Antimycin a Inhibits QE -Quenching by a Protonophoric Mechanism

1995 ◽  
pp. 2055-2058
Author(s):  
Christine T. Yerkes ◽  
Antony R. Crofts
Keyword(s):  
Antimycin A

The Calorimetric-respirometric Ratio: Its Potential as a Cytotoxicity Test

1994 ◽  
Vol 22 (5) ◽  
pp. 364-376
Author(s):  
Richard B. Kemp ◽  
Catherine Stephansen ◽  
Sajid Mohamed ◽  
R.W. John Meredith
Keyword(s):  
Heat Flux ◽  
Salt Solution ◽  
Krebs Cycle ◽  
Cytotoxicity Test ◽  
Antimycin A ◽  
Rich Medium ◽  
Animal Cells ◽  
Normal Input ◽  
High Level ◽  
L929 Mouse

The ratio between heat flux and oxygen flux, the calorimetric ratio, is an enthalpy budget device used to identify anaerobic pathways in the presence of respiration. Ratios that are more exothermic (i.e. more negative) than the average for catabolic substrates (-450kJ mol O2 ± 5%; Thornton's rule), are usual for cells established in culture, including suspension-adapted LS-L929 mouse fibroblasts. A common reason for this is a high level of glycolysis, to produce lactate, simultaneously with aerobic pathways. To test the idea that the calorimetric-respirometric (CR) ratio is a revealing cytotoxic endpoint, LS cells grown in serum-rich medium were insulted with known metabolic poisons. Malonate, 2,4-dinitrophenol (2,4-DNP) and a mixture of antimycin A and rotenone increased the CR ratio to degrees largely explained by greater lactate flux, the CR700 values being 22μM malonate, 56μM 2,4-DNP and, for the mixture, 2μM antimycin A and 5μM rotenone. Higher concentrations of 2,4-DNP gave an “exothermic gap” for which there was no explained pathway. Iodoacetate decreased the CR ratio while inhibiting glycolysis, a result which can be explained by the hypothesis that substrates available in the serum were degraded by mitochondrial pathways and thereby substituted for the normal input from the Krebs cycle, which had been arrested by pyruvate starvation. In a balanced salt solution containing only 5.5mM glucose, the metabolic rate slowed and the CR ratio was more exothermic (CR700 = 6μM), giving a “gap” for which there was no explanation. Ten MEIC chemicals gave CR700 endpoints which closely corresponded to the order of toxicity for a battery of tests using animal cells. The CR method thus provides a good basis for investigating the mechanisms by which chemicals have toxic effects on cells.

Separation of carotid body chemoreceptor responses to O2 and CO2 by oligomycin and by antimycin A

1982 ◽  
Vol 242 (3) ◽  
pp. C200-C206 ◽  
Author(s):  
E. Mulligan ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Carbonic Anhydrase ◽  
Partial Pressure ◽  
Carotid Body ◽  
Body Tissue ◽  
Antimycin A ◽  
Tissue Ph ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Metabolic Hypothesis

The cat carotid chemoreceptor O2 and CO2 responses can be separated by oligomycin and by antimycin A. Both of these agents greatly diminish or abolish the chemoreceptor O2 response but not the nicotine or CO2 responses. After either oligomycin or antimycin, the responses to increases and decreases in arterial CO2 partial pressure (PaCO2) consisted of increases and decreases in activity characterized respectively by exaggerated overshoots and undershoots. These were eliminated by the carbonic anhydrase inhibitor, acetazolamide, suggesting that they resulted from changes in carotid body tissue pH. The steady-state PaCO2 response remaining after oligomycin was no longer dependent on arterial O2 partial pressure (PaO2). All effects of antimycin were readily reversible in about 20 min. The separation of the responses to O2 and CO2 indicates that there may be at least partially separate pathways of chemoreception for these two stimuli. The similarity of the oligomycin and antimycin results supports the metabolic hypothesis of chemoreception.

scholarly journals Effects of antimycin A and 2-deoxyglucose on secretion in human platelets. Differential inhibition of the secretion of acid hydrolases and adenine nucleotides

1979 ◽  
Vol 182 (2) ◽  
pp. 413-419 ◽  
Author(s):  
Holm Holmsen ◽  
Linda Robkin ◽  
H. James Day
Keyword(s):  
Shape Change ◽  
Adenine Nucleotides ◽  
Human Platelets ◽  
Dense Granule ◽  
Metabolic Inhibitors ◽  
Antimycin A ◽  
Acid Hydrolase ◽  
Acid Hydrolases ◽  
Dense Granule Secretion ◽  
Granule Secretion

1. Shape change, aggregation and secretion of dense-granule constituents in platelets differ in their dependence on cellular energy metabolism. The possibility that such a difference also exists between secretion of dense-granule constituents and acid hydrolases was investigated. 2. Human platelets were incubated with [14C]adenine in plasma, and then washed and resuspended in salt solutions. The effects of incubating the cells with antimycin A and 2-deoxyglucose on the concentrations of [14C]ATP, ADP, AMP, IMP and inosine plus hypoxanthine and on thrombin-induced secretion of ATP plus ADP and acid hydrolases were studied. The metabolic inhibitors only affected 14C-labelled nucleotides, whereas thrombin only liberated unlabelled ATP and ADP. 3. The extent of secretion decreased progressively with time during incubation with the metabolic inhibitors. At any time the secretion of acid hydrolases, β-N-acetylglucosaminidase, β-glucuronidase and β-galactosidase was inhibited to a greater extent than secretion of ATP plus ADP (dense-granule secretion). 4. Incubation with the metabolic inhibitors shifted the log (dose)–response relationship to higher thrombin concentrations, and with a greater shift for acid hydrolase secretion than for dense-granule secretion. 5. Antimycin, when present alone, caused a marked decrease in the rate of acid hydrolase secretion, but had no effect on dense-granule secretion. 6. These results further support the view that acid hydrolase secretion and dense-granule secretion are separate processes with different requirements for ATP energy. Acid hydrolase secretion, but not dense-granule secretion, appears to depend on a simultaneous rapid generation of ATP, which can be accomplished by oxidative, but not by glycolytic, ATP production.

Antimycin A induced cardioprotection is dependent on pre-ischemic p38-MAPK activation but independent of MKK3

2005 ◽  
Vol 39 (4) ◽  
pp. 709-717 ◽  
Author(s):  
A KABIR ◽  
X CAO ◽  
D GOROG ◽  
M TANNO ◽  
R BASSI ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Antimycin A ◽  
Mapk Activation
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