compared these with estimates of choline intake derived from 3-d food records kept by subjects immediately before study enrollment. Mean choline intake in this subject population met or slightly exceeded the current Adequate Intake (AI) of 7 mg/(kg . d) set by the Institute of Medicine. Men and women consumed similar amounts of choline per day (8.4 and. 6.7 mg/kg, respectively; P = 0.11). Choline intakes estimated from the 3-d food records were significantly lower than this (when expressed as mg/kg, or as total mg, but not when normalized to energy intake), suggesting underreporting of food intake. Intake of betaine, which may spare choline utilization as a methyl-group donor, was 5.3 mg/(kg . d) in men and 4.7 mg/(kg . d) in women. Intake of folate, vitamin B-12, and methionine + cysteine, were similar and sufficient in all subjects. The current recommended AI for choline seems to be a good approximation of the actual intake of this nutrient.

Adult↗
PubMed1997

Characterization of human erythrocyte choline transport in chronic renal failure.

BACKGROUND: Membrane transport of choline cations is elevated in renal failure in erythrocytes and cerebral tissue but the origins and clinical importance of this are unknown. METHODS: The membrane transport changes have been characterized using erythrocytes from patients on maintenance haemodialysis (HD), patients on continuous ambulatory peritoneal dialysis (CAPD), and control subjects. Data were obtained from cells depleted of intracellular choline to create zero-trans (ZT) conditions for choline influx. [14C]-choline influx measurements provided a kinetic description of choline flux as the sum of a saturable transport system (defined by Vmax and Km) and an apparent diffusion pathway. Inhibition of choline transport by hemicholinium-3 (HC-3), quinine and N-ethylmaleimide (NEM) has been studied. Actions of three cationic polyamine putative uraemic toxins (putrescine, spermidine, spermine) were tested in control erythrocytes. RESULTS: Mean (SEM) Vmax (ZT) was increased in HD at 45.0 (3.0) mumol/l cells/h and in CAPD at 46.6 (2.5) mumol/l cells/h compared to controls (30.0 (2.0) mumol/l cells/h). Mean Km (ZT) was not significantly altered in HD or CAPD (HD: 6.1 (1.6) microM; CAPD: 5.5 (0.7) microM; control: 5.1 (0.9) microM). The sensitivity of choline transport to the inhibitors tested was not altered in HD. 1.0 mM quinine, 2.0 mM NEM and 1.0 mM HC-3 caused 75-90% inhibition of transport in both HD and controls. For inhibition of ZT influx of 25 microM choline the mean IC50 of quinine was 90 (9) microM in HD and 101 (13) microM in controls (n.s.). The ZT influx of 200 microM choline was not altered by any of the polyamines at concentrations up to 1.0 mM. CONCLUSIONS: Membrane choline transport in CRF remains protein-mediated and exhibits normal substrate and inhibitor affinities; high values of Vmax seem to occur through increased surface expression of an active normal choline transporter. Increases in plasma polyamines cannot explain the choline transport changes in CRF.

Biological Transport↗
PubMed1998

Prenatal availability of choline modifies development of the hippocampal cholinergic system.

Choline supplementation during fetal development [embryonic days (E) 11-17] permanently enhances memory performance in rats. To characterize the neurochemical mechanisms that may mediate this effect, we investigated the development of indices of the cholinergic system in the hippocampus: choline acetyltransferase (ChAT), acetylcholinesterase (AChE), synthesis of acetylcholine (ACh) from choline transported by high-affinity choline uptake (HACU), and potassium-evoked ACh release. During E11-E17, Sprague-Dawley pregnant rats consumed 0 [choline-deficient (ChD)], 1.3 [control (ChC)], and 4.6 [choline-supplemented (ChS)] mmol/(kg x day) of choline, respectively. On postnatal days 17 and 27, hippocampi of the ChD animals had the highest AChE and ChAT activities, and increased synthesis of ACh from choline transported by HACU, concomitant with reductions of tissue ACh content relative to the ChC and ChS rats and an inability to sustain depolarization-evoked ACh release relative to the ChS animals. In contrast, AChE and ChAT activities, and ACh synthesized from choline transported by HACU, were lowest in ChS rats whereas depolarization-evoked ACh release was the highest. This pattern of changes suggests that the hippocampus of the ChD animals is characterized by fast ACh recycling and efficient choline reutilization for ACh synthesis, presumably to maintain adequate ACh release despite the decrease of the ACh pool, whereas in the ChS animals ACh turnover and choline recycling is slower while the evoked release of ACh is high. Together, the data show a complex adaptive response of the hippocampal cholinergic system to prenatal choline availability and provide a novel example of developmental plasticity in the nervous system governed by the supply of a single nutrient.

Acetylcholine↗
PubMedDate not supplied

Carbon-11 choline positron emission tomography in musculoskeletal tumors: comparison with fluorine-18 fluorodeoxyglucose positron emission tomography.

PURPOSE: Recently, a new positron emission tomography (PET) tracer, carbon-11 choline, has been introduced in oncology investigations, but the role of choline PET in musculoskeletal tumor evaluation has not been previously examined. This is the first trial to investigate the utility of choline PET in evaluating musculoskeletal tumors in comparison with fluorine-18 fluoro-2-deoxy-D-glucose (FDG) PET. METHOD: Thirty-three patients were examined with both choline PET and FDG PET, of which standardized uptake values (SUVs) were used for evaluation of the lesions. To decide the appropriate cutoff value and compare the two PET studies, receiver operating characteristic curve analysis was used. The binomial test was used for comparison of sensitivities between choline PET and FDG PET. RESULTS: A significant correlation (r = 0.537, P = 0.0013) between choline and FDG SUVs was noted for all lesions (n = 33). Mean SUVs for malignant tumors were significantly higher than those for benign lesions in both choline PET and FDG PET. Using a cutoff value of 2.7 for choline SUVs, the sensitivity for correctly diagnosing malignancy was 92.3% (12/13) with a specificity of 90.0% (18/20), resulting in an accuracy rate of 90.9%. With use of a cutoff value of 3.3 for SUVs in FDG PET, the sensitivity was 84.6% (11/13) with a specificity of 80.0% (16/20), resulting in an accuracy rate of 81.8%. The receiver operating characteristic curves of two analyses showed that the mean area under the curve value of choline PET (0.9577 +/- 0.041) was significantly greater (P = 0.0488) than that of FDG PET (0.8192 +/- 0.0806). There was no significant difference in sensitivity and specificity between choline PET and FDG PET analysis using either the binomial test (P = 0.4531) or McNemar test (P = 0.371). CONCLUSION: Choline PET analysis may not be inferior to FDG PET analysis for differentiating malignant from benign musculoskeletal tumors. The advantages of choline PET were shorter examination time and little retention in the bladder; therefore, this modality may be useful for preoperative planning for musculoskeletal tumors, especially for lesions around the hip joints.

Adolescent↗
PubMed1990

Choline uptake by cerebral capillary endothelial cells in culture.

A passage of choline from blood to brain and vice versa has been demonstrated in vivo. Because of the presence of the blood-brain barrier, such passage takes place necessarily through endothelial cells. To get a better understanding of this phenomenon, the choline transport properties of cerebral capillary endothelial cells have been studied in vitro. Bovine endothelial cells in culture were able to incorporate [3H]choline by a carrier-mediated mechanism. Nonlinear regression analysis of the uptake curves suggested the presence of two transport components in cells preincubated in the absence of choline. One component showed a Km of 7.59 +/- 0.8 microM and a maximum capacity of 142.7 +/- 9.4 pmol/2 min/mg of protein, and the other one was not saturable within the concentration range used (1-100 microM). When cells were preincubated in the presence of choline, a single saturable component was observed with a Km of 18.5 +/- 0.6 microM and a maximum capacity of 452.4 +/- 42 pmol/2 min/mg of protein. [3H]Choline uptake by endothelial cells was temperature dependent and was inhibited by the choline analogs hemicholinium-3, deanol, and AF64A. The presence of ouabain or 2,4-dinitrophenol did not affect the [3H]choline transport capacity of endothelial cells. Replacement of sodium by lithium and cell depolarization by potassium partially inhibited choline uptake. When cells had been preincubated without choline, recently transported [3H]choline was readily phosphorylated and incorporated into cytidine-5'-diphosphocholine and phospholipids; however, under steady-state conditions most (63%) accumulated [3H]choline was not metabolized within 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

RBC-choline: changes by lithium and relation to prophylactic response.

Red blood cell (RBC)- and plasma-choline levels were measured in patients on lithium (n = 96), antidepressants (n = 32) and neuroleptics (n = 51), and in 25 healthy drug-free controls. Lithium patients exhibited highly increased RBC- and slightly increased plasma-choline levels compared with controls (P less than 0.001 and P less than 0.05, respectively); the choline ratio (RBC-/plasma-choline) was elevated almost to the same extent as RBC-choline (P less than 0.001). With antidepressants RBC-choline and choline ratios were slightly reduced (P less than 0.05), whereas neuroleptics showed no effect on choline levels. 79% of lithium patients were responders (reduction in hospitalizations with lithium), 21% were non-responders (no reduction or increase in hospitalizations). Choline ratio exhibited a significant relation to prophylactic lithium response, but lithium ratio did not. The percentage of non-responders was significantly higher in patients with a choline ratio exceeding 100 than in patients with a choline ratio below this cut-off (P less than 0.01). Thus, the increase of RBC-choline and choline ratios appears to be an effect specific for lithium and might be related to the outcome of lithium prophylaxis.

Age Factors↗