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Journal of General Microbiology Feb 1980Oligomycin (3 microgram ml-1) inhibited glucose utilization in Trypanosoma brucei S42 as shown by measurements of oxygen uptake and pyruvate production. Carbonyl cyanide...
Oligomycin (3 microgram ml-1) inhibited glucose utilization in Trypanosoma brucei S42 as shown by measurements of oxygen uptake and pyruvate production. Carbonyl cyanide 3-chlorophenylhydrazone, an uncoupler of oxidative phosphorylation, did not relieve this inhibition, although some relief was afforded by the alternative substrate glycerol. Naturally dyskinetoplastic Trypanosoma evansi MIAG 105 was less sensitive to inhibition by oligomycin although glycerol relief was still observed, relecting the differential sensitivity of the two pathways. With glucose present as the substrate, 45Ca2+ transport was inhibited by oligomycin in T. brucei, but was stimulated in T. evansi. These results are discussed in terms of alternative systems for maintaining cytoplasmic Ca2+ concentrations in normal and dyskinetoplastic strains of trypanosome.
Topics: Animals; Biological Transport; Calcium; Glucose; Oligomycins; Oxygen Consumption; Pyruvates; Sodium-Potassium-Exchanging ATPase; Trypanosoma; Trypanosoma brucei brucei
PubMed: 6246194
DOI: 10.1099/00221287-116-2-391 -
FEBS Letters Mar 1977
Topics: Adenosine Triphosphatases; Ionophores; Kinetics; Mitochondria; Nigericin; Oligomycins; Saccharomyces cerevisiae; Valinomycin; Venturicidins
PubMed: 140066
DOI: 10.1016/0014-5793(77)80089-6 -
FEBS Letters Jul 1973
Topics: Crosses, Genetic; DNA; Drug Resistance, Microbial; Erythromycin; Ethidium; Extrachromosomal Inheritance; Mitochondria; Mutation; Oligomycins; Recombination, Genetic; Suppression, Genetic; Yeasts
PubMed: 4729489
DOI: 10.1016/0014-5793(73)80208-x -
PloS One 2016The maximal capacity of the mitochondrial electron transport system (ETS) in intact cells is frequently estimated by promoting protonophore-induced maximal oxygen...
The maximal capacity of the mitochondrial electron transport system (ETS) in intact cells is frequently estimated by promoting protonophore-induced maximal oxygen consumption preceded by inhibition of oxidative phosphorylation by oligomycin. In the present study, human glioma (T98G and U-87MG) and prostate cancer (PC-3) cells were titrated with different concentrations of the protonophore CCCP to induce maximal oxygen consumption rate (OCR) within respirometers in a conventional growth medium. The results demonstrate that the presence of oligomycin or its A-isomer leads to underestimation of maximal ETS capacity. In the presence of oligomycin, the spare respiratory capacity (SRC), i.e., the difference between the maximal and basal cellular OCR, was underestimated by 25 to 45%. The inhibitory effect of oligomycin on SRC was more pronounced in T98G cells and was observed in both suspended and attached cells. Underestimation of SRC also occurred when oxidative phosphorylation was fully inhibited by the ATP synthase inhibitor citreoviridin. Further experiments indicated that oligomycin cannot be replaced by the adenine nucleotide translocase inhibitors bongkrekic acid or carboxyatractyloside because, although these compounds have effects in permeabilized cells, they do not inhibit oxidative phosphorylation in intact cells. We replaced CCCP by FCCP, another potent protonophore and similar results were observed. Lower maximal OCR and SRC values were obtained with the weaker protonophore 2,4-dinitrophenol, and these parameters were not affected by the presence of oligomycin. In permeabilized cells or isolated brain mitochondria incubated with respiratory substrates, only a minor inhibitory effect of oligomycin on CCCP-induced maximal OCR was observed. We conclude that unless a previously validated protocol is employed, maximal ETS capacity in intact cells should be estimated without oligomycin. The inhibitory effect of an ATP synthase blocker on potent protonophore-induced maximal OCR may be associated with impaired metabolism of mitochondrial respiratory substrates.
Topics: Cell Line, Tumor; Cell Respiration; Electron Transport; Humans; Mitochondria; Oligomycins; Oxidative Phosphorylation; Oxygen Consumption
PubMed: 26950698
DOI: 10.1371/journal.pone.0150967 -
Pesticide Biochemistry and Physiology Jun 2021Botrytis cinerea is one of the most destructive fungal pathogens which can cause gray mold diseases of numerous plant species, while the frequent applications of...
Botrytis cinerea is one of the most destructive fungal pathogens which can cause gray mold diseases of numerous plant species, while the frequent applications of fungicides also result in the fungicide-resistances of B. cinerea. In this study, a new Streptomyces strain FX13 was obtained to show biocontrol potentials against fungicide-resistant B. cinerea B3-4. Its in vitro and in vivo antifungal mechanisms were further investigated. The results showed that the culture extract of strain FX13 could significantly inhibit the mycelia growth of B. cinerea B3-4 with the EC value of 5.40 mg L, which was greatly lower than those of pyrisoxazole, boscalid and azoxystrobin. Further bioassay-guided isolation of the extract had yielded the antifungal component SA1, which was elucidated as a 26-membered polyene macrolide of oligomycin A. SA1 could inhibit the mycelia growth, spore germination, germ tube elongation and sporogenesis of B. cinerea B3-4 in vitro, and also showed significant curative and protective effects against gray mold on grapes in vivo. Moreover, SA1 could result in the loss of membrane integrity and the leakage of cytoplasmic contents, which might be related to the accumulation of reactive oxygen species (ROS) and membrane lipid peroxidation. Besides, intracellular adenosine triphosphatase (ATPase) activity and adenosine triphosphate (ATP) content of B. cinerea B3-4 decreased after SA1-treatment. Overall, the oligomycin A-producing strain FX13 could inhibit fungicide-resistant B. cinerea B3-4 in vitro and in vivo, also highlighting its biocontrol potential against gray mold.
Topics: Botrytis; Fungicides, Industrial; Oligomycins; Plant Diseases; Streptomyces
PubMed: 33993959
DOI: 10.1016/j.pestbp.2021.104834 -
The Journal of Antibiotics Aug 1972
Topics: Adenosine Triphosphatases; Anti-Bacterial Agents; Drug Resistance, Microbial; Mitochondria; Mutation; Oligomycins; Saccharomyces cerevisiae
PubMed: 4265192
DOI: No ID Found -
Biochimica Et Biophysica Acta Apr 1968
Topics: Antimetabolites; Cyclohexanes; Depression, Chemical; Energy Transfer; Glucose; Imides; Oligomycins; Oxidation-Reduction; Saccharomyces
PubMed: 5655440
DOI: 10.1016/0005-2728(68)90199-0 -
Comparative Biochemistry and... 1976
Topics: Adenosine Triphosphatases; Aerobiosis; Anaerobiosis; Animals; DNA; Diptera; Genetic Variation; Genotype; Kinetics; Mitochondria; Oligomycins; Phenotype; Saccharomyces cerevisiae; Species Specificity; Trypanosoma; Trypanosoma brucei brucei
PubMed: 133016
DOI: 10.1016/0305-0491(76)90167-x -
Somatic Cell Genetics Nov 1979Fourteen oligomycin-resistant LM(TK-) clones were isolated following the mutagenesis of minicells. In the absence of oligomycin, the mutants grew with population...
Fourteen oligomycin-resistant LM(TK-) clones were isolated following the mutagenesis of minicells. In the absence of oligomycin, the mutants grew with population doubling times similar to that of the wild type (1 day). In 3 or 5 microgram oligomycin/ml the doubling times of the mutants were 1.2-2.5 days. Both stable and unstable classes were represented among the oligomycin-resistant mutants. Mitochondrial ATPase activities of the mutants were 1.3-1130 times more resistant to oligomycin than the wild type. The mitochondrial ATPase of OLI 14 was found to be bound firmly to the mitochondrial membrane, showed no alteration in the pH optimum compared to wild-type, and exhibited increased resistance to DCCD and venturicidin. These results are consistent with the conclusion that oligomycin resistance in these mutants results from altered mitochondrial ATPase.
Topics: Adenosine Triphosphatases; Animals; Cell Line; Clone Cells; Drug Resistance; Mice; Mitochondria; Mutation; Oligomycins; Phenotype
PubMed: 161820
DOI: 10.1007/BF01542644 -
Biochimica Et Biophysica Acta Mar 1994Incubation of cultured ventricular cardiomyocytes with high oligomycin concentrations (100 micrograms/ml), either alone or combined with 2-deoxyglucose (20 mM), led to...
Incubation of cultured ventricular cardiomyocytes with high oligomycin concentrations (100 micrograms/ml), either alone or combined with 2-deoxyglucose (20 mM), led to the rapid depletion of cellular ATP. Inositol (poly)phosphate production decreased, and 6-keto PGF1 alpha production was increased. In cells depleted of ATP, either by low oligomycin concentrations or by sodium azide, 6-keto PGF1 alpha was not appreciably increased. There was a 25% rise in the release of fatty acids from the sn-2 position in glycerophospholipids. We suggest that oligomycin at high concentrations causes the release of free arachidonic acid from phospholipids either by non-PIP2-specific PLC and DG lipase or by phospholipase D, phosphatidic acid phosphatase and DG lipase. The effect is unrelated to decreased cellular ATP content.
Topics: 6-Ketoprostaglandin F1 alpha; Adenosine Triphosphate; Animals; Cells, Cultured; Deoxyglucose; Inositol Phosphates; Myocardium; Oligomycins; Rats
PubMed: 8130261
DOI: 10.1016/0005-2760(94)90152-x