Disease relevance of citric acid

• In a double-blind study, 12 patients on chronic hemodialysis received daily an average of 1.3 meq/kg body weight of oral sodium citrate for 8 weeks and a placebo solution for 8 weeks [1].
• Sodium citrate corrected predialysis metabolic acidosis (plasma pH 7.41 compared to 7.35; serum bicarbonate, 21.1 compared to 17.0 meq/L) and the plasma arterial PCO2 was higher (33.8 compared to 31.2) [1].
• Weight gain between dialysis periods was 0.4 kg higher with sodium citrate (2.9 compared to 2.5 kg) [1].
• Here we find that Escherichia coli IscU fails to assemble iron-sulfur clusters when the accessible "free" iron in solution is limited by an iron chelator sodium citrate [2].
• The development of metabolic alkalosis during plasmapheresis can be explained by the large sodium citrate load given during the procedure [3].

High impact information on citric acid

• An equimolar amount of sodium given as sodium citrate induced no change in blood pressure [4].
• Five techniques were performed using fibroblasts: with vinblastine (A); without drugs (B); with sodium citrate (C); without drugs but with heat serum inactivation (D); and with sodium citrate and heat serum inactivation (E) [5].
• Remarkably, IscA, an iron-sulfur cluster assembly protein with an iron association constant of 3.0 x 10(19) m(-1), is able to overcome the iron limitation due to sodium citrate and deliver iron for the IscS-mediated iron-sulfur cluster assembly in IscU [2].
• Randomized, clinical trial comparison of trisodium citrate 30% and heparin as catheter-locking solution in hemodialysis patients [6].
• Recently, trisodium citrate (TSC) has been advocated because of its antimicrobial properties and local anticoagulation [6].

Chemical compound and disease context of citric acid

• Correspondingly, maximum response to hexamethonium bromide, a ganglion blocker, was greater in sodium chloride-loaded angiotensin II rats (77.7 +/- 4.6 mm Hg) than that in angiotensin II (59.7 +/- 5.1 mm Hg) or in sodium citrate-loaded angiotensin II (57.7 +/- 4.2 mm Hg) rats [7].
• A crystal of the FabI protein from Escherichia coli has been obtained from polyethylene glycol (M(r) = 400) solution with sodium citrate at pH 8.5, by the hanging-drop technique at 4 degrees C. The crystal belongs to the hexagonal space group P6(1)22 (or P6(5)22) with cell dimensions of a = b = 81.1 A and c = 331.5 A [8].
• Large crystals of lipase from Pseudomonas cepacia have been grown at room temperature from solutions containing 2-methyl-2,4-pentanediol and sodium citrate [9].
• CONCLUSIONS: A CRRT protocol using regional 2% trisodium citrate anticoagulation is not associated with significant bleeding complications or citrate toxicity, and represents a simplified approach compared with previous applications using 4% trisodium citrate [10].
• In two patients (F.I., G.F.) no thrombocytopenia was observed when platelets were counted by fingerstick method but there was a 20% platelet decrease in blood samples collected in sodium citrate and a 50% decrease in samples collected in EDTA [11].

Biological context of citric acid

• Venous blood was drawn directly into prewarmed (37 degrees C) plastic syringes containing anticoagulants (3.2% trisodium citrate solution) plus a platelet aggregation inhibitor [12].
• A comparison of two sodium citrate concentrations in two evacuated blood collection systems for prothrombin time and ISI determination [13].
• We measured ex vivo (basal) and in vitro (thrombin-induced) platelet activation in sodium citrate, ethylenediaminetetraacetic acid (EDTA), and Citrate Theophylline Dipyridamole Adenosine (CTAD) whole blood specimens [14].
• The ionic strength dependence of Kcat/Kapp is identical with that of sodium chloride, sodium phosphate, and sodium citrate, thus ruling out any possibility that the phenomena arise from a specific, partially competitive binding of Na+ to the enzyme active site [15].
• Observations made using the Advia 120 Hematology System platelet density parameter, MPC, in the absence of thrombin were 25.7 +/- 0.9 g/dl, 27.9 +/- 0.9 g/dl and 24.8 +/- 1.2 g/dl in sodium citrate, EDTA and CTAD whole blood specimens, respectively [14].

Anatomical context of citric acid

• Chick gastrula mesodermal cells, known as highly migratory, were dissociated into single cells in sodium citrate buffer, conjugated with paramagnetic beads activated by tosyl-residue (4.5 microns in diameter) and seeded onto coverglasses coated with fibronectin [16].
• The effect of sodium citrate on the stimulation of polymorphonuclear leukocytes [17].
• Hypocitraturia was associated with increased activity of sodium-citrate cotransporter in renal cortical brush-border membranes (BBM) in the high casein group [18].
• However, cryogel formation from CF plasma was reduced significantly by 1) slow thawing at 4 degrees C rather than quick thawing at 20 and 0 or 20 and 4 degrees C, 2) the use of 1:16.6 sodium citrate rather than 1:12.5 ACD-A, or 3) the addition of intact platelets, platelet lysate, membranes, or cytosol to CF plasma before freezing [19].
• The yield of progenitor cells was similarly enhanced when trisodium citrate, a chelating substance, was added to the filtration medium [20].

Associations of citric acid with other chemical compounds

• Sodium chloride increased mean arterial blood pressure in the salt-sensitive subjects; sodium citrate did not [21].
• The efficacy of whole blood preservation in acid citrate dextrose (ACD-A) and citrate-phosphate dextrose (CPD) anticoagulants containing half-strength trisodium citrate concentrations, was determined by biochemical and cellular assessment during 28 day storage at 4 degrees--6 degrees [22].
• This study thus demonstrates that, although blood pressure in salt-sensitive individuals is raised by sodium chloride only, both sodium chloride and sodium citrate evoke similar increases in pressor response to norepinephrine and angiotensin II [23].
• The characterization of the spike was performed by postcolumn reverse isotope dilution analysis (this is, by postcolumn addition of a solution of 200 ng mL-1 natural iron in sodium citrate/citric acid of pH 4) [24].
• Also, the diastereomers of aspartic acid, glutamic acid, and proline were resolved using a 10 mM sodium citrate buffer (pH 4.4) [25].

Gene context of citric acid

• Crystals of human RCC1 suitable for X-ray analysis have been obtained using the seeding technique in hanging drops with sodium citrate as a precipitant [26].
• VEGF was not different and PF4 was very low or undetectable in Edinburgh plasma and CTAD plasma, while it was significantly higher in sodium citrate plasma [27].
• BTG and PF4 release from blood anticoagulated with sodium citrate was inhibited by AD6 during a 3 h incubation [28].
• Crystals of yeast IDH have been obtained and optimized using sodium citrate, a competitive inhibitor of the enzyme, as the precipitating agent [29].
• A new assay was developed, and the following steady-state kinetic constants were determined for 1-deoxy-D-xylulose 5-phosphate synthase A and B: K(m)(pyruvate) = 0.61 and 3.0 mM, K(m)(D-glyceraldehyde 3-phosphate) = 150 and 120 microM, and V(max) = 1.9 and 1.4 micromol/min/mg in 200 mM sodium citrate (pH 7.4) [30].

Analytical, diagnostic and therapeutic context of citric acid

• The solution with sodium citrate base was as effective as WHO-oral rehydration solution for management of diarrhoea [31].
• Crystallization trials using both these salts were carried out, and although no condition could as yet be found for obtaining crystals with ammonium sulphate solutions, crystals of the enzyme have been obtained with sodium citrate [32].
• Ultrafiltration rate was maintained at 2.0 liters/hr and citrate-based replacement fluid (trisodium citrate 13.3 mM, sodium chloride 100 mM, magnesium chloride 0.75 mM, dextrose 0.2%) was infused proximal to the filter to maintain the desired fluid balance [33].
• Blood samples were obtained by aseptic venipuncture and anticoagulated with 3.8% sodium citrate [34].
• BACKGROUND: Regional anticoagulation with trisodium citrate is an effective form of anticoagulation for continuous renal replacement therapy (CRRT) for patients with contraindications to heparin [10].

References