PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PICRATES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 91 records · Page 5Linked to original sources
PubMed1995

Analgesic efficacy of topical butamben picrate.

Over the past generation, advents in topical antibiotics and oral analgesia have obscured butamen and its family of topical anesthetics. Using a modified version of the McGill University pain questionnaire, this study attempts to establish the efficacy and clinical utility of this overlooked topical anesthetic.

Adolescent↗
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↗
PubMed1985

Picric acid methods greatly overestimate serum creatinine in mice: more accurate results with high-performance liquid chromatography.

The creatinine levels of blood and urine from humans, rats, and mice were measured by high-performance liquid chromatography. These were compared to the alkaline picrate analysis of creatinine performed by standard colorimetric, kinetic, and AutoAnalyzer techniques. For human serum and urine the values obtained using the HPLC technique gave good agreement with four out of five alkaline picrate techniques. For black or white mice, the serum creatinine concentration was 8.7 +/- 0.4 microM by HPLC but 44.9 +/- 1.9 microM by the lowest alkaline picrate method. Mouse urine creatinine concentrations were 3.24 +/- 0.19 mM by HPLC and 4.59 +/- 0.39 mM by the nearest alkaline picrate method. Rat serum creatinine concentrations analyzed by HPLC were about half the values obtained by AutoAnalyzer. Mouse and rat samples seemed to have substances which gave nonspecific color and thus interfered with the analysis of creatinine by the alkaline picrate methods. While the alkaline picrate analysis of creatinine was adequate for human samples, it was necessary to use HPLC to accurately measure rodent creatinine. The fractional excretion of creatinine was determined by measuring creatinine in mouse urine and plasma by both the kinetic and HPLC methods and comparing these values to urine and plasma inulin. Using the kinetic method, creatinine was cleared at 43 +/- 3% of the rate of inulin. Using the HPLC method, creatinine was cleared at 170 +/- 11% of the rate of inulin.

Animals↗
PubMed2001

Converging catabolism of 2,4,6-trinitrophenol (picric acid) and 2,4-dinitrophenol by Nocardioides simplex FJ2-1A.

Initial F420-dependent hydrogenation of 2,4,6-trinitrophenol (picric acid) generated the hydride sigma-complex of picrate and finally the dihydride complex. With 2,4-dinitrophenol the hydride sigma-complex of 2,4-dinitrophenol is generated. The hydride transferring enzyme system showed activity against several substituted 2,4-dinitrophenols but not with mononitrophenols. A Km-value of 0.06 mM of the hydride transfer for picrate as substrate was found. The pH optima of the NADPH-dependent F420 reductase and for the hydride transferase were 5.5 and 7.5, respectively. An enzymatic activity has been identified catalyzing the release of stoichometric amounts of 1 mol nitrite from 1 mol of the dihydride sigma-complex of picrate. This complex was synthesized by chemical reduction of picrate and characterized by 1H and 13C NMR spectroscopy. The hydride sigma-complex of 2,4-dinitrophenol has been identified as the denitration product. The nitrite-eliminating activity was enriched and clearly separated from the hydride transferring enzyme system by FPLC. 2,4-Dinitrophenol has been disproven as a metabolite of picrate (Ebert et al. 1999) and a convergent catabolic pathway for picrate and 2,4-dinitrophenol with the hydride sigma-complex of 2,4-dinitrophenol as the common intermediate has been demonstrated.

2,4-Dinitrophenol↗
PubMed1974

Trinitrophenol: a membrane-impermeable uncoupler of oxidative phosphorylation.

Picrate (trinitrophenol) is a unique uncoupler of oxidative phosphorylation. Unlike the commonly used uncouplers (e.g., 2,4-dinitrophenol, pentachlorophenol, m-chlorocarbonylcyanide phenylhydrazone, and 5-chloro-3-t-butyl-2'-chloro-4'-nitrosalicylanilide), picrate seems to penetrate the mitochondrial inner membrane very slowly. Consequently, it is ineffective when added to intact mitochondria or to mitochondria depleted of their outer membranes. In contrast, when added to phosphorylating submitochondrial particles prepared by sonication in which the inner membrane orientation is inside-out, picrate binds to the uncoupler-binding sites and uncouples oxidative phosphorylation. This unique property of picrate has made it possible to compare the potencies of picrate and dinitrophenol for (a) uncoupling and (b) increasing the proton permeability of submitochondrial particle vesicles. At 50% uncoupling concentration, dinitrophenol increased the proton permeability of submitochondrial particle vesicles by 9- to 12-fold. In contrast, at 100% uncoupling concentrations or higher, picrate augmented the proton permeability of the particles by only about 3-fold. These results indicate that facilitation of transmembrane proton equilibration does not determine the degree of uncoupling, and lead to the corollary conclusion that the magnitude of transmembrane proton gradient need not be the quantitative driving force for ATP synthesis.

Animals↗
PubMed1999

Simple method for determination of thiocyanate in urine.

BACKGROUND: It would be useful to develop a simple kit method for determination of thiocyanate in urine, which could be used to monitor cyanide overload in cassava-consuming populations. METHODS: The method was based on the quantitative oxidation of thiocyanate in acid permanganate at room temperature in a closed vial with liberation of HCN, which reacted with a picrate paper. For semiquantitative analysis in the field, the colored picrate paper was matched with a color chart prepared using known amounts of KSCN. In the laboratory, a more accurate result was obtained by elution of the colored complex in water and measurement of the absorbance at 510 nm. Over the range 0-100 mg/L, there was a linear relationship given by the equation: thiocyanate content (mg/L) = 78 x absorbance. RESULTS: The picrate thiocyanate method gave no interference with urine samples containing protein at less than 7 g/L, 21 amino acids, histamine, glucose, NaCl, urea, blood, and linamarin. For 53 urine samples analyzed by an accurate column method and the thiocyanate picrate method, a regression line gave very good agreement (r(2) = 1. 000). Quantitative recoveries of thiocyanate added to urine samples were obtained with the picrate method. CONCLUSIONS: A simple picrate kit for determination of thiocyanate in urine was developed and is available free of charge for workers in developing countries.

Adult↗
PubMed2007

Hydrogen-bond interactions of nicotine and acetylcholine salts: a combined crystallographic, spectroscopic, thermodynamic and theoretical study.

The hydrogen-bond (HB) interactions of the monocharged active forms of nicotine and acetylcholine (ACh) have been compared theoretically by using density functional theory (DFT) calculations and experimentally on the basis of crystallographic observations and the measurement of equilibrium constants in solution. The 2,4,6-trinitrophenolate (picrate) counterion was used to determine the experimental HB basicity of the cations despite its potential multisite HB acceptor properties. The preferred HB interaction site of the ammonium picrate salts was determined from a survey of crystallographic data found in the Cambridge Structural Database (CSD) and is supported by theoretical calculations. Two distinct classes of ammonium groups were characterised depending on the absence (quaternary ammonium) or presence (tertiary, secondary and primary ammoniums) of an N(+)HO hydrogen bond linking the two ions. The crystal structure of nicotinium picrate was determined and compared with that of ACh. This analysis revealed the peculiar behaviour of the ammonium moiety of nicotinic acetylcholine receptor (nAChR) ligands towards the picrate anion. Dedicated methods have been developed to separate the individual contributions of the anion and cation accepting sites to the overall HB basicity of the ion pairs measured in solution. The HB basicities of the picrate anions associated with the two different ammonium classes were determined in dichloromethane solution by using several model ion pairs with non-basic ammonium cations. The experimental and theoretical studies performed on the nicotine and ACh cations consistently show the significant HB ability of the acceptor site of nAChR agonists in their charged form. Both the greater HB basicity of the pyridinic nitrogen over the carbonyl oxygen and the greater HB acidity of the N(+)H unit relative to N(+)CH could contribute to the higher affinity for nAChRs of nicotine-like ligands relative to ACh-like ligands.

Acetylcholine↗