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PubMed1992

Degradation of 2,4-dinitrophenol by two Rhodococcus erythropolis strains, HL 24-1 and HL 24-2.

Two Rhodococcus erythropolis strains, HL 24-1 and HL 24-2, were isolated from soil and river water by their abilities to utilize 2,4-dinitrophenol (0.5 mM) as the sole source of nitrogen. Although succinate was supplied as a carbon and energy source during selection, both isolates could utilize 2,4-dinitrophenol also as the sole source of carbon. Both strains metabolized 2,4-dinitrophenol under concomitant liberation of stoichiometric amounts of nitrite and 4,6-dinitrohexanoate as a minor dead-end metabolite.

2,4-Dinitrophenol↗

PubMed1984

[Effect of carrageenan, galactose and 2,4-dinitrophenol on leukocyte phagocytosis of Staphylococcus aureus and E. coli].

The influence of carrageenan (0.1, 0.05 and 0.01%), galactose (1 X 10(-1), 1 X 10(-2) and 5 X 10(-2) mol/l) and 2,4-dinitrophenol (5 X 10(-4), 1 X 10(-4), 5 X 10(-5) and 1 X 10(-5) mol/l) on the phagocytosis of Staphylococcus aureus SG 511 and E. coli 04/K31 by polymorphonuclear neutrophil granulocytes was studied. At the same time the capacity of the germs to grow and multiply in presence of different concentrations of the analysed compounds was tested. The phagocytosis of Staphylococcus aureus SG 511 was not inhibited by carrageenan, galactose and 2,4-dinitrophenol, but an influence on the phagocytosis of E. coli 04/K31 could be clearly demonstrated (0.1 and 0.05% carrageenan, 1 X 10(-1) mol/l galactose, 5 X 10(-4) and 1 X 10(-4) mol/l 2,4-dinitrophenol). The multiplication of Staphylococci and E. coli was not influenced by all three compounds.

2,4-Dinitrophenol↗

PubMed1984

Effects of 2,4-dinitrophenol and other metabolic inhibitors on the thermograms of Ehrlich ascites carcinoma cells registered with a microcalorimeter.

The heat produced by Ehrlich ascites carcinoma cells was measured microcalorimetrically to investigate the characteristics of the energetics of these cells. 2,4-Dinitrophenol and other inhibitors were used to obtain the standard thermograms. The heat level of starved Ehrlich ascites carcinoma cells (endogenous) was almost constant and linear and depended on the cell number used in the experiments (about 1 cal/1 X 10(8) cells/hr). The endogenous heat generation was suppressed strongly by potassium cyanide but not by iodoacetic acid or 2,4-dinitrophenol. On the other hand, heat evolution was directly related to the amount of glucose added to the medium but not to the number of cells (19 cal/mmol of glucose). The addition of iodoacetic acid markedly suppressed heat generation, but potassium cyanide did not. In contrast, glucose with dinitrophenol increased heat production markedly to about 10% higher than that of the control, possibly due to the uncoupled energy from oxidative phosphorylation. Malonic acid (1 mM) suppressed slightly the endogenous heat but caused a 15% reduction in exogenous heat. The amount of heat produced by the addition of glucose (19 cal/mmol) was equivalent to 40% of the theoretical value of energy released through glycolysis (47 cal/mmol). Thus, the heat produced by exogenous glucose appears to be mainly dependent on glycolysis.

2,4-Dinitrophenol↗

PubMed1994

Immunohistochemical and biochemical indicators of muscle damage in vitro: the stability of control muscle and the effects of dinitrophenol and calcium ionophore.

The biochemical, histological and ultrastructural effects of 2,4-dinitrophenol and the calcium ionophore, A23187, on rat soleus muscle incubated in vitro have been examined to test the hypothesis that immunohistochemical techniques can be used to recognize early structural features of fibre damage. In control muscles, despite mild glycogen depletion and a mild reduction in protein synthetic rate in the central portion of the muscle, fibres throughout the muscle appear to be viable with normal cytoskeletal and contractile protein architecture, normal concentrations of high energy phosphates and no creatine kinase efflux. Dinitrophenol causes rapid creatine kinase efflux, extensive loss of immunolabelling for desmin and dystrophin, and abnormal myosin immunolabelling. Creatine kinase efflux and the changes in desmin and dystrophin are reduced by the exclusion of calcium. A23187 causes more gradual creatine kinase efflux associated with changes in myosin immunolabelling, but loss of desmin and dystrophin immunolabelling is restricted to a few of the most peripheral fibres. The results suggest that immunohistochemical methods can be used to reveal differences in the intracellular mechanisms of muscle damage. Although both dinitrophenol and A23187 may act, in part, through calcium-mediated processes, their effects on cytoskeletal proteins differ. Creatine kinase efflux after A23187 may not be due to gross sarcolemmal damage.

2,4-Dinitrophenol↗

PubMed1980

Effects of phenol and dinitrophenol on acid and alkaline phosphatases in tissues of a fish (Notopterus notopterus).

Specimens of a fresh water fish, Notopterus notopterus were exposed to either phenol (12.56 mg/L), dinitrtophenol (1.34 mg/L), or a mixture of the two (6.28 mg phenol + 0.67 mg dinitrophenol/L) for 72-hr. Surviving fish were sacrificed at 24-, 48-, and 72-hr after exposure, and tissue samples were taken for determining the acid phosphatase and alkaline phosphatase activities. Phenol, dinitrophenol, and mixtures of both, inhibited the activity of both enzymes in the kidney, heart, brain, gills, muscles, stomach, intestine, and pyloric caeca. dinitrophenol exerted more inhibition than phenol. In general, mixtures of phenol and dinitrophenol are somewhat more effective than either compound alone in the inhibition of enzyme activities.

Acid Phosphatase↗

PubMed1978

The hyperpolarizing and depolarizing effects of 2,4-dinitrophenol on Ehrlich cells.

The ability of glucose to reverse the effects of dinitrophenol on amino acid uptake in Ehrlich cells is a function of pH. At pH 6.0, the presence of glucose does not reverse the inhibitory action of the uncoupler. Nearly complete restoration occurs with glucose at pH 7.4. At pH 8, the presence of glucose may cause a modest increase in amino acid uptake in presence of dinitrophenol. At all pH values, glucose restores ATP and cellular K+ to the control levels at the same pH. Although the cytoplasmic pH changes with changes in the external pH, the cell interior is more alkaline than the medium near pH 6.0 and more acid than the medium at pH 7.8 even after 45 min incubation at 37 degrees C. With dinitrophenol and in presence of glucose the difference in pH between the medium and the cell is minimal at both pH 6.0 and 7.8.

Adenosine Triphosphate↗

PubMed2005

Dinitrophenol-induced mitochondrial uncoupling in vivo triggers respiratory adaptation in HepG2 cells.

Here, we show that 3 days of mitochondrial uncoupling, induced by low concentrations of dinitrophenol (10 and 50 microM) in cultured human HepG2 cells, triggers cellular metabolic adaptation towards oxidative metabolism. Chronic respiratory uncoupling of HepG2 cells induced an increase in cellular oxygen consumption, oxidative capacity and cytochrome c oxidase activity. This was associated with an upregulation of COXIV and ANT3 gene expression, two nuclear genes that encode mitochondrial proteins involved in oxidative phosphorylation. Glucose consumption, lactate and pyruvate production and growth rate were unaffected, indicating that metabolic adaptation of HepG2 cells undergoing chronic respiratory uncoupling allows continuous and efficient mitochondrial ATP production without the need to increase glycolytic activity. In contrast, 3 days of dinitrophenol treatment did not change the oxidative capacity of human 143B.TK(-) cells, but it increased glucose consumption, lactate and pyruvate production. Despite a large increase in glycolytic metabolism, the growth rate of 143B.TK(-) cells was significantly reduced by dinitrophenol-induced mitochondrial uncoupling. We propose that chronic respiratory uncoupling may constitute an internal bioenergetic signal, which would initiate a coordinated increase in nuclear respiratory gene expression, which ultimately drives mitochondrial metabolic adaptation within cells.

2,4-Dinitrophenol↗

PubMed1967

The time-course of the synthesis of adenosine triphosphate in Ehrlich ascites-tumour cells, and the effect of 2,4-dinitrophenol.

1. In Ehrlich ascites-tumour cells kept in nitrogen at 20 degrees for 20-30min., the ATP concentration falls from about 15mumoles/g. dry wt. to 2-3mumoles/g. dry wt. 2. If oxygen is admitted to such cells, the ATP concentration rises again in 1-2min. to about 15mumoles/g. dry wt. 3. If glucose is added, in nitrogen, there is a slower increase in ATP concentration to about 6mumoles/g. dry wt., followed by a fall and then by a still slower rise. 4. With glucose and oxygen, the ATP concentration rises rapidly in 1min. to about 8mumoles/g. dry wt., then falls, and finally increases slowly to reach 15mumoles/g. dry wt. in 2hr. 5. 2,4-Dinitrophenol (0.3mm) has little effect on these processes. 6. At 1.0mm, 2,4-dinitrophenol completely inhibits the ATP synthesis dependent on the endogenous respiration, while leaving that in the presence of glucose only a little impaired in rate, and considerably greater in magnitude. 7. ATP synthesis in the presence of glucose and 1.0mm-2,4-dinitrophenol is about three times as fast in oxygen as in nitrogen.

Adenosine Triphosphate↗

PubMed1975

The effect of 2, 4-dinitrophenol on the growth of Bordetella pertussis in chick tracheal organ culture.

Among various metabolic inhibitors tested, only 2, 4-dinitrophenol inhibited the growth of Bordetella pertussis in chick tracheal organ culture at concentrations nontoxic both for bacterial organisms and for ciliary motility of the tracheal fragments. Although this effect of 2, 4-dinitrophenol was reversible in its early stage, longer treatment with this inhibitor resulted in an irreversible inhibition of bacterial growth due to secondary damage of the tracheal fragments. From these observations, it was postulated that the energy required for bacterial growth might be derived from cellular metabolism sensitive to inhibition with 2, 4-dinitrophenol.

Animals↗

PubMed1979

Effects of 2,4-dinitrophenol amylobarbitone and certain other drugs on the rate of oxygen consumption and force of contraction of isolated curarized diaphragm muscle of the rat.

1 A technique has been developed for studying over periods of 10 min or longer the effects of drugs on both the force of electrically-induced contractions and the oxygen consumption of an isolated, curarized, mammalian, skeletal muscle preparation.2 The resting oxygen consumption of the muscle was increased substantially by 2,4-dinitrophenol in concentrations (0.02 mM and higher) that eventually produced contracture. Two other uncoupling agents, 4,6-dinitro-o-cresol and carbonylcyanide-p-trifluoromethoxyphenylhydrazone, behaved similarly.3 The oxygen consumption over 10 min of the stimulated muscle was also increased by 2,4-dinitrophenol (0.05 mM), although the strength of the ;maximal' contractions was lessened.4 Amylobarbitone increased the strength of contraction at a concentration (0.2 mM) that did not affect oxygen consumption significantly. Amylobarbitone and pentobarbitone also increased it at a concentration (1 mM) that depressed oxygen consumption. They decreased both strength of contraction and oxygen consumption at a concentration of 5 mM. Phenobarbitone had a weaker action.5 S-n-decyl-thiouronium increased oxygen consumption when given at a concentration (1 mM) that diminished strength of contraction and eventually produced contracture of the muscle.6 Both S-methyl-thiouronium (1 mM) and 4-aminopyridine (0.1 mM and 0.5 mM) increased strength of contraction without increasing oxygen consumption. Neither strength of contraction nor oxygen uptake was affected by ouabain (up to 0.01 mM) or by phenformin (0.1 mM).7 It is concluded that the response to 2,4-dinitrophenol is due mainly, if not wholly, to its known ability to uncouple oxidative phosphorylation; that the response to the barbiturates is due to a combination of a known metabolic action (viz., blocking of the respiratory chain) and a stimulant action on muscle; and the response to S-n-decyl-thiouronium to a disruptive action on cell membranes. The disproportionate actions of 4-aminopyridine and S-methyl-thiouronium on strength of contraction relative to oxygen consumption are also attributed to a non-metabolic action.

Amobarbital↗

PubMed1999

3-nitroadipate, a metabolic intermediate for mineralization of 2, 4-dinitrophenol by a new strain of a Rhodococcus species.

The bacterial strain RB1 has been isolated by enrichment cultivation with 2,4-dinitrophenol as the sole nitrogen, carbon, and energy source and characterized, on the basis of 16S rRNA gene sequence comparison, as a Rhodococcus species closely related to Rhodococcus opacus. Rhodococcus sp. strain RB1 degrades 2,4-dinitrophenol, releasing the two nitro groups from the compound as nitrite. The release of nitro groups from 2,4-dinitrophenol occurs in two steps. First, the 2-nitro group is removed as nitrite, with the production of an aliphatic nitro compound identified by 1H nuclear magnetic resonance and mass spectrometry as 3-nitroadipate. Then, this metabolic derivative is further metabolized, releasing its nitro group as nitrite. Full nitrite assimilation upon reduction to ammonia requires that an additional carbon source be supplied to the medium.

2,4-Dinitrophenol↗

PubMed1975

Inhibition by 2,4-dinitrophenol of 9,10-dimethyl-1,2-benzanthracene carcinogenesis in the hamster cheek pouch.

After topical treatment of cheek pouches of 10 hamsters with 9,10-dimethyl-1,2-benzanthracene and 2,4-dinitrophenol for 10 weeks no carcinomas developed in any of the animals. After treatment of 10 animals with the carcinogen only, there were 49 carcinomas in the 8 survivors. Inhibition of chemical carcinogenesis by dinitrophenol was tentatively attributed to suppression of ATP synthesis and to activation of ATPase by dinitrophenol.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1980

Metabolism of 3,3'-Diiodothyronine and 3'-monoiodothyronine, and effect of potassium cyanide and dinitrophenol and glucuronidation of thyroxine in cultured rat hepatoma cells.

Rat hepatoma cells (R117-21B) metabolized 3,3'diiodothyronine and 3'-monoiodothyronine by sulfation and glucuronidation. Glucuronidation of iodothyronines (a mixture of 3,3'-diiodothyronine, approximately 99%, and 3'-monoiodothyronine, approximately 10%(was very rapid and 83% of the total 125I in the medium was their glucuronides after 8 hr incubation with the cells at 37 degrees C. Iodothyronine sulfates (approximately 9% of the total 125I) were also detected. No clear increase in free iodide was observed during the 8 hr incubation. The effect of KCN or dinitrophenol on glucuronidation of thyroxine was investigated. Both drugs inhibited glucuronidation, and dinitrophenol was more effective than KCN. Dinitrophenol accelerated the liberation of 125I- in the metabolism of thyroxine in the cultured rat hepatoma cells.

Animals↗

PubMed2005

[Use of dinitrophenols in ion-pair extraction spectrophotometry of cationic tensides].

The application of 2,4-dinitrophenol and 2,6-dinitrophenol as reagents for a ion pair extraction spectrophotometry was tested. The ion pair extraction spectrophotometry experiments were carried out using a simplified procedure (test tube method). Four cationic tensides were used as model analytes. After the optimal conditions of the assay were being determined, the influence of the concentration excess of the reagents on the absorbance of the chloroform extract was investigated. Calibration curves were constructed; an estimation of limits of quantitation was performed and apparent molar absorption coefficients were determined. The obtained results show that both investigated dinitrophenols are suitable for the studied purpose.

Dinitrophenols↗

PubMed1976

[Influence of strophanthin and 2,4-dinitrophenol to the scopolamine-evoked acetylcholine release in rat cortex].

In rats narcotized by urethan we investigated the effect of 2,4-dinitrophenol and ouabain with regard to the cortical release of acetylcholine stimulated by scopolamine and to the acetylcholine content of telencephalon changed in that way. Dinitrophenol increased the liberating effect of scopolamine. In the presence of dinitrophenol and scopolamine ouabain reduced acetylcholine synthesis resulting in an strong decrease of acetylcholine content on persistent diminished increase of acetylcholine release.

Acetylcholine↗

PubMed1963

QUANTITATIVE STUDIES OF THE EFFECT OF ORGANIC SUBSTRATES AND 2,4-DINITROPHENOL ON HETEROTROPHIC CARBON DIOXIDE FIXATION IN HYDROGENOMONAS FACILIS.

McFadden, Bruce A. (Washington State University, Pullman), and H. Robert Homann. Quantitative studies of the effect of organic substrates and 2,4-dinitrophenol on heterotrophic carbon dioxide fixation in Hydrogenomonas facilis. J. Bacteriol. 86:971-977. 1963.-Whole cells of Hydrogenomonas facilis under heterotrophic conditions fixed levels of C(14)O(2) which depended upon the nature of the carbon source being oxidized. It was established that oxidative rates varied as a function of p(CO2). Therefore, all studies were conducted in the presence of 1.5 mole% CO(2) in the gas phase. With glucose-grown cells supplied with glucose as substrate, the heterotrophic fixation was curtailed 98% by the addition of 8.3 x 10(-4)m 2,4-dinitrophenol (DNP). A coupling between reductive fixation of CO(2) and heterotrophic oxidation of substrate is consistent with the observed effect of DNP. The efficiency of coupling of fixation with oxidation was studied for acetate, d-glucose, l-glutamate, d,l-lactate, d-ribose, and succinate as substrates. Kinetic studies showed that the efficiency of coupling (expressed as disintegrations per minute of C(14) per microliter of O(2)) was initially time-variable for all substrates; however, it approached a constant value after 30 to 45 min for acetate, glutamate, lactate, and succinate. The initial variation of the ratio with time was due primarily to C(14)O(2) uptake, which was nonlinear with time. Control studies in the absence of exogenous substrate indicated that CO(2) fixation may also be linked to oxidation of endogenous stores accumulated during heterotrophic growth. d-Ribose appears to be the most promising substrate for short-term fixation studies owing to the rapid incorporation of C(14) and the unusually low endogenous fixation rate by cells grown on ribose. Calculations reveal that, after isotopic equilibrium has occurred, the amount of CO(2) utilized during glucose oxidation is almost 50% of O(2) uptake during the same interval. Even during succinate oxidation, which was shown to be coupled much less effectively with CO(2) fixation, the CO(2) utilized during the same interval is 8% of O(2) uptake.

2,4-Dinitrophenol↗

PubMed1971

Microcalorimetric Measurements of the Heat Evolution and Its Sensitivity to Dinitrophenol during Different Stages of Synchronous Cultures of Scenedesmus.

The applicability of the LKB flow microcalorimeter in a microalgal system was tested. Respiration and its sensitivity to 2,4-dinitrophenol during different stages of a synchronous culture of Scenedesmus obtusiusculus were studied. In cells harvested during the first 8 hours of illumination, heat evolution was 10 to 15 microwatts per 10 million cells and then rose to a peak of about 80 microwatts per 10 million when the cells were harvested in the beginning of the dark period, just before the onset of the divisions. Calculated per milligram dry weight, the highest values were about 140 microwatts, also obtained early in the dark period, after which the values dropped. They were roughly 90 microwatts per milligram at the onset of light and a little below 70 microwatts per milligram after 8 hours of illumination. Thus, the synthesis of new cell material does not give rise to actively respiring mitochondria during the first half of the light period, after which the situation is reversed. Low concentrations of dinitrophenol increased heat evolution, and high concentrations were inhibitory. Cells from the early stages of development were more sensitive to dinitrophenol than older cells. Young cells gave a transient peak of heat evolution even when the steady state was inhibited. Coupled oxidative phosphorylation seems necessary for substrate mobilization and transport to the mitochondria of the young cells. Possibly, young cells use mainly fatty acids and old cells carbohydrates as their main substrate for respiration.

Journal Article↗

PubMed2005

Tetramethylammonium 2,5-dinitrophenolate monohydrate.

The crystal structure of the title compound, C4H12N+.C6H3N2O5-.H2O, is built up from tetramethylammonium cations, 2,5-dinitrophenolate anions and water molecules. The nitro groups are almost coplanar with the aryl ring, which exhibits significant distortion from an ideal hexagonal form. The X-ray geometry of the tetramethylammonium cation shows slight distortion from the tetrahedral symmetry predicted by molecular orbital calculations. The O-H...O hydrogen-bonded water and 2,5-dinitrophenolate units are related by an inversion center and form dimers. The 2,5-dinitrophenolate anions, related by an inversion center and translation, are stacked to form a column along the [100] direction.

Journal Article↗