Kinetic formulation of oxygen consumption and denitrification processes in soil

1997 ◽  
Vol 77 (2) ◽  
pp. 253-260 ◽  
Author(s):  
C. M. Cho ◽  
D. L. Burton ◽  
C. Chang
Keyword(s):  
Oxygen Consumption ◽  
Microbial Population ◽  
Relative Magnitude ◽  
Inhibitory Effect ◽  
Zero Order ◽  
Kinetic Formulation ◽  
Nitrous Oxide Reduction ◽  
Key Words Oxygen Consumption ◽  
Denitrification Kinetics ◽  
Kinetic Expression

A kinetic expression for oxygen, nitrate, nitrite and nitrous oxide reduction in soil was developed. The formulation was based on competitive Michaelis-Menten kinetics for a steady microbial population whose respiratory activity was assumed to be constant so that the number of electrons produced per unit of time was constant. Competition among the electron acceptors was characterized by their affinity toward the electron and by their concentration. Several different values for the affinity coefficients were used to simulate the concentration of O2, NO3−, NO2−, N2O and N2 at various times. When relative magnitudes of affinity coefficients were chosen to be 100 000, 1, 100 and 0.1, for O2, NO3−, NO2− and N2O, respectively, the temporal plot of concentration showed that the disappearance of O2 and NO3− was zero order. The accumulation of NO2− was very small and it was rapidly reduced to N2O. The production rate of N2O was nearly zero order but the magnitude of the rate was rather small as opposed to the rate of disappearance of NO3−. The reduction of N2O to N2 took place only after NO3− had almost disappeared. With these competition parameters NO3− was stable in the presence of O2. The reduction of N2O was also very much retarded in the presence of NO3−. NO2− was relatively unstable, even in the presence of O2, and it was further reduced to N2O. With the relative magnitude of the chosen affinity coefficients, the kinetic formulation effectively simulated the "inhibitory" effect of O2 upon the denitrification process, and the "inhibitory" effect of NO3− and NO2− upon the reduction of N2O to N2. Key words: Oxygen consumption, denitrification, kinetics, competition

Halothane Selectively Inhibits Nonshivering Thermogenesis 

1995 ◽  
Vol 82 (2) ◽  
pp. 491-501 ◽  
Author(s):  
Andrea Dicker ◽  
Kerstin B. E. Ohlson ◽  
Lennart Johnson ◽  
Barbara Cannon ◽  
Sten G.E. Lindahl ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Inhibitory Effect ◽  
Nonshivering Thermogenesis ◽  
Halothane Anesthesia ◽  
Control Series ◽  
Mechanically Ventilated ◽  
Anesthetized Rats ◽  
Rate Of Oxygen Consumption ◽  
Spontaneously Breathing ◽  
Thermogenic Response

Background During halothane anesthesia, infants fail to increase oxygen consumption in response to a cold stimulus in the form of an increase in temperature gradient between body and environment. Based on recent observations with isolated brown-fat cells, it seemed feasible that this inability to respond could be due to an inhibition of nonshivering thermogenesis during halothane anesthesia. Methods The rate of oxygen consumption was measured in cold-acclimated hamsters and rats. The rate evoked by norepinephrine injection in hamsters at an environmental temperature of approximately 24 degrees C was used as a measure of the capacity for nonshivering thermogenesis. Anesthesia was induced by 3% halothane and maintained by 1.5% halothane. One experimental series with spontaneously breathing hamsters and a second control series with spontaneously breathing rats and with rats whose lungs were mechanically ventilated were conducted. Results Norepinephrine injection led to a fourfold increase in the rate of oxygen consumption in control hamsters; after this response had subsided, a second injection led to a similar effect. Halothane anesthesia caused an approximately 20% decrease in resting metabolic rate (P < 0.05) and a 70% inhibition of the thermogenic response to norepinephrine (P < 0.001). The halothane concentration yielding half-maximal inhibitory effect was estimated to be less than 1.0%. After the animals had recovered from halothane anesthesia, a completely restored thermogenic response to norepinephrine was observed. The inhibitory effect of halothane also was observed in hamsters maintained at normothermia and was therefore not secondary to the slight hypothermia that otherwise developed during anesthesia. In a series of control experiments, it was confirmed that rats also showed large thermogenic responses to norepinephrine injections, and it was found that, in spontaneously breathing halothane-anesthetized rats, the thermogenic response to norepinephrine was also much inhibited. Further, in halothane-anesthetized rats whose lungs were mechanically ventilated, and where blood gases were kept at virtually normal levels, the thermogenic response to norepinephrine was found to be similarly markedly inhibited. Conclusions A much diminished or abolished thermogenic response to injected norepinephrine was demonstrated in halothane-anesthetized animals. This implies that there would be a diminished ability to elicit nonshivering thermogenesis even when this process is physiologically induced. Such a diminished ability could in part explain the susceptibility of neonates and infants to hypothermia during halothane anesthesia.

Inhibitory Effect of Thyroxine Analogues on Oxygen Consumption in Mice

Nature ◽  
1949 ◽  
Vol 164 (4173) ◽  
pp. 699-700 ◽  
Author(s):  
N. F. MACLAGAN ◽  
M. M. SHEAHAN ◽  
J. H. WILKINSON
Keyword(s):  
Oxygen Consumption ◽  
Inhibitory Effect

scholarly journals Regulation of erythropoietin production is related to proximal tubular function

1989 ◽  
Vol 256 (5) ◽  
pp. F942-F947 ◽  
Author(s):  
K. U. Eckardt ◽  
A. Kurtz ◽  
C. Bauer
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Sensor ◽  
Collecting Duct ◽  
Inhibitory Effect ◽  
Tubular Function ◽  
Sodium Reabsorption ◽  
Renal Oxygen Consumption ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Renal Oxygen

Regulation of renal erythropoietin (EPO) production is based on an intrarenal oxygen sensor. Whereas the sensitivity of this oxygen sensor to variations in renal oxygen supply is well established, the influence of changes in renal oxygen consumption has not yet been elucidated. Diuretic drugs, which inhibit active sodium reabsorption, reduce tubular oxygen consumption. We therefore investigated the effects of acetazolamide, furosemide, hydrochlorothiazide, and amiloride, known to preferentially inhibit sodium reabsorption at different segments of the nephron, on hypoxia-induced EPO formation in mice. Those drugs that are considered to act mainly in the loop of Henle, distal tubule, and collecting duct (furosemide, hydrochlorothiazide, and amiloride) did not impair EPO formation. Acetazolamide on the other hand, which is thought to act predominantly at the proximal tubular site, significantly reduced EPO formation in response to normobaric hypoxia (8 and 14% O2) and functional anemia (0.1% carbon monoxide). This inhibitory effect of acetazolamide was dose dependent and correlated with the natriuresis induced. It appeared not to depend on the metabolic acidosis induced by the drug, since the simultaneous administration of sodium bicarbonate, which restored standard bicarbonate levels to normal, did not diminish the inhibitory effect of acetazolamide on EPO production. In conclusion the data suggest that the regulation of EPO production is likely to be related to proximal tubular function.

scholarly journals The biosynthesis of intestinal mucins. The effect of salicylate on glycoprotein biosynthesis by sheep colonic and human gastric mucosal tissues in vitro

1968 ◽  
Vol 106 (3) ◽  
pp. 645-658 ◽  
Author(s):  
P W Kent ◽  
A. Allen
Keyword(s):  
Oxygen Consumption ◽  
Amino Sugar ◽  
Inhibitory Effect ◽  
Total Radioactivity ◽  
Human Gastric Mucosa ◽  
Enzyme Preparations ◽  
Acetylneuraminic Acid ◽  
Control Value ◽  
Glycoprotein Biosynthesis

1. Incubation of sheep colonic mucosal scrapings in Krebs–Ringer buffer for 2½hr. in the presence of salicylate (15mm) resulted in decreased incorporation of radioactivity into the epithelial glycoprotein from the following labelled precursors: 16·6μm-d-[2−14C]glucose (83·9% inhibition), 20μm-l-[U−14C]threonine (82%) and 35SO42−(79%). Oxygen uptake measured simultaneously was diminished to 41% of the control value. 2. At lower concentrations of salicylate (e.g. 3·75mm), incorporation of 20μm-l-[U−14C]threonine was little affected (3–6% inhibition), whereas utilization of 4μm-d-[U−14C]glucose and 35SO42− was inhibited (41–48% and 40–59% of the control values respectively). 3. Analysis of the papain-digested glycoprotein from tissue incubations with 16·6μm-d-[2−14C]glucose in the presence of salicylate (3·75mm) showed large decreases in labelling of N-acetylneuraminic acid and N-glycollylneuraminic acid residues (57% and 34% of the control values respectively) and of hexosamine constituents (glucosamine, 55% inhibition; galactosamine, 33% inhibition). Labelling of neutral sugars (galactose and fucose) was relatively little affected (9 and 11% inhibition respectively). 4. Glucose 6-phosphate transaminase and glucosamine 6-phosphate acetylase in particle-free enzyme preparations of the sheep tissue were unaffected by salicylate at the above concentrations. Acetyl-CoA synthetase was markedly inhibited. 5. Human gastric mucosa (from operation), on incubation as above, had in one experiment an oxygen consumption of 9·9μl./hr./mg. dry wt. of tissue and incorporated 5μm-d-[U−14C]glucose (15·8% of the total radioactivity added) into bound hexosamine (20·6% of the total radioactivity incorporated), hexoses (glucose and galactose, 5·7%) and fucose (14·2%). The presence of salicylate (15mm) decreased the incorporation of 5μm-d-[U−14C]glucose into the glycoprotein by 74%, all sugar constituents being affected, without influence on the rate of oxygen consumption. 6. The results suggest an inhibitory effect of salicylate on glycoprotein biosynthesis at the level of the amino sugar intermediates.

Acute effects of epidermal growth factor on Na+, K+-ATPase-dependent oxygen consumption and the amount of the enzyme units in enterocytes isolated from the jejunum of chickens

1998 ◽  
Vol 78 (3) ◽  
pp. 327-333 ◽  
Author(s):  
H. Park ◽  
B. W. McBride ◽  
L. P. Milligan ◽  
L. M. Trouten-Radford
Keyword(s):  
Oxygen Consumption ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Intracellular Ph ◽  
Basolateral Membrane ◽  
Fixed Number ◽  
Short Term ◽  
Key Words Oxygen Consumption ◽  
Epidermal Growth

Enterocytes from jejunum of male White Leghorn chickens aged 14 d and 20 wk were used to investigate the short-term effect of epidermal growth factor (EGF) on total O2 uptake (TO2) and Na+, K+-dependent O2 uptake (OSO2) and intracellular pH (pHi). Total O2 uptake and OSO2 was decreased (P < 0.05) in enterocytes, isolated from both young and adult birds as concentration of EGF increased in the incubation medium from 0 to 100 ng mL−1. The energy required to support Na+, K+-ATPase activity in jejunal enterocytes obtained from 2-wk-old and 20-wk-old birds was 33–37% and 31–34% of total O2 uptake, respectively. No changes were observed in the amount of the maximal binding sites for 3H-ouabain in enterocytes incubated with EGF; the regulation had not caused rapid decrease in the amount of Na+, K+-ATPase units in the basolateral membrane of enterocytes. Epidermal growth factor caused short-term reduction of pHi as did amiloride. Seemingly, an acute action of EGF in chicken enterocytes in vitro is to reduce the activity of a fixed number of Na+, K+-ATPase units in enterocytes by decreasing Na+, H+-antiport-dependent Na+ influx. Key words: Oxygen consumption, enterocytes, Na+, K+-ATPase, ouabain, epidermal growth factor, intracellular pH, chicks

scholarly journals THE APPLICATION OF THE MATHEMATICAL MODEL FOR PREDICTING THE THRESHOLD CONCENTRATIONS OF THE INFLUENCE OF PESTICIDES ON THE SANITARY STATUS OF WATERS

2018 ◽  
Vol 97 (6) ◽  
pp. 520-524
Author(s):  
Olga S. Pivneva
Keyword(s):  
Mathematical Model ◽  
Oxygen Consumption ◽  
Experimental Studies ◽  
Oxygen Demand ◽  
Equation System ◽  
Inhibitory Effect ◽  
Water Bodies ◽  
Screening Methods ◽  
Real Risk ◽  
Biochemical Oxygen Consumption

Introduction. The rapid growth in the production and use of pesticides poses a real risk of the possible contamination of water bodies, which determines the urgency of the improving the methods of hygienic rating of pesticide preparations in water bodies, as well as the search for screening methods for establishing threshold concentrations.The issues of the need to improve the methodological approaches to the hygienic regulation of pesticide products in water of water bodies are considered, the need for further scientific study of this issue is shown. Material and methods. There are presented results of ourselves laboratory studies on the effect of herbicides of the sulfonylurea class on the processes of self-purification of reservoirs according to the Biological Oxygen Demand (BOD) index. In the work there were used substances of the sulfonylureas derivatives with a multi-directional mechanism of action that exerts both a stimulating and inhibitory effect on the course of processes of the biochemical oxygen consumption. With the use of the formula (Gotovtsev A.V., 2016), the total biochemical oxygen consumption for sulfonylurea derivatives was calculated from the two experimentally measured BOD values. Results. The data of biochemical oxygen consumption for two substances, obtained as a result of experimental studies, are presented. Selected substances have a multi-directional effect on the course of biochemical processes: stimulation - deviation of BOD from the control (%); inhibition - deviation of BOD from the control (%). There was made an estimation of the possible use of the formula for calculating the total biochemical oxygen consumption obtained in the solution of the modified Streeter-Phelps equation system for pesticides of the sulfonylurea class. The formula was applied as a mathematical model for the predictive assessment of the establishment of threshold concentrations of pesticides on the effect on the sanitary regime of water bodies (accordingly to BOD index). Discussion. In the paper, experimental and calculated values of biochemical oxygen consumption were compared, which shows the possibility of using this mathematical method for predicting the effect of pesticidal preparations of this class on the processes of self-purification of water reservoirs. Conclusion. There was shown the possibility of using mathematical modeling methods, in particular, the modified Streeter-Phelps system of equations in the practice of sanitary and hygienic investigations.

scholarly journals Hypoxia-inducible factor-1α is the therapeutic target of the SGLT2 inhibitor for diabetic nephropathy

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ryoichi Bessho ◽  
Yumi Takiyama ◽  
Takao Takiyama ◽  
Hiroya Kitsunai ◽  
Yasutaka Takeda ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Oxygen Consumption ◽  
Target Genes ◽  
Hypoxia Inducible Factor ◽  
Sglt2 Inhibitor ◽  
Inhibitory Effect ◽  
Sglt2 Inhibitors ◽  
Proximal Tubular Epithelial Cells ◽  
Renal Proximal Tubular

Abstract Previous studies have demonstrated intrarenal hypoxia in patients with diabetes. Hypoxia-inducible factor (HIF)-1 plays an important role in hypoxia-induced tubulointerstitial fibrosis. Recent clinical trials have confirmed the renoprotective action of SGLT2 inhibitors in diabetic nephropathy. We explored the effects of an SGLT2 inhibitor, luseogliflozin on HIF-1α expression in human renal proximal tubular epithelial cells (HRPTECs). Luseogliflozin significantly inhibited hypoxia-induced HIF-1α protein expression in HRPTECs. In addition, luseogliflozin inhibited hypoxia-induced the expression of the HIF-1α target genes PAI-1, VEGF, GLUT1, HK2 and PKM. Although luseogliflozin increased phosphorylated-AMP-activated protein kinase α (p-AMPKα) levels, the AMPK activator AICAR did not changed hypoxia-induced HIF-1α expression. Luseogliflozin suppressed the oxygen consumption rate in HRPTECs, and subsequently decreased hypoxia-sensitive dye, pimonidazole staining under hypoxia, suggesting that luseogliflozin promoted the degradation of HIF-1α protein by redistribution of intracellular oxygen. To confirm the inhibitory effect of luseogliflozin on hypoxia-induced HIF-1α protein in vivo, we treated male diabetic db/db mice with luseogliflozin for 8 to 16 weeks. Luseogliflozin attenuated cortical tubular HIF-1α expression, tubular injury and interstitial fibronectin in db/db mice. Together, luseogliflozin inhibits hypoxia-induced HIF-1α accumulation by suppressing mitochondrial oxygen consumption. The SGLT2 inhibitors may protect diabetic kidneys by therapeutically targeting HIF-1α protein.

scholarly journals Inhibitory Effect of Water on Oxygen Consumption by Plant Materials

1960 ◽  
Vol 35 (2) ◽  
pp. 184-188 ◽  
Author(s):  
Takao Ohmura ◽  
Robert W. Howell
Keyword(s):  
Oxygen Consumption ◽  
Inhibitory Effect ◽  
Plant Materials ◽  
Effect Of Water

KINETIC FORMULATION OF THE DENITRIFICATION PROCESS IN SOIL

1979 ◽  
Vol 59 (3) ◽  
pp. 249-257 ◽  
Author(s):  
C. M. CHO ◽  
J. G. MILLS
Keyword(s):  
Enzyme Kinetics ◽  
Maximum Concentration ◽  
Initial Rate ◽  
Zero Order ◽  
Gas Mixture ◽  
Disappearance Rate ◽  
High Accumulation ◽  
Kinetic Formulation ◽  
Initial Concentration ◽  
Denitrification Process

Kinetic formulation of denitrification process in soil was developed based on a model of competitive Michaelis-Menten type enzyme kinetics. Several values of parameters were chosen to plot the concentrations of NO−3, NO−2, N2O-N and N2-N at various times of incubation under different initial concentrations of NO−3. According to the model the disappearance rate of NO−3 was found to be independent of initial concentration of NO−3 and was nearly constant, similar to zero order rate of disappearance. The initial rate of NO−2 formation was independent of the NO−3 concentration. However, the maximum concentration of NO−2 and the time at which the maximum was found were found to be dependent upon the NO−3 concentration. When there was very little accumulation of NO−2 in the system, the initial rate of N2O formation was found to be independent of NO−3 concentration. However, if there was high accumulation of NO−2, the initial rate of N2O formation became inversely related to NO−3 concentration. The initiation of N2 formation was generally slower as the concentration of NO−3 increased. The composition of gas mixture, N2O and N2, was found to vary depending upon the initial NO−3 concentration and with the time of incubation. The formulation presented herein describes the features of denitrification experimentally observed fairly well.

Doxorubicin and epirubicin iron-induced generation of free radicals In vitro. A comparative study

1987 ◽  
Vol 7 (8) ◽  
pp. 653-658 ◽  
Author(s):  
Kjell Grankvist ◽  
Roger Henriksson
Keyword(s):  
Oxygen Consumption ◽  
Free Radicals ◽  
Myocardial Injury ◽  
Oxygen Free Radicals ◽  
Oxygen Electrode ◽  
Inhibitory Effect ◽  
Free System ◽  
A Cell ◽  
Strong Inhibitory Effect

To ascertain any differences in myocardial injury exerted by the anthracyclines doxorubicin and epirubicin, their ability to generate oxygen free radicals when mixed with Fe(II) was examined in vitro using an oxygen electrode. 5–250 μg/ml doxorubicin or epirubicin consumed oxygen when mixed with 50 or 100 μmol/1 Fe(II). Addition of 75 μmol/1 cytochrome C showed that of the consumed oxygen, approximately 80% entered the monovalent pathway of oxygen reduction. The strong inhibitory effect of 250 mg/1 catalase indicates that most of the superoxide radicals generated are further reduced to hydrogen peroxide by both anthracyclines. Addition of metal chelators DTPA (100/μmol/1), or DDTC (50 μmol/1) did not affect oxygen consumption, whereas EDTA (100/μmol/1) or desferrioxamine (100 μmol/1) with anthracyclines and Fe(II) rather stimulated oxygen consumption. It is concluded that there are no significant differences in the amount or proportion of generated oxygen free radicals between doxorubicin and epirubicin when mixed with Fe(II) in a cell-free system in vitro. Thus, the ability of the anthracyclines, in conjunction with iron alone, to generate radicals does not explain the differences of the drugs in causing myocardial injury.

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