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PubMed1968

Mechanism of choline O-sulphate utilization in fungi.

1. The position of the enzyme blocks in a number of parathiotrophic mutants of Aspergillus nidulans A 69 and mutants A and C of a biotinless mutant of Aspergillus nidulans were examined by nutritional and heterokaryosis experiments and by assay in vitro of enzyme systems and specific enzymes. 2. The mutants were in five groups: A and C blocked at sulphate transport; gamma at ATP sulphurylase; iota at adenosine 5'-sulphatophosphate kinase; eta at the adenosine 3'-phosphate 5'-sulphatophosphate reductase system; alpha, beta and zeta between sulphite and thiosulphate. 3. The ability of the various mutants to synthesize choline O-sulphate in vivo and in vitro and to utilize choline O-sulphate as a source of sulphur indicated that the utilization of endogenously formed choline O-sulphate involved the splitting off of inorganic sulphate, which was then reduced. 4. Choline O-sulphate acted as a source of choline for cholineless strains of Neurospora crassa, suggesting that choline O-sulphate breakdown occurred by simple hydrolysis involving a choline sulphatase. 5. After de-repression of mycelia by growing for a period on a sulphur-free medium the presence of choline sulphatase in physiologically significant amounts was demonstrated in all the A. nidulans strains tested. 6. Choline O-sulphate is transported across the mycelial wall by a mechanism different to that responsible for inorganic sulphate transport.

Adenine Nucleotides↗
PubMed1982

The incorporation of solubilized choline-transport activity into liposomes.

The choline-transport system has been solubilized from synaptic plasma membrane by using either sodium cholate or Triton X-100, and re-incorporated into unilamellar liposomes by using the technique of cholate dialysis. The criteria of choline-transport activity were saturability by excess choline, inhibition by hemicholinium-3, and trans-activation (i.e. stimulation of the uptake of [3H]choline into liposomes by preloading them with non-radioactive choline). Liposomes prepared from detergent extracts of synaptic plasma membrane and added lipid showed uptake of [3H]choline fulfilling these three criteria. Data on choline-transport activity of liposomes at various choline concentrations could be interpreted as implying that the transport system has two apparent Km values (2-5 microM and 50-100 microM), or alternatively that the system is composed of two or more negatively co-operating subunits (or units). It was shown by t.l.c. that the transported radioactivity was choline and that it was not significantly acetylated. Replacing Na+ by K+ on the outside of these liposomes partially inhibited uptake, and the formation of a potential gradient (inside negative) with valinomycin increased the total but not the saturable components of uptake when liposomes were prepared in a K+ medium, and transferred to an Na+ medium.

Adenosine Triphosphate↗
PubMed2000

Do sequence repeats play an equivalent role in the choline-binding module of pneumococcal LytA amidase?

LytA amidase breaks down the N-acetylmuramoyl-l-alanine bonds in the peptidoglycan backbone of Streptococcus pneumoniae. Its polypeptide chain has two modules: the NH(2)-terminal module, responsible for the catalytic activity, and the COOH-terminal module, constructed by six tandem repeats of 20 or 21 amino acids (p1-p6) and a short COOH-terminal tail. The polypeptide chain must contain at least four repeats to efficiently anchor the autolysin to the choline residues of the cell wall. Nevertheless, the catalytic efficiency decreases by 90% upon deletion of the final tail. The structural implications of deleting step by step the two last (p5 and p6) repeats and the final COOH-tail and their effects on choline-amidase interactions have been examined by comparing four truncated mutants with LytA amidase by means of different techniques. Removal of this region has minor effects on secondary structure content but significantly affects the stability of native conformations. The last 11 amino acids and the p5 repeat stabilize the COOH-terminal module; each increases the module transition temperature by about 6 degrees C. Moreover, the p5 motif also seems to participate, in a choline-dependent way, in the stabilization of the NH(2)-terminal module. The effects of choline binding on the thermal stability profile of the mutant lacking the p5 repeat might reflect a cooperative pathway providing molecular communication between the choline-binding module and the NH(2)-terminal region. The three sequence motives favor the choline-amidase interaction, but the tail is an essential factor in the monomer <--> dimer self-association equilibrium of LytA and its regulation by choline. The final tail is required for preferential interaction of choline with LytA dimers and for the existence of different sets of choline-binding sites. The p6 repeat scarcely affects the amidase stability but could provide the proper three-dimensional orientation of the final tail.

Choline↗
PubMed2004

Genome-wide analysis reveals inositol, not choline, as the major effector of Ino2p-Ino4p and unfolded protein response target gene expression in yeast.

In the yeast Saccharomyces cerevisiae, the transcription of many genes encoding enzymes of phospholipid biosynthesis are repressed in cells grown in the presence of the phospholipid precursors inositol and choline. A genome-wide approach using cDNA microarray technology was used to profile the changes in the expression of all genes in yeast that respond to the exogenous presence of inositol and choline. We report that the global response to inositol is completely distinct from the effect of choline. Whereas the effect of inositol on gene expression was primarily repressing, the effect of choline on gene expression was activating. Moreover, the combination of inositol and choline increased the number of repressed genes compared with inositol alone and enhanced the repression levels of a subset of genes that responded to inositol. In all, 110 genes were repressed in the presence of inositol and choline. Two distinct sets of genes exhibited differential expression in response to inositol or the combination of inositol and choline in wild-type cells. One set of genes contained the UASINO sequence and were bound by Ino2p and Ino4p. Many of these genes were also negatively regulated by OPI1, suggesting a common regulatory mechanism for Ino2p, Ino4p, and Opi1p. Another nonoverlapping set of genes was coregulated by the unfolded protein response pathway, an ER-localized stress response pathway, but was not dependent on OPI1 and did not show further repression when choline was present together with inositol. These results suggest that inositol is the major effector of target gene expression, whereas choline plays a minor role.

Basic Helix-Loop-Helix Proteins↗
PubMed2005

Phosphorylation of the yeast choline kinase by protein kinase C. Identification of Ser25 and Ser30 as major sites of phosphorylation.

The Saccharomyces cerevisiae CKI1-encoded choline kinase catalyzes the committed step in phosphatidylcholine synthesis via the Kennedy pathway. The enzyme is phosphorylated on multiple serine residues, and some of this phosphorylation is mediated by protein kinase A. In this work we examined the hypothesis that choline kinase is also phosphorylated by protein kinase C. Using choline kinase as a substrate, protein kinase C activity was dose- and time-dependent and dependent on the concentrations of choline kinase (K(m) = 27 microg/ml) and ATP (K(m) = 15 microM). This phosphorylation, which occurred on a serine residue, was accompanied by a 1.6-fold stimulation of choline kinase activity. The synthetic peptide SRSSSQRRHS (V5max/K(m) = 17.5 mm(-1) micromol min(-1) mg(-1)) that contains the protein kinase C motif for Ser25 was a substrate for protein kinase C. A Ser25 to Ala (S25A) mutation in choline kinase resulted in a 60% decrease in protein kinase C phosphorylation of the enzyme. Phosphopeptide mapping analysis of the S25A mutant enzyme confirmed that Ser25 was a protein kinase C target site. In vivo the S25A mutation correlated with a decrease (55%) in phosphatidylcholine synthesis via the Kennedy pathway, whereas an S25D phosphorylation site mimic correlated with an increase (44%) in phosphatidylcholine synthesis. Although the S25A (protein kinase C site) mutation did not affect the phosphorylation of choline kinase by protein kinase A, the S30A (protein kinase A site) mutation caused a 46% reduction in enzyme phosphorylation by protein kinase C. A choline kinase synthetic peptide (SQRRHSLTRQ) containing Ser30 was a substrate (V(max)/K(m) = 3.0 mm(-1) micromol min(-1) mg(-1)) for protein kinase C. Comparison of phosphopeptide maps of the wild type and S30A mutant choline kinase enzymes phosphorylated by protein kinase C confirmed that Ser30 was also a target site for protein kinase C.

Adenosine Triphosphate↗
PubMed1992

Choline: an important nutrient in brain development, liver function and carcinogenesis.

Choline is required to make certain phospholipids which are essential components of all membranes. It is a precursor for biosynthesis of the neurotransmitter acetylcholine and also is an important source of labile methyl groups. Much attention has been given to the effect of supplemental choline upon brain function, i.e., enhancement of acetylcholine synthesis and release. In addition, choline supplements administered to rats in utero or shortly after birth permanently after brain function. The mechanisms for this effect is unknown and under investigation at this time. Healthy humans fed diets deficient in choline, and humans fed parenterally have decreased plasma choline concentrations and develop liver dysfunction that is similar to that seen in choline-deficient animals. In experimental animals, fatty liver occurs in choline deficiency because phosphatidylcholine synthesis is required for very low-density lipoprotein secretion. This accumulation of lipids in liver may explain why choline-deficient rats spontaneously develop hepatocarcinoma. We found that choline deficiency was associated with the accumulation of 1,2-diacylglycerol, an activator of protein kinase C. Several lines of evidence indicate that cancers might develop secondary to abnormalities in protein kinase C-mediated signal transduction.

Alanine Transaminase↗
PubMedDate not supplied

The effect of lecithin supplementation on plasma choline concentrations during a marathon.

BACKGROUND: Previous studies have shown that plasma and urinary free choline concentrations decrease significantly during a marathon, and that these decreases may be associated with decreased performance. OBJECTIVE: In a pilot study, we sought to determine whether lecithin supplementation prior to a marathon would maintain plasma free and urinary choline concentrations and improve performance versus placebo. METHODS: 12 accomplished marathon runners, males (7) and females (5), 21 to 50 years of age were randomized to receive lecithin (4 capsules BID; PhosChol 900) or placebo beginning one day prior to the 2000 Houston-Methodist Health Care Marathon. The lecithin supplement provided approximately 1.1 g of choline on a daily basis (2.2 g total). Runners estimated finish time based on recent performance and training. Fasting, pre- and post-marathon plasma and a five-hour urine collection were analyzed for free choline and plasma for phospholipid-bound choline. Pre-race predicted, as well as the actual finish time, were recorded. RESULTS: All subjects completed the marathon. Plasma free choline decreased significantly in the placebo group and increased significantly in the lecithin group (9.6 +/- 3.6 to 7.0 +/- 3.6 nmol/mL vs. 8.0 +/- 1.2 to 11.7 +/- 3.6 nmol/mL, p = 0.001 for the delta between groups). No significant changes in plasma phospholipid-bound choline concentration were observed. There was a non-significant decrease in urine free choline in both groups. Actual finish time was 256.3 +/- 46.3 minutes for the lecithin group vs. 240.8 +/- 62.0 for the placebo group and the actual:predicted time was 1.03 +/- 0.06 (lecithin) and 1.07 +/- 0.08 (placebo), p = 0.36. CONCLUSION: Short-term lecithin supplementation prior to a marathon maintains normal plasma free choline concentration during the race, but failed to improve performance.

Adult↗
PubMed2006

Block of muscle nicotinic receptors by choline suggests that the activation and desensitization gates act as distinct molecular entities.

Ion channel block in muscle acetylcholine nicotinic receptors (AChRs) is an extensively reported phenomenon. Yet, the mechanisms underlying the interruption of ion flow or the interaction of the blocker with the channel's gates remain incompletely characterized. In this paper, we studied fast channel block by choline, a quaternary-ammonium cation that is also an endogenous weak agonist of this receptor, and a valuable tool in structure-function studies. Analysis of the single-channel current amplitude as a function of both choline concentration and voltage revealed that extracellular choline binds to the open-channel pore with millimolar apparent affinity (K(B) congruent with 12 mM in the presence of approximately 155 mM monovalent and 3.5 mM divalent, inorganic cations), and that it permeates the channel faster than acetylcholine. This, together with its relatively small size ( approximately 5.5 A along its longest axis), suggests that the pore-blocking choline binding site is the selectivity filter itself, and that current blockages simply reflect the longer-lived sojourns of choline at this site. Kinetic analysis of single-channel traces indicated that increasing occupancy of the pore-blocking site by choline (as judged from the reduction of the single-channel current amplitude) is accompanied by the lengthening of (apparent) open interval durations. Consideration of a number of possible mechanisms firmly suggests that this prolongation results from the local effect of choline interfering with the operation of the activation gate (closure of blocked receptors is slower than that of unblocked receptors by a factor of approximately 13), whereas closure of the desensitization gate remains unaffected. Thus, we suggest that these two gates act as distinct molecular entities. Also, the detailed understanding gained here on how choline distorts the observed open-time durations can be used to compensate for this artifact during activation assays. This correction is necessary if we are to understand how choline binds to and gates the AChR.

Animals↗
PubMed1968

Concentrative accumulation of choline by human erythrocytes.

Influx and efflux of choline in human erythrocytes were studied using (14)C-choline. When incubated at 37 degrees C with physiological concentrations of choline erythrocytes concentrate choline; the steady-state ratio is 2.08 +/- 0.23 when the external choline is 2.5 microM and falls to 0.94 +/- 0.13 as the external concentration is raised to 50 microM. During the steady state the influx of choline is consistent with a carrier system with an apparent Michaelis constant of 30 x 10(-6) and a maximum flux of 1.1 micromoles per liter cells per min. For the influx into cells preequilibrated with a choline-free buffer the apparent Michaelis constant is about 6.5 x 10(-6)M and the maximum flux is 0.22 micromole per liter cells per min. At intracellular concentrations below 50 micromole per liter cells the efflux in the steady state approximates first order kinetics; however, it is not flux through a leak because it is inhibited by hemicholinium. Influx and efflux show a pronounced exchange flux phenomenon. The ability to concentrate choline is lost when external sodium is replaced by lithium or potassium. However, the uphill movement of choline is probably not coupled directly to the Na(+) electrochemical gradient.

Biological Transport, Active↗
PubMed1976

Significance of choline synthesis in the oxidation of the methionine methyl group in rats.

Experiments were conducted to assess the significance of de novo choline synthesis in the oxidative metabolism of the methyl group of L-methionine in the rat. Comparison of the rates of 14CO2 production by rats fed diets containing equimolar or equal methyl loads of [methyl-14C]methionine, [methyl-14C] choline, [methyl-14C] betaine and [methyl-14C] sarcosine revealed that the methyl groups of choline, betaine and sarcosine were oxidized at rates nearly equivalent to or exceeding that of the methionine methyl group. However, the results of a second series of in vivo experiments using non-radioactive choline or betaine as intermediary trapping pools indicated that little newly formed radioactive choline was released from tissue phospholipid choline during the period of rapid 14CO2 production from [14CH3] methionine. Incorporation of the methionine methyl group into phospholipid choline by incubated liver slices was strongly inhibited by 2-methoxyethanol without a parallel inhibition of methionine methyl group oxidation. Results of these in vitro studies also indicated that the metabolic pathway responsible for the transfer of the methionine methyl group into choline and that responsible for its oxidation to CO2 differ widely in the ease with which they can be saturated by L-methionine. It is concluded that essentially all of the methionine methyl group oxidation in vitro and that occurring during the absorptive period in vivo must depend primarily on pathways other than those leading to the synthesis of choline.

Adaptation, Physiological↗
PubMed1989

Conversion of dietary choline to trimethylamine and dimethylamine in rats: dose-response relationship.

Trimethylamine (TMA) and dimethylamine (DMA) are normal components of human urine and are precursors of dimethylnitrosamine, a potent carcinogen. In part, DMA and TMA are products of the metabolism of dietary choline by intestinal bacteria. Most TMA formed in the intestinal tract is later oxidized and excreted as trimethylamine oxide (TMAO). Humans treated with large doses of choline smell "fishy" (the odor of TMA). Humans ingest choline as part of foods, and yet rarely smell fishy, suggesting that TMA formation must depend upon the dose of choline ingested. We found that, in adult rats, at low doses of choline (1.5 mmol/kg body wt) only 9 mumol choline (6% of the dose) reached the part of the intestine which is colonized by bacteria (the cecum and colon). After administration of 15 mmol choline/kg body wt, 237 mumol (16% of the dose) reached the cecum and colon. At both doses, 64-65% of the administered choline was absorbed from the intestine by 3 h after the dose. We found that orally administered choline slightly increased TMA and TMAO excretion at doses of choline smaller than 7 mmol/kg body wt, but that there was a disproportionately large increase in TMA excretion per 24 h when larger doses were administered (from 11 mumol TMA and 100 mumol TMAO per kg body wt in controls to 226 mumol TMA and 3617 mumol TMAO per kg body wt in rats treated with 15 mmol choline/kg body wt).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Choline supplementation alters carnitine homeostasis in humans and guinea pigs.

We have previously shown that supplementary choline causes significant decreases in urinary excretion of carnitine in humans. The objectives of the present work were to study this interaction in a different human population and on other body pools of carnitine in an animal model. In young adult women, daily choline supplementation (20 mg/kg body wt) resulted in a 75% lower urinary carnitine excretion than in controls, without significantly altering plasma carnitine concentrations. Supplementary choline was added to the ground diet of Sprague-Dawley rats (2.5 g/kg diet) and guinea pigs (3 g/kg diet). Choline supplementation had no effect on plasma concentrations or urinary excretion of carnitine in the rats. In guinea pigs, however, choline supplementation resulted in a significantly lower urinary excretion and higher plasma total carnitine concentrations. The skeletal muscle carnitine concentration was higher in the choline-supplemented guinea pigs, but not significantly higher in other tissues. These studies demonstrated that choline supplementation results in decreased urinary excretion of carnitine in young adult women, that guinea pigs are a suitable animal model for studying the effect of choline supplementation on carnitine status in humans, and that choline results in a conservation of carnitine in guinea pigs and perhaps in humans.

3-Hydroxybutyric Acid↗
PubMed2005

Dietary S-methylmethionine, a component of foods, has choline-sparing activity in chickens.

Acid hydrolysis of dehulled soybean meal (SBM) and corn gluten meal (CGM) followed by chromatographic amino acid analysis (ninhydrin detection) revealed substantial quantities of S-methylmethionine (SMM) in both ingredients (1.65 g SMM/kg SBM; 0.5 g SMM/kg CGM). Young chicks were used to quantify the methionine- (Met) and choline-sparing bioactivity of crystalline L-SMM, relative to L-Met and choline chloride standards in 3 assays. A soy isolate basal diet was developed that could be made markedly deficient in Met, choline, or both. When singly deficient in choline or in both choline and Met, dietary SMM addition produced a significant (P < 0.01) growth response. In Assay 2, dietary SMM did not affect (P > 0.10) growth of chicks fed a Met-deficient, choline-adequate diet. A standard-curve growth assay revealed choline bioactivity values (wt:wt) of 14.2 +/- 0.8 and 25.9 +/- 5.1 g/100 g SMM based on weight gain and gain:food responses, respectively. A fourth assay, using standard-curve procedures, showed choline bioactivity values of 20.1 +/- 1.1 and 22.9 +/- 1.7 g/100 g SMM based on weight gain and gain:food responses, respectively. It is apparent that SMM in foods and feeds has methylation bioactivity, and this has implications for proper assessment of dietary Met and choline requirements as well as their bioavailability in foods and feeds.

Animals↗
PubMed2004

Evaluation of the potential of triethanolamine to alter hepatic choline levels in female B6C3F1 mice.

Triethanolamine (TEA), a widely used nongenotoxic alcohol-amine, has recently been reported to cause an increased incidence of liver tumors in female B6C3F1 mice, but not in males nor in Fischer 344 rats. Choline deficiency induces liver cancer in rodents, and TEA could compete with choline uptake into tissues. The potential of TEA to cause choline deficiency in the liver of these mice as a mode of tumorigenesis was investigated. Groups of female B6C3F1 mice were administered 0 (vehicle) or a maximum tolerated dosage (MTD) of 1000 mg/kg/day TEA (Trial I) and 0, 10, 100, 300, or 1000 mg/kg/day TEA (Trial II) in acetone vehicle via skin painting 5 days/week for 3 weeks. Female CDF(R) rats were also administered 0 or an MTD dosage of 250 mg/kg/day TEA (Trial II) in a similar manner. No clinical signs of toxicity were noted, and upon sacrifice, levels of hepatic choline, its primary storage form, phosphocholine (PCho), and its primary oxidation product, betaine, were determined. A statistically significant decrease in PCho and betaine, was observed at the high dosage (26-42%) relative to controls and a dose-related, albeit variable, decrease was noted in PCho levels. Choline levels were also decreased 13-35% at the high dose level in mice. No changes in levels of choline or metabolites were noted in treated rats. A subsequent evaluation of the potential of TEA to inhibit the uptake of (3)H-choline by cultured Chinese Hamster Ovary Cells revealed a dose-related effect upon uptake. It was concluded that TEA may cause liver tumors in mice via a choline-depletion mode of action and that this effect is likely caused by the inhibition of choline uptake by cells.

Administration, Topical↗
PubMed1996

Dietary choline supplementation in pregnant rats increases hippocampal phospholipase D activity of the offspring.

Supplementation with choline during pregnancy in rats causes a long-lasting improvement of visuospatial memory of the offspring. The biochemical mechanism of this effect may be related to the function of choline as a precursor of phosphatidylcholine (PC), the substrate of a receptor-stimulated enzyme, phospholipase D (PLD). PLD activation initiates the sequential formation of two intracellular messengers, phosphatidic acid and 1,2-sn-diacylglycerol. We hypothesized that prenatal choline status may cause long-term modulation of PLD-catalyzed PC hydrolysis in the hippocampus, a brain region implicated in visuospatial memory functions. PLD activity was determined in hippocampal slices prelabeled with [3H]glycerol or [3H]oleic acid by measuring the PLD-catalyzed formation of [3H]phosphatidylpropanol in the presence of 1-propanol. Slices were obtained from male pups born to mothers consuming a control diet, a choline-supplemented diet, or a choline-free diet from days 11 to 17 of pregnancy. The radiolabeling of phospholipid classes was unaffected by the treatments. Prenatal choline supplementation significantly increased basal PLD activity in [3H]glycerol-labeled slices [by 46% of controls on postnatal day (P) 7 and by 36% on P21], and [3H]oleate-labeled slices (by 91% on P7), as well as glutamate-stimulated PLD activity in [3H]oleate-labeled slices (by 60% on P7). Prenatal choline deficiency failed to alter PLD activity. The actions of choline apparently required intact cells because in vitro assays of PLD activity in hippocampal homogenates, using fluorescent NBD-PC as substrate, revealed no differences between groups. The results show that prenatal choline supplementation up-regulates basal and receptor-stimulated PLD activity in the hippocampus during postnatal development.

Animals↗
PubMed2006

Staging performance of carbon-11 choline positron emission tomography/computed tomography in patients with bone and soft tissue sarcoma: comparison with conventional imaging.

The present study was conducted to compare the diagnostic accuracy between carbon-11 choline (11C-choline) positron emission tomography (PET)/computed tomography (CT) and conventional imaging for the staging of bone and soft tissue sarcomas. Sixteen patients who underwent 11C-choline PET/CT prior to treatment were evaluated retrospectively for staging accuracy. Conventional imaging methods consisted of 99,mTc-hydroxymethylene diphosphonate bone scintigraphy, chest CT and magnetic resonance imaging of the primary site. The images were reviewed and a consensus was reached by two board-certified radiologists who were unaware of any clinical or radiological information using hard-copy films and multimodality computer platform. Tumor stage was confirmed by histological examination and/or by an obvious progression in number and/or size of the lesions on follow-up examinations. Reviewers examining both 11C-choline PET/CT and conventional imaging classified T stage in all patients. Interpretation based on 11C-choline PET/CT, the Node (N) stage was correctly diagnosed in all patients, whereas the accuracy of conventional imaging in N stage was 63%. Tumor Node Metastasis (TNM) stage was assessed correctly with 11C-choline PET/CT in 15 of 16 patients (94%) and with conventional imaging in eight of 16 patients (50%). The overall TNM staging and N staging accuracy of 11C-choline PET/CT were significantly higher than that of conventional imaging (P < 0.05). 11C-choline PET/CT is more accurate than conventional imaging regarding clinical staging of patients with bone and soft tissue sarcomas. A whole body 11C-choline PET/CT might be acceptable for imaging studies of tumor staging prior to treatment.

Adolescent↗
PubMed1977

Choline kinase and ethanolamine kinase are separate, soluble enzymes in rat liver.

Choline kinase and ethanolamine kinase are located in the cytosol from rat liver and have been copurified more than 500-fold by affinity chromatography [P. J. Brophy and D. E. Vance (1976) FEBS Lett. 62, 123-125]. Kinetic properties of the two activities were determined. Choline kinase had a Km for choline of 0.033 mM and ethanolamine was a competitive inhibitor (Ki = 6.2 mM). Ethanolamine kinase had a Km for ethanolamine of 7.7 mM and choline was a 'mixed' type of inhibitor with a Ki of 0.037 mM. Both enzymes activities responded in a similar fashion to the adenylate energy charge. Betaine and choline phosphate partially inhibited both kinases with a 93% inhibition of the ethanolamine kinase by 5 mM choline phosphate. CTP and ethanolaminephosphate partially inhibited the ethanolamine kinase, but not the choline kinase. Other metabolites tested had negliglible effects on both kinases. The affinity-column-purified enzyme was analyzed by disc gel electrophoresis which resolved the two activities. Hence, although many of the properties of the two activities are similar, choline kinase and ethanolamine kinase must be separate enzymes. Analysis of rat liver cytosol by disc gel electrophoresis indicated four isoenzymes for choline kinase and ethanolamine kinase.

Adenine Nucleotides↗
PubMedDate not supplied

Uptake of 1:2-14C-choline by the guinea-pig lung in vitro: and the effects of p-terphenyl hemicholinium-3.

1. The perfused guinea-pig lung in vitro released a total of 290 +/- 24 nmol choline after 65 min. At the end of perfusion, there were 525 +/- 36 nmol choline and 11.6 +/- 0.5 mg lecithin per g of lung tissue. 2. When perfused with 1:2-(14) C-choline at 20 nmol (20 nCi)/ml for 70 min, the level of choline in the perfusion fluid remained at 20 nmol/ml; but 65% of radioactivity was abstracted by the lung. 21% of the sequestered radioactivity was in choline phospholipids, chiefly lecithin. 3. The p-terphenyl analogue of hemicholinium no. 3 (TPHC-3), when added into the perfusion fluid at concentration 30 nmol/ml, increased significantly both the 14C-choline uptake and the conversion of 14C-choline to 14C-lecithin in the lung. However, it did not change the total tissue concentration of choline and lecithin in the lung. 4. The lung seems to have separate uptake and release mechanisms for choline and these are in equilibrium. 5. The effects of TPHC-3 on the lung in this study may be secondary to its respiratory depressant action.

Animals↗