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At least 19 recordsLinked to original sources
PubMed1978

Modification of the alkaline picrate assay for creatinine to prevent spuriously elevated values by keto acids.

Acetoacetate and pyruvate, sometimes present in patients' serum in abnormal amounts, interfere, like other keto acids, with the determination by some usual procedures of creatinine. Acetoacetate can be responsible for overestimation of "creatinine" in the order of 400 mumol/l in sera of ketotic diabetics, fasting subjects and other patients with ketosis. The pseudocreatinine reaction of acetoacetate increases with increasing concentration of NaOH and picrate. Pyruvate causes falsely elevated values, especially at high picrate concentrations. The effect of acetoacetate at 25 degrees C has ceased 90 sec after the start of the reaction. We propose a continuous flow method with relatively low concentrations of NaOH and picrate, and a kinetic method at 25 degrees C with a measuring time of between 90 and 270 sec after mixing sample and reagents. In this way the interference by acetoacetate and pyruvate is eliminated or reduced. We found excellent correlation between the proposed method for a centrifugal analyzer and a manual reference method, based on the adsorption of creatinine to fuller's earth.

Creatinine↗
PubMed1978

Specific method for serum creatinine determination based on ion exchange chromatography and an automated alkaline picrate reaction -- a proposed reference method.

A proposed reference method for serum creatinine has been developed under the auspices of the Committee on Reference Methods and Reference Materials of the Canadian Society of Clinical Chemists. A serum ultrafiltrate at pH 2.0 is applied through a closed sample loop injection system to a short column containing cationic resin of high resolving power. Elution with sodium citrate buffer by means of minipump at constant rate passes the eluate into alkaline picrate reagents in a continuous flow system (Technicon AAIII pump, AAII colorimeter 50 mm x 1.5 mm flow cell, narrow band width filter). The colour reaction peak is monitored visually to verify specificity and the area is calculated electronically. Specificity has been demonstrated by use of Jaffé-reactive substances such as glucose, sodium acetoacetate, L-ascorbic acid, pyruvic acid, L-dopa and glycocyamidine and also by use of an alternate colour reaction, sodium 3,5-dinitrobenzoate in place of alkaline picrate in the analysis of serum pools. Routine methods in common use, i.e., manual and automated alkaline picrate procedures, demonstrated a statistically significant high bias in interlaboratory studies in which this procedure was used for reference.

Autoanalysis↗
PubMed1978

[Effect of selective application of sodium picrate to the hypogastric ganglion in the hypogastric nerve-vas deferens preparation of the guinea pig (author's transl)].

Effect of sodium picrate (picric acid-Na; PA) on the hypogastric ganglion in the hypogastric nerve-vas deferens preparation of the guinea pig was studied and the results are as follows: PA or acetylcholine (ACh) at doses (g/ml) of 10(-5) approximately 10(-4) applied to the ganglion increased the height of the response (R-NS) of the vas deferens to the hypogastric nerve stimulation. Neither drug restored R-NS blocked by hexamethonium 3 X 10(-5). Effects of PA and ACh on R-NS were potentiated by neostigmine 10(-7) and the potentiation was considerably greater for ACh than for PA. Effects of PA on R-NS were not influenced by pretreatment with atropine. Both PA and ACh recovered R-NS which was partially reduced by hemicholinium-3 (HC-3), although the recovery of R-NS by PA was rapidly abolished more than that by ACh when these drugs were repeatedly applied in the presence of HC-3 3 X 10(-5). PA markedly recovered the R-NS reduced by morphine 10(-4) and ACh slightly restored that R-NS. These results suggest that the site of action of PA on the hypogastric ganglion of the guinea pig is different from that of ACh and the effect of PA on R-NS may be due to the acceleration of ACh-release from preganglionic nerve endings.

Acetylcholine↗
PubMed1976

Reaction of alkaline sodium picrate with creatinine: I. Kinetics and mechanism of formation of the mono-creatinine picric acid complex.

Spectrophotometric, kinetic, and nuclear magnetic resonance studies indicate that alkaline sodium picrate and creatinine react to form a 1/1 aduct between picric and creatinine, with a stability constant of log K= 4.26. Kinetic studies indicate that the forward reaction is first order with respect to picric acid, hydroxide, and creatinine concentration. The reverse reaction, the dissociation of the 1/1 complex, shows a complex dependence on hydroxide concentration. The expression for the observed pseudo-first-order rate constant in the presence of excess picric acid is: Kobsd = K1K0[P][OH] +[K2[OH]x. A value of K1K0 = 5.0 (mol/liter)-2s-1 is obtained. For accurate analytical results with this reaction, hydroxide concentration must be maintained at a constant value for both samples and standards.

Chemical Phenomena↗
PubMed1977

Accelerating effect of 2,4,6-trinitrophenol on the glycolytic rate of human red cells.

A number of instantaneous changes occurred when picrate was added to a suspension of human red cells in steady state with respect to glycolysis and ion distribution across the membrane at pH 7.40. The rate of glycolysis increased, without change in glycolytic quotient, to a new steady-state value, the effect reaching a maximum of 1.75 times the rate of the control at 0.5 mM picrate. Inorganic phosphate (P(i)) was released at a relatively constant rate, increasing with picrate concentration to 1.0 mmol P(i)/liter cells x h at 5-6 mM picrate. The steady- state concentrations of ATP and 1,3-diphosphoglycerate (1,3-DPG) decreased to new stable values within 15-45 min after the addition of picrate. The ATP level was affected only at picrate concentrations of 1 mM or more, and the level of ATP stabilized at 75 percent of the control values at 4 mM of picrate. In contrast, 1,3-DPG concentrations decreased to 40 percent of the control value of 0.5 mM picrate. Higher concentrations of picrate resulted in only a small additional decrease in the stationary concentration of 1,3-DGP. A net efflux of cellular potassium at constant rate took place. This net efflux was an almost linear function of picrate concentration in the range of 0.1-3 mM. At the latter concentration the net efflux amounted to about 2.7 meq/liter cells x h and a further increase in picrate concentration caused only a minor increase in the potassium efflux. Possible mechanisms for the effects of picrate on human red cell glycolysis are discussed.

Adenosine Diphosphate↗
PubMed1975

Mitochondrial ATP-Pi exchange complex and the site of uncoupling of oxidative phosphorylation.

Five enzyme complexes, which are concerned with electron transport and oxidative phosphorylation, have been isolated from beef heart mitochondria. Enzyme complexes I, II, III and IV are the electron transfer complexes discovered in 1961. Complex V is an energy-conserving complex. It catalyzes ATP-Pi exchange and ATP hydrolysis. The exchange reaction is sensitive to uncouplers, rutamycin, valinomycin plus K-+, dicyclorexylcarboditmide, arsenate, azide, and adenylyl imidodiphosphate. It is also specific for ATP; ITP, GTP and UTP are essentially ineffective. Studies with the photoaffinity labeling uncoupler, 2-azido-4-nitrophenol (NPA), have shown that the mitochondrial uncoupler-binding sites are located exclusively in complex V. Complexes I, III and IV, which carry the three coupling sites of the respiratory chain, had negligible capacity for the binding of NPA, whereas the uncoupler-binding capacity of complex V appeared to be increased two- to threefold as compared to mitochondria. Complexes I, II, III, IV and V are obtained from the same batch of mitochondria by a simple fractionation procedure, which employs cholate, deoxycholate, ammonium acetate and ammonium sulfate. Studies with NPA have shown that mitochondria contain per milligram protein about 0.6 nmole of uniformly reacting uncoupler binding site. All of the uncouplers tested appeared to interact competitively with this site. Photoaffinity labeling with tritiated NPA has shown that a major portion of NPA binds to a polypeptide of molecular weight between 26,000 and 30,000. Other studies on the mechanism of uncoupling have shown that picrate is a membrane-impermeable uncoupler. It cannot uncouple mitochondria. However, it is an effective uncoupler of ATP synthesis and ATP-induced transhydrogenation or reverse electron transfer when used in conjunction with sonicated submitochondrial particles, which have an inside-out orientation of the inner membrane with respect to the medium. In these particles, picrate binds to the same uncoupler-binding site as NPA and other uncouplers. However, unlike the membrane-permeable uncouplers, picrate is a poor protonophore. It has a very small effect on the proton permeability of phosphorylating submitochondrial vesicles, even at two to three times the concentration needed for complete uncoupling. The increase in the proton permeability of submitochondrial vesicles caused by such high concentrations of picrate (500 mum) can be achieved with approximately 5 mum 2,4-dinitrophenol. At this concentration, dinitrophenol results in only about 20% uncoupling.

Adenosine Triphosphate↗
PubMed1976

Facilitated transport of di- and trinitrophenolate ions across lipid membranes by valinomycin and nonactin.

The conductance of black lipid membranes in the presence of 2,4,6-trinitrophenol (or 2,4-dinitrophenol) is considerably enhanced, if the cation carriers valinomycin, enniatin B or nonactin are added. The effect is, however, largely independent of the cation concentration and is identical for the cations Li+, Na+ and Ba2+. This finding, as well as the sign and magnitude of the diffusion potential in the presence of a gradient of picrate are consistent with the assumption that the transport of picrate anions is facilitated by the above-mentioned macrocyclic compounds, but that cations are not directly involved. A model is suggested which, based on the generation of mobile defect structures by the incorporation of large molecules, allows one to explain facilitated transport without the assumption of stable chemical bonds between a carrier and its transported substrate. If K+ is present in the aqueous phase, the conductance is largely determined by the permeation of the cation complexes of valinomycin and nonactin. The conductance is, however, increases by adsorption of picrate anions to the membrane surface. The negative surface potential generated by the adsorption layer seems to be responsible for the saturation of the conductance at high picrate concentrations in the absence of valinomycin and nonactin.

Anti-Bacterial Agents↗
PubMed1977

Determination of serum creatinine by reaction with methyl-3,5-dinitrobenzoate in Methyl Sulfoxide.

Creatinine in serum is determined with a new reagent system consisting of methyl-3,5-dinitrobenzoate and tetramethyl ammonium hydroxide in 50% methyl sulfoxide. The method shows excellent correlation with manual and automated alkaline picrate procedures and has comparable sensitivity. The proposed method has advantages over the dinitrobenzoyl chloride assay system in terms of sensitivity, reagent stability and precision. The day-to-day coefficient of variation is 2.9-3.8%, while within day is 1.5-2.1%. The standard curve is linear beyond 20 mg/dl creatinine. Compared to the picrate method, the proposed assay is less than one half as susceptible to a combination of known interfering agents. Based on the present studies, it is recommended as an excellent alternative to the commonly used picrate procedures.

Acetoacetates↗
PubMed1977

Serum creatinine assay by use of 3,5-dinitrobenzoates: a critique.

Methyl-3,5-dinitrobenzoate and 3,5-dinitrobenzoyl chloride are demonstrated to react with creatinine through their conversion to 3,5-dinitrobenzoate. Analytical recovery of creatinine added to serum is improved by an "acid-supernate" modification, which is also much less susceptible to a combination of known interfering agents than is the picrate procedure. The "neutral-supernate" procedure shows negligible interference by cephalothin as compared to commonly used picrate procedures. Replacement of tetramethylammonium hydroxide by sodium hydroxide was also tested. The interrelationships between dimethyl sulfoxide concentration, recoveries of creatinine, and slopes of correlations (r greater than .992) of various dinitrobenzoate and picrate methods are critically assessed. Because of its precision, greater specificity, and other criteria, we recommend the methyl-3,5-dinitrobenzoate (or 3,5-dinitrobenzoic acid) neutral-supernate method for routine applications.

Cephalothin↗
PubMed1976

Transport of pyruvate nad lactate into human erythrocytes. Evidence for the involvement of the chloride carrier and a chloride-independent carrier.

The kinetics and activation energy of entry of pyruvate and lactate into the erythrocyte were studied at concentrations below 4 and 15mM respectively. The Km and Vmax. values for both substrates are reported, and it is shown that pyruvate inhibits competitively with respect to lactate and vice versa. In both cases the Km for the carboxylate as a substrate was the same as its Ki as an inhibitor. Alpha-Cyano-4-hydroxycinnamate and its analogues inhibited the uptake of both lactate and pyruvate competitively. Inhibition was also produced by treatment of cells with fluorodinitrobenzene but not with the thiol reagents or Pronase. At high concentrations of pyruvate or lactate (20mM), uptake of the carboxylate was accompanied by an efflux of Cl-ions. This efflux of Cl- was inhibited by alpha-cyano-4-hydroxycinnamate and picrate and could be totally abolished by very low (less than 10 muM) concentrations of the inhibitor of Cl- transport, 4,4'-di-isothiocyanostilbene-2,2'-disulphonic acid. This inhibitor titrated out the chlordie efflux induced by pyruvate, bicarbonate, formate and fluoride, in each case total inhibition becoming apparent when approximately 1.2x10(6) molecules of inhibitor were present per erythrocyte, that is, about one inhibitor molecule per molecule of the Cl- carrier. Evan when Cl- efflux was totally blocked pyruvate and lactate uptake occurred. Kinetic evidence is presented which suggests that the Cl- carrier can transport pyruvate and lactate with a high Km and high Vmax., but that an additional carrier with a low Km and a low Vmax. also exists. This carrier catalyses the exchange of small carboxylate anions with intracellular lactate, is competitively inhibited by alpha-cyano-4-hydroxycinnamate and non-competitively inhibited by picrate. The Cl- carrier shows a reverse pattern of inhibition. It is concluded that net efflux of lactic acid from the cell must occur on the Cl- carrier and involve exchange with HCO3 - followed by loss of CO2. The low Km carrier might be used in pyruvate/lactate or acetoacetate/beta-hydroxybutyrate exchanges involved in transferring reducing power across the cell membrane. The possibility that the Cl- carrier exists in cells other than the erythrocyte is discussed. It is concluded that its presence in other cell membranes together with a low intracellular Cl- concentration would explain why the pH in the cytoplasm is lower than that of the blood, and why permeable carboxylate anions do not accumulate within the cell when added from outside.

Biological Transport, Active↗