The inhibitory effect of the artificial electron donor system, phenazine methosulfate-ascorbate, on bacterial transport mechanisms

1977 ◽  
Vol 7 (1) ◽  
pp. 49-59 ◽  
Author(s):  
R. G. Eagon ◽  
B. D. Gitter ◽  
J. J. Rowe
Keyword(s):  
Electron Donor ◽  
Inhibitory Effect ◽  
Bacterial Transport ◽  
Transport Mechanisms ◽  
Phenazine Methosulfate ◽  
Donor System

The effect of phenazine methosulfate-ascorbate on bacterial active transport and adenosine triphosphate formation: inhibition of Pseudomonas aeruginosa and stimulation of Escherichia coli

1979 ◽  
Vol 25 (7) ◽  
pp. 798-802 ◽  
Author(s):  
R. G. Eagon ◽  
T. W. Hodge III ◽  
J. B. Rake ◽  
J. M. Yarbrough
Keyword(s):  
Escherichia Coli ◽  
Pseudomonas Aeruginosa ◽  
Active Transport ◽  
Adenosine Triphosphate ◽  
Electron Donor ◽  
Energy Sources ◽  
Phenazine Methosulfate ◽  
Atp Formation ◽  
Stimulation Of ◽  
Donor System

The artificial electron-donor system, phenazine methosulfate (PMS) ascorbate, inhibited active transport of glucose by Pseudomonas aeruginosa irrespective of whether the incubation systems were in air, flushed with oxygen, or gassed with nitrogen under anaerobic denitrifying conditions. Active transport of glucose by P. aeruginosa was also inhibited by reduced 5-N-methyl-phenazonium-3-sulfonate, a membrane-impermeable electron donor. PMS–ascorbate caused rapid depletion of intracellular adenosine triphosphate (ATP) when added to respiring cell suspensions of P. aeruginosa either in the presence or absence of glucose or succinate as oxidizable energy sources. In contrast, under identical conditions, Escherichia coli formed ATP with PMS–ascorbate as the sole oxidizable energy source and ATP formation continued when glucose or succinate was present in addition to PMS–ascorbate in the incubation system.

Polypeptides of the Thylakoid Membrane and Their Functional Characterization

1978 ◽  
Vol 33 (9-10) ◽  
pp. 723-730 ◽  
Author(s):  
Georg H. Schmid ◽  
Wilhelm Menke ◽  
Alfons Radunz ◽  
Friederike Koenig
Keyword(s):  
Molecular Weight ◽  
Electron Transport ◽  
Electron Donor ◽  
Photosystem I ◽  
Thylakoid Membrane ◽  
Apparent Molecular Weight ◽  
Variable Fluorescence ◽  
Phenazine Methosulfate ◽  
Cyclic Photophosphorylation ◽  
High Concentrations

Abstract From stroma-freed chloroplasts of Antirrhinum majus polypeptides with the apparent molecular weights 44 000, 26 000 and 20 000 were isolated.The antiserum to a polypeptide with the moleculair weight 44 000 inhibits the photoreduction of anthraquinone-2-sulfonate with dichlorophenol indophenol/ascorbate when the concentration of the electron donor dichlorophenol indophenol is low. The antiserum enhances the rate of phenazine methosulfate-mediated cyclic photophosphorylation. The variable fluorescence yield is increased by the antiserum . It is assumed that this polypeptide plays a role in electron transport between the two photosystems. From two polypeptides with the apparent molecular weight 26 000 one seems to belong to the reaction center of photosystem II as it inhibits the photooxidation of tetramethyl benzidine and diphenyl carbazide with suitable electron acceptors and inhibits electron transport between water and silicomolybdate. Variable fluorescence is not or not too strong decreased by the antiserum . The other polypeptide of the apparent molecular weight 26 000 inhibits the photoreduction of anthraquinone-2-sulfonate with high concentrations of dichlorophenol indophenol as the electron donor. Phenazine methosulfate-mediated cyclic photophosphorylation is also inhibited by the antiserum . Therefore, we should like to associate it with the reaction center of photosystem I. The antiserum to the polypeptide with the apparent molecular weight 20 000 inhibits the photoreduction of anthraquinone-2-sulfonate with low and high concentrations of the electron donor dichlorophenol indophenol. It enhances phenazine methosulfate-mediated cyclic photophosphorylation. The polypeptide, therefore, should be functionally involved on the acceptor side of photosystem I.The results obtained up-to-now on the function and localization of the polypeptides in the thylakoid membrane are summarized.

Nb-doped CaO: an efficient electron donor system

2014 ◽  
Vol 26 (31) ◽  
pp. 315004 ◽  
Author(s):  
Stefano Prada ◽  
Livia Giordano ◽  
Gianfranco Pacchioni
Keyword(s):  
Electron Donor ◽  
Donor System

scholarly journals Glutathione-glutaredoxin is an efficient electron donor system for mammalian p53R2–R1-dependent ribonucleotide reductase

2019 ◽  
Vol 294 (34) ◽  
pp. 12708-12716 ◽  
Author(s):  
Rajib Sengupta ◽  
Lucia Coppo ◽  
Pradeep Mishra ◽  
Arne Holmgren
Keyword(s):  
Electron Donor ◽  
Ribonucleotide Reductase ◽  
Donor System

A Proposed Mechanism for Diuron-Induced Phytotoxicity

Weed Science ◽  
1972 ◽  
Vol 20 (4) ◽  
pp. 357-363 ◽  
Author(s):  
Charles E. Stanger ◽  
Arnold P. Appleby
Keyword(s):  
Electron Donor ◽  
Time Course ◽  
Spinacia Oleracea ◽  
Electron Flow ◽  
Chlorophyll Degradation ◽  
Protective Mechanism ◽  
Carotenoid Pigments ◽  
Complete Protection ◽  
Mechanisms Of Toxicity ◽  
Donor System

Chloroplasts isolated from spinach(Spinacia oleraceaL.) leaves were used to study mechanisms of toxicity from 3-(3,4-dichlorophenyl)-1,1-dimethylurea (diuron). Light was needed to initiate diuron injury. The addition of ascorbate plus 2,6-dichlorophenylindolephenol (DPIP) as an electron donor system completely protected the chloroplasts from diuron-induced toxicity. The protective effect from the electron donor system occurred only in functional chloroplasts. Diuron caused rapid and extensive chlorophyll degradation at chlorophyll: diuron ratios of 200:1 and lower. At higher ratios the effect was much less measurable. The electron donor system gave complete protection in the presence of methylamine HCl, a known inhibitor of photophosphorylation, indicating that a deficiency of ATP was not the primary cause of diuron toxicity. Time-course studies showed that carotenoid pigments began to degrade before initiation of chlorophyll degradation. These results are interpreted as supporting a hypothesis that diuron induces phytotoxicity by catalyzing lethal photosensitized oxidations in the cell. This may occur as a result of (a) a greater concentration of oxidized chlorophyll caused by an interruption of electron flow and (b) an inhibition of NADPH formation which is necessary to maintain a functional carotenoid protective mechanism.

scholarly journals Ouabain Induced Seizures: Site of Production and Response to Anticonvulsants

1978 ◽  
Vol 5 (4) ◽  
pp. 405-411 ◽  
Author(s):  
Duncan L.W. Davidson ◽  
Yasuo Tsukada ◽  
André Barbeau
Keyword(s):  
Cerebral Cortex ◽  
Reticular Formation ◽  
Dorsal Hippocampus ◽  
Mesencephalic Reticular Formation ◽  
Cerebellar Nuclei ◽  
Inhibitory Effect ◽  
Transport Mechanisms ◽  
Limbic Seizures ◽  
Temporal Lobe Seizures ◽  
Low Volume

SUMMARY:Ouabain, an inhibitor of Na+-K+-ATP'ase, has been administered intraventricularly to rats to study the effect of impairment of membrane transport mechanisms on the genesis of seizures. Running and leaping seizures occur rapidly after injection oj ouabain in a low volume (10μl) when the maximal uptake of ouabain (39.8%) is in the hippocampus. Generalized clonic-lonic seizures are induced by higher volume injections (50μl) associated with wider distribution of ouabain, including the cerebellum and brainstem.Ouabain was injected into cerebral cortex, caudate nucleus, dorsal hippocampus, fastigeal nucleus, ventrolateral mesencephalic reticular formation and cerebellar cortex. The cerebellar injections produced both running and leaping and generalized clonic-lonic seizures. It is suggested that this results from decreased inhibitory effect of vermal and paravermal Purkinje cells on intra-cerebellar nuclei, which alters cerebellar influence on the reticular formation and the limbic system.Diphenylhydantoin, phenobarbitone, phenacemide, carbamezepine and clonazepam but not ethosuximide are effective against generalized clonic-lonic seizures, suggesting that this is a model for “grand mat” but not “petit mal” seizure mechanisms. It is furthermore suggested that running and leaping are subcortical, probably limbic, seizures that are most relevant as a model for temporal lobe seizures.

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