Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CITRATES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources

The effects of citrate on hydroxyapatite induced calcium oxalate crystallization and on the formation of calcium phosphate crystals.

The addition of different amounts of hydroxyapatite crystals (HAP) to a solution, metastably supersaturated with respect to calcium oxalate (CaOx) resulted in heterogenous crystallization at seed concentrations exceeding 0.2 mmol/l. The induction period varied between 1 and more than 8 h with the shortest period for a seed concentration of 2 mmol/l. Addition to the system of 1 and 2% of whole urine and citrate in concentrations corresponding to approximately 1% of that found in normal urine inhibited the crystallization for as long as 4 h. In a system supersaturated with respect to calcium phosphate (CaP) the total number of crystals was markedly reduced by citrate concentrations exceeding 0.5 mmol/l. The fractions of medium sized and large crystals were sharply reduced and small crystals predominated at higher citrate concentrations. This might indicate effects of citrate on both crystal growth and crystal aggregation. We conclude that increased citrate concentrations during treatment with alkali leads to a significant inhibition of CaOx growth on HAP as well as to a prevention of the formation of large CaP crystals from solutions supersaturated with respect to CaP.

Calcium Oxalate↗

Effects of different doses of alkaline citrate on urine composition and crystallization of calcium oxalate.

Prophylactic treatment with alkaline citrate in patients with recurrent calcium oxalate (CaOx) stone disease results in reduced CaOx supersaturation and increased urinary citrate. The effects of a single evening dose were compared with those of two and three daily doses in six recurrent CaOx stone formers with hypercalciuria, hypocitraturia or raised calcium/citrate quotients. While on a standardized hospital diet the patients were given 7.5 g (28 mmol) of sodium potassium citrate (URALYT-U) in one, two, and three doses. Fractional urine collections during 24 hours were analyzed for pH, composition, and crystallization risk (CR). All dosage regimens had favourable effects on urinary calcium, citrate, calcium/citrate quotients, and CaOx-CR. The most sustained effect was recorded with three divided doses. Single evening doses resulted in the most pronounced effects between 22.00-06.00 h, thereby counteracting the increased risk of CaOx crystallization during that period. In terms of 24h urine composition the best effect was recorded with alkaline citrate administered three times daily, but because of the favourable response by a single evening dose between 22.00-06.00 h the assumption was made that this dosage regimen might be sufficient to reduce the risk of CaOx crystallization and stone formation. However, the validity of such an assumption can only be established by long-term clinical studies.

Calcium Oxalate↗

The effect of sodium bicarbonate and sodium citrate ingestion on anaerobic power during intermittent exercise.

The effect of sodium bicarbonate and sodium citrate ingestion on cycling performance in three 30 s Wingate Anaerobic Tests separated by 6 min recovery periods has been studied using 6 male subjects. Subjects ingested either sodium bicarbonate (B), sodium bicarbonate plus sodium citrate (BC), sodium citrate (C) or sodium chloride (P) 2.5 h prior to exercise in a dose of 0.3 g kg-1 body weight. Pre-exercise blood pH was 7.44 +/- 0.06, 7.42 +/- 0.05, 7.41 +/- 0.05 and 7.38 +/- 0.04 in the C, BC, B and P conditions respectively. Mean and peak power output were significantly reduced by successive Wingate tests but not significantly affected by the treatments. Performance in the second and third tests was highest following C, BC and B ingestion. The total work done in the 3 tests was 103%, 102% and 101% of that achieved in the P condition after C, BC and B ingestion respectively. The increased alkali reserve recorded subsequent to bicarbonate and citrate treatment reduced mean post-exercise acidosis, although pH was significantly higher only in the C condition (p less than 0.05) compared to P after each exercise bout. No significant differences in plasma lactate concentration were recorded at any time. Citrate ingestion appears to be most effective in elevating blood pH and [HCO3-], and in enhancing performance in short-term intermittent exercise. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood and has a small, but non-significant, effect on anaerobic power and capacity as measured in a series of 3 Wingate Anaerobic Tests.

Acid-Base Equilibrium↗

Oxalate accumulation from citrate by Aspergillus niger. I. Biosynthesis of oxalate from its ultimate precursor.

Carbon-14 was incorporated from citrate-1,5-14C, glyoxylate-14C(U), or glyoxylate-1-14C into oxalate by cultures of Aspergillus niger pregrown on a medium with glucose as the sole source of carbon. Glyoxylate-14C(U) was superior to glyoxylate-1-14C and citrate-1,5-14C as a source of incorporation. By addition of a great amount of citrate the accumulation of oxalate was accelerated and its maximum yield increased. In a cell-free extract from mycelium forming oxalate from citrate the enzyme oxaloacetate hydrolase (EC3.7.1.1) was identified. Its in vitro activity per flask exceeded the rate of in vivo accumulation of oxalate. Glyoxylate oxidizing enzymes (glycolate oxidase, EC1.1.3.1; glyoxylate oxidase, EC1.2.3.5;NAD(P)-dependent glyoxylate dehydrogenase; glyoxylate dehydrogenase, CoA-oxalylating, EC1.2.1.7) could not be detected in cell-free extracts. It is concluded that in cultures accumulating oxalate from citrate after pregrowth on glucose, oxalate arises by hydrolytic cleavage of oxaloacetate but not by oxidation of glyoxylate.

Aspergillus↗

Citrate inhibition of rat-kidney cortex phosphofructokinase.

The regulatory properties of citrate on the activity of phosphofructokinase (PFK) purified from rat-kidney cortex has been studied. Citrate produces increases in the K0.5 for Fru-6-P and in the Hill coefficient as well as a decrease in the Vmax of the reaction without affecting the kinetic parameters for ATP as substrate. ATP potentiates synergistically the effects of citrate as an inhibitor of the enzyme. Fru-2,6-P2 and AMP at concentrations equal to Ka were not able to completely prevent citrate inhibition of the enzyme. Physiological concentrations of ATP and citrate produce a strong inhibition of renal PFK suggesting that may participate in the control of glycolysis in vivo.

Adenosine Triphosphate↗

Transport of malate and citrate into rat brain mitochondria under hypoxia and anesthesia.

Hypoxia and anesthesia inhibited penetration of malate and citrate into the brain mitochondria by 60% and 40%, respectively. Anesthetized animals exposed to low oxygen tension showed similar changes as those subjected to hypoxia without anesthesia. Recovery from anesthesia was rapid and the rates of citrate and malate uptake returned to the control values in approximately 60 min. In the case of hypoxia, days were required to restore the control values of citrate and malate uptake. Free fatty acids had no effect on the entry of malate and citrate into the mitochondria. However, changes in the levels of protein --SH groups were observed which may be responsible for the impaired transport of citrate and malate under hypoxic condition.

Anesthesia↗

Citrate and urease-induced crystallization in synthetic and human urine.

The effects of citrate on the different phases of urease-induced crystallization were studied using Coulter counter techniques and optical microscopy. Citrate increased urine pH and markedly delayed the initiation of the crystallization (nucleation) in both human and synthetic urine. In synthetic urine, particle aggregation and especially particle growth were delayed and inhibited by citrate. In human urine, aggregation was distinctly inhibited by citrate. It appears that the susceptibility of urine to form crystals in the presence of urease activity is influenced by its citrate concentration.

Adult↗

Sodium citrate supplementation in inborn argininosuccinate lyase deficiency: a study in a 5-year-old patient under total parenteral nutrition.

The effects of sodium citrate supplementation to improve aspartic acid supply in a 5-year-old girl with argininosuccinate lyase deficiency were studied over a period of 5 years under constant and total parenteral nutrition. Daily increasing doses of sodium citrate (0-8 mmol/kg) were continuously infused i.v.. Her standard therapy with arginine hydrochloride (4 mmol/kg/day) and sodium benzoate (200 mg/kg/day) was continued. Serum citrulline concentrations were reduced by citrate supplementation (161.8-41.7 mumol/l). Correspondingly serum concentrations of argininosuccinate and its anhydrides rose (270-458 mumol/l), positively correlated with the doses of sodium citrate. Renal elimination of argininosuccinate did not change measurably. There was no improvement in plasma ammonia concentration, which remained between 88 and 136 mumol/l. A long-standing hepatomegaly did not improve. The patient developed a significant alkalosis with blood pH-values increasing up to 7.55. The alkalosis lead to a reduction in renal ammonium elimination by at least 5.3 mmol/kg per day; the portion of ammonium-nitrogen decreased from 54.2% to finally 9% of total urinary nitrogen. Nevertheless total urinary nitrogen elimination, as measured by pyrochemiluminescence, improved by 24.5% during the 5 days and rose from 2065 mg nitrogen/day to 2570 mg/day. This improvement could not be explained by the metabolites determined and corresponded with an increase in chemically undefined nitrogen excretion, which rose from 0% to 65.9% of total urinary nitrogen. Further investigations are necessary to elucidate the nature of these unexplained nitrogen-containing compounds. CONCLUSION. Sodium citrate supplementation improved renal nitrogen elimination in a patient with argininosuccinate lyase deficiency in the observation period of 5 days by up to 24.5%.

Alkalosis↗

[Effect of different concentrations of various zinc complexes (picolinate, citrate, 8-hydroxyquinolate) in comparison with sulfate on zinc supply status in rats].

12 groups of 8 young male Sprague-Dawley rats received a semisynthetic casein-diet, whose zinc concentration (1.3 ppm) was adjusted to 5, 10 and 15 ppm by supplementation of various Zn complexes or salts like Zn citrate, Zn picolinate, Zn 8-hydroxyquinolate and Zn sulfate. After 24 days all animals were killed and examined on parameters of zinc supply status. The weight gain of the animals with 5 ppm dietary zinc was strongly reduced compared to groups with the higher dietary zinc content. The type of the supplemented Zn compound showed in no way an influence on the live-weight of the animals. The zinc concentration of the tissues, too, was only dependent on the level of the dietary zinc concentration and not on the type of supplemented zinc compound. The activity of the alkaline phosphatase in serum, a zinc metalloenzyme, was altogether reduced in the zinc-deficient animals with 5 ppm dietary zinc content, but showed a significant higher activity in the citrate and 8-hydroxyquinolate group than in the sulfate and picolinate group. Also the percent zinc-binding capacity of serum, a good indicator for estimating the zinc supply status of rats, showed a better zinc supply of the citrate group with 5 as well as 10 ppm dietary zinc, compared with the other groups on the same dietary zinc content. The serum zinc concentration of rats with 5 ppm as Zn citrate was more than twice higher than in animals given zinc as picolinate, 8-hydroxyquinolate or sulfate. The results indicate a better utilization of zinc chelated by citric acid than by picolinic acid, 8-hydroxyquinoline or as salt like sulfate. But the higher bioavailability of zinc in human milk should not only be attributed to the presence of citrate.

Alkaline Phosphatase↗

The effect of citrate loading on exercise performance, acid-base balance and metabolism.

Nine subjects (VO2max 65 +/- 2 ml.kg-1.min-1, mean +/- SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g.kg-1 body mass) or a sodium chloride placebo (P, 0.045 g.kg-1 body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% VO2max, followed by exercise to exhaustion at 95% VO2max. Pre-exercise arterialized-venous [H+] was lower in C (36.2 +/- 0.5 nmol.l-1; pH 7.44) than P (39.4 +/- 0.4 nmol.l-1; pH 7.40); the plasma [H+] remained lower and [HCO3-] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% VO2max was similar in C (310 +/- 69 s) and P (313 +/- 74 s). Cardiorespiratory variables (ventilation, VO2, VCO2, heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195 +/- 19 mumol.l-1; P, 81 +/- 7 mumol.l-1) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% VO2max. Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.

Acid-Base Equilibrium↗

Resolution of Ga-67 citrate uptake in the left neck mass of Hodgkin's disease and reversion of double scoliosis of cervical-thoracic and lower lumbar vertebrae.

A 6-yr-old boy underwent a total body Ga-67 citrate imaging study because of a large mass of Hodgkin's lymphoma in the left neck and the left anterior chest wall region. The images showed intense uptake in the left neck extending anteroinferiorly to the left upper chest wall corresponding to the left neck and chest region. In addition, there was mild cervical-upper thoracic scoliosis with convexity to the right and mild scoliosis of the lower lumbar scoliosis with concavity to the left. After three cycles of chemotherapy, in the follow-up Ga-67 citrate total body images seven months after his first Ga-67 citrate imaging, the intense uptake in the left neck and the left upper chest wall had been resolved and the scoliosis of the cervical-thoracic and lower lumbar spine had also been reversed to normal. This case shows that a Ga-67 citrate imaging study is useful for first diagnosis and subsequent monitoring of the therapeutic effects in a follow-up imaging. Also Ga-67 citrate imaging provided evidence that the scoliosis had been reversed.

Antineoplastic Combined Chemotherapy Protocols↗

Biochemical controls of citrate synthase in chickpea bacteroids.

Bacteroids formed by Mesorhizobium ciceri CC 1192 in symbiosis with chickpea plants (Cicer arietinum L.) contained a single form of citrate synthase [citrate oxaloacetate-lyase (CoA-acetylating) enzyme; EC 4.1.3.7], which had the same electrophoretic mobility as the enzyme from the free-living cells. The citrate synthase from CC 1192 bacteroids had a native molecular mass of 228 +/- 32 kDa and was activated by KCl, which also enhanced stability. Double reciprocal plots of initial velocity against acetyl-CoA concentration were linear, whereas the corresponding plots with oxaloacetate were nonlinear. The Km value for acetyl-CoA was 174 microM in the absence of added KCl, and 88 microM when the concentration of KCl in reaction mixtures was 100 mM. The concentrations of oxaloacetate for 50% of maximal activity were 27 microM without added KCl and 14 microM in the presence of 100 mM KCl. Activity of citrate synthase was inhibited 50% by 80 microM NADH and more than 90% by 200 microM NADH. Inhibition by NADH was linear competitive with respect to acetyl-CoA (Kis = 23.1 +/- 3 microM) and linear noncompetitive with respect to oxaloacetate (Kis = 56 +/- 3.8 microM and Kii = 115 +/- 15.4 microM). NADH inhibition was relieved by NAD+ and by micromolar concentrations of 5'-AMP. In the presence of 50 or 100 mM KCl, inhibition by NADH was apparent only when the proportion of NADH in the nicotinamide adenine dinucleotide pool was greater than 0.6. In the microaerobic environment of bacteroids, NADH may be at concentrations that are inhibitory for citrate synthase. However, this inhibition is likely to be relieved by NAD+ and 5'-AMP, allowing carbon to enter the tricarboxylic acid cycle.

Citrate (si)-Synthase↗

Characterization of the intron-containing citrate synthase gene from the alkanotrophic yeast Candida tropicalis: cloning and expression in Saccharomyces cerevisiae.

Citrate synthase, an essential enzyme of the tricarboxylic acid cycle in mitochondria, was purified from acetate-grown Candida tropicalis. Results from SDS-PAGE and gel filtration showed that this enzyme was a dimer composed of 45-kDa subunits. A citrate synthase cDNA fragment was amplified by the 5'-RACE method. Nucleotide sequence analysis of this cDNA fragment revealed that the deduced amino acid sequence contained an extended leader sequence which is suggested to be a mitochondrial targeting signal, as judged from helical wheel analysis. Using this cDNA probe, one genomic citrate synthase clone was isolated from a yeast lambdaEMBL3 library. The nucleotide sequence of the gene encoding C. tropicalis citrate synthase, CtCIT, revealed the presence of a 79-bp intron in the N-terminal region. Sequences essential as yeast splicing motifs were present in this intron. When the CtCIT gene including its intron was introduced into Saccharomyces cerevisiae using the promoter UPR-ICL, citrate synthase activity was highly induced, which strongly indicated that this intron was correctly spliced in S. cerevisiae.

Amino Acid Sequence↗

Concentrated urine and diluted urine: the effects of citrate and magnesium on the crystallization of calcium oxalate induced in vitro by an oxalate load.

Supplementation of certain calcium crystallization inhibitors, such as citrate and magnesium, and the dilution of urine with water are now considered consolidated practice for the prevention of calcium kidney stones. The aim of this study is to verify, using tried and true in vitro methods, whether the effect of these inhibitors can manifest itself in different ways depending on whether the urine is concentrated or diluted. Calcium oxalate crystallization was studied on 4-h urine of 20 male idiopathic calcium oxalate stone formers, first under low hydration conditions (non-diluted urine) and then under high hydration conditions (diluted urine). Both the diluted and the non-diluted urine samples were subjected to three types of load: (a) an oxalate concentration increment of 1.3 mmol/l only; (b) an oxalate concentration increment of 1.3 mmol/l with a citrate concentration increment of 1.56 mmol/l; (c) an oxalate concentration increment of 1.3 mmol/l with a magnesium concentration increment of 2.08 mmol/l. In non-diluted urine, the addition of the citrate and magnesium did not modify the crystallization parameters under study. In contrast, in the diluted urine the addition of the citrate and magnesium led to a reduction in the total quantity of crystals (equivalent to 35-45%) and their aggregates (equivalent to 30-40%); at the same time, there was an increase in the diameter of the monohydrate calcium oxalate crystals, which also underwent a morphological change. In conclusion, the inhibitory effects of citrate and magnesium on the crystallization of calcium oxalate do not manifest themselves in highly concentrated urine.

Calcium Oxalate↗

Ferrus calcium citrate is absorbed better than iron bisglycinate in patients with Crohn's disease, but not in healthy controls.

Our purpose was to compare the absorption of iron bisglycinate and ferrous calcium citrate in volunteers using an oral iron tolerance test. Twenty volunteers, 10 healthy controls and 10 with stable Crohn's disease, agreed to participate in the study. All were given 50 mg of elemental iron as iron bisglycinate or ferrous calcium citrate. Serum iron levels were monitored for 4 hr. After a week, each received the other regimen. Using the area under the curve as indicator, the oral iron absorption test revealed that absorption of iron post-ingestion of ferrous calcium citrate was better than after ingestion of iron bisglycinate for the group as a whole (P < 0.03). Volunteers with Crohn's disease absorbed ferrous calcium citrate better than iron bisglycinate (P=0.005). No difference was noted in the absorption of either preparation by healthy volunteers. Ferrus calcium citrate is apparently more effective than iron bisglycinate in patients with Crohn's disease.

Adult↗

Hemodynamic effects of sildenafil citrate (Viagra) on segmental branches of bilateral renal arteries.

INTRODUCTION: Erectile dysfunction (ED) is one of the most encountered male health problem and sildenafil citrate is used worldwide for treatment of ED. Aim of the present study was to determine and evaluate hemodynamic effects of sildenafil citrate on segmental branches of bilateral renal arteries of cases with ED. PATIENTS AND METHODS: Total of 35 male patients aging between 34 and 56 years were recruited into study. Patients were evaluated with renal color Doppler sonography (CDS) before and after (45-75 min) peroral sildenafil citrate (50 mg) administration. Peak systolic flow rate (V(max)), end diastolic flow rate (V(min)), resistive index (RI) and pulsatility index (PI) of renal artery segmental branches were determined before and after sildenafil citrate administration. RESULTS: V(min) measured at right lower segment was significantly reduced after sildenafil administration (p = 0.030). Accordingly mean RI and PI of right lower segment of renal artery slightly increased after drug administration (p = 0.007 and p = 0.012, respectively). The measurements on other segments had no significant change after sildenafil treatment when compared to baseline values. On this single dose administration no side effect was recorded. CONCLUSION: Findings of the present study demonstrated that peroral sildenafil citrate usage had slight effects on hemodynamic parameters of lower segmental branch of right renal artery. This result could not be interpreted as robust evidence for hemodynamic changes of renal arteries associated with sildenafil usage nevertheless warrants more comprehensive research with larger number of patients.

Adult↗

Superoxide-dependent redox cycling of citrate-Fe3+: evidence for a superoxide dismutaselike activity.

Citrate-Fe3+, reportedly a physiological chelate, exhibits superoxide dismutaselike activity, as evidenced by the inhibition of xanthine oxidase-dependent cytochrome c reduction; the dismutation of xanthine oxidase-generated superoxide to hydrogen peroxide and oxygen, and the enhanced disproportionation of potassium superoxide. The catalytic activity of citrate-Fe3+ corresponds, on a molar basis, to 0.03% of that of copper- and zinc-containing superoxide dismutase. Although weak, this activity enables citrate-Fe3+ to inhibit superoxide and ADP-Fe3+ -dependent peroxidation of extracted microsomal lipids. Also, the dismutase activity of citrate-Fe3+ interferes with its ability to promote lipid peroxidation. It is proposed that chelation of Fe3+ by citrate may represent a protective mechanism against the deleterious consequences of superoxide generation.

Chelating Agents↗

Properties and organ distribution of ATP citrate (pro-3S)-lyase.

1. The lipogenic enzyme ATP citrate lyase (ATP:citrate oxaloacetate-lyase (pro-3S-CH2COO-acetyl-CoA; ATP-dephosphorylating), EC 4.1.3.8) is partially purified from human liver by ammonium sulfate fractionation and anionexchange chromatography. 2. Km values for the substrates are 1.1 x 10(-5) 1.3 x 10(-3), and 1.2 x 10(-4) M for CoASH, ATP and citrate, respectively. The hypolipidemic drug L(-)-hydroxycitrate is a competitive inhibitor with respect to citrate (Ki = 3 x 10(-4) M). 3. Specific activities measured in liver, adipose tissue and intestinal mucosa (autopsic and biopsic material) are in the range of 1 mU/mg protein suggesting that the citrate pathway does not significantly contribute to human lipogenesis. No stimulation is found after a 3-day carbohydrate-rich diet. 4. Specific activities of other key-enzymes of the acetyl-CoA production from carbohydrates (pyruvate dehydrogenase, cytosolic acetyl-CoA synthetase) are of the same low magnitude.

ATP Citrate (pro-S)-Lyase↗