Electron transport pathways for the oxidation of endogenous substrate(s) in Acidithiobacillus ferrooxidans

2006 ◽  
Vol 52 (4) ◽  
pp. 317-327 ◽  
Author(s):  
Yongqiang Chen ◽  
Isamu Suzuki
Keyword(s):  
Electron Transport ◽  
Electron Acceptor ◽  
Acidithiobacillus Ferrooxidans ◽  
Complex I ◽  
Iron Chelators ◽  
Endogenous Respiration ◽  
Sugar Alcohols ◽  
Transport Pathways ◽  
Endogenous Substrate ◽  
Transport Inhibitors

Oxidation of endogenous substrate(s) of Acidithiobacillus ferrooxidans with O2 or Fe3+ as electron acceptor was studied in the presence of uncouplers and electron transport inhibitors. Endogenous substrate was oxidized with a respiratory quotient (CO2 produced/O2 consumed) of 1.0, indicating its carbohydrate nature. The oxidation was inhibited by complex I inhibitors (rotenone, amytal, and piericidin A) only partially, but piericidin A inhibited the oxidation with Fe3+ nearly completely. The oxidation was stimulated by uncouplers, and the stimulated activity was more sensitive to inhibition by complex I inhibitors. HQNO (2-heptyl-4-hydroxyquinoline N-oxide) also stimulated the oxidation, and the stimulated respiration was more sensitive to KCN inhibition than uncoupler stimulated respiration. Fructose, among 20 sugars and sugar alcohols including glucose and mannose, was oxidized with a CO2/O2 ratio of 1.0 by the organism. Iron chelators in general stimulated endogenous respiration, but some of them reduced Fe3+ chemically, introducing complications. The results are discussed in view of a branched electron transport system of the organism and its possible control.Key words: Acidithiobacillus ferrooxidans, endogenous respiration, uncouplers, electron transport.

Effects of electron transport inhibitors and uncouplers on the oxidation of ferrous iron and compounds interacting with ferric iron inAcidithiobacillus ferrooxidans

2005 ◽  
Vol 51 (8) ◽  
pp. 695-703 ◽  
Author(s):  
Yongqiang Chen ◽  
Isamu Suzuki
Keyword(s):  
Electron Transport ◽  
Cytochrome Oxidase ◽  
Complex I ◽  
Ferric Iron ◽  
Complex Iii ◽  
Transport Pathway ◽  
Low Concentrations ◽  
Transport Inhibitors ◽  
A Site ◽  
Electron Transport Pathway

Oxidation of Fe2+, ascorbic acid, propyl gallate, tiron, L-cysteine, and glutathione by Acidithiobacillus ferrooxidans was studied with respect to the effect of electron transport inhibitors and uncouplers on the rate of oxidation. All the oxidations were sensitive to inhibitors of cytochrome c oxidase, KCN, and NaN3. They were also partially inhibited by inhibitors of complex I and complex III of the electron transport system. Uncouplers at low concentrations stimulated the oxidation and inhibited it at higher concentrations. The oxidation rates of Fe2+and L-cysteine inhibited by complex I and complex III inhibitors (amytal, rotenone, antimycin A, myxothiazol, and HQNO) were stimulated more extensively by uncouplers than the control rates. Atabrine, a flavin antagonist, was an exception, and atabrine-inhibited oxidation activities of all these compounds were further inhibited by uncouplers. A model for the electron transport pathways of A. ferrooxidans is proposed to account for these results. In the model these organic substrates reduce ferric iron on the surface of cells to ferrous iron, which is oxidized back to ferric iron through the Fe2+oxidation pathway, leading to cytochrome oxidase to O2. Some of electrons enter the uphill (energy-requiring) electron transport pathway to reduce NAD+. Uncouplers at low concentrations stimulate Fe2+oxidation by stimulating cytochrome oxidase by uncoupling. Higher concentrations lower Δp to the level insufficient to overcome the potentially uphill reaction at rusticyanin-cytochrome c4. Inhibition of uphill reactions at complex I and complex III leads to Δp accumulation and inhibition of cytochrome oxidase. Uncouplers remove the inhibition of Δp and stimulate the oxidation. Atabrine inhibition is not released by uncouplers, which implies a possibility of atabrine inhibition at a site other than complex I, but a site somehow involved in the Fe2+oxidation pathway.Key words: Acidithiobacillus ferrooxidans, electron transport, uncouplers, uphill electron transport pathway.

Effects of Diphenylether Herbicides on Reactions of Mitochondria and Chloroplasts

Weed Science ◽  
1970 ◽  
Vol 18 (5) ◽  
pp. 636-642 ◽  
Author(s):  
D. E. Moreland ◽  
W. J. Blackmon ◽  
H. G. Todd ◽  
F. S. Farmer
Keyword(s):  
Electron Transport ◽  
Oxygen Uptake ◽  
Spinacia Oleracea ◽  
White Potato ◽  
Light Reaction ◽  
Site Of Action ◽  
Transport Inhibitors ◽  
Atp Generation ◽  
A Site ◽  
Limited Oxygen

Effects of three diphenylether herbicides [2,4-dichlorophenyl-p-nitrophenyl ether (nitrofen); 2,4,6-trichlorophenyl-4′-nitrophenyl ether (hereinafter referred to as MC-1478); and 2,4′-dinitro-4-trifluoromethyl-diphenylether (hereinafter referred to as C-6989)] were measured on phosphorylation and electron transport in spinach(Spinacia oleraceaL.) chloroplasts, and mung bean(Phaseolus aureusL., var. Jumbo) and white potato tuber(Solarium tuberosumL.) mitochondria. All of the diphenylethers acted primarily as inhibitors of chloroplast noncyclic electron transport, and the coupled photophosphorylation. The compounds ranked in the following decreasing order of inhibitory effectiveness: MC-1478 ≥ C-6989 >> nitrofen. A site of action close to light reaction II was suggested. At high molar concentrations, marginal interference with cyclic electron transport or phosphorylation was obtained. In mitochondria, MC-1478 and nitrofen acted primarily as electron transport inhibitors with malate, NADH, and succinate as substrates. MC-1478 was a slightly stronger inhibitor than nitrofen. Only slight stimulation of ADP-limited oxygen uptake was obtained during the oxidation of NADH and succinate; whereas, strong inhibition of oxygen uptake was obtained with malate. C-6989 also weakly stimulated ADP-limited oxygen uptake with NADH and succinate but differed from the two chlorinated diphenylethers in that electron transport was not inhibited when ADP was present in excess. Interference with ATP generation could be one of the mechanisms through which the phytotoxicity of diphenylether herbicides is expressed.

Effects of Difenzoquat on Photoreactions and Respiration in Wheat (Triticum aestivum) and Wild Oat (Avena fatua)

Weed Science ◽  
1983 ◽  
Vol 31 (5) ◽  
pp. 693-699 ◽  
Author(s):  
Blaik P. Halling ◽  
Richard Behrens
Keyword(s):  
Triticum Aestivum ◽  
Electron Transport ◽  
Electron Acceptor ◽  
Photosynthetic Electron Transport ◽  
Significant Inhibition ◽  
Avena Fatua ◽  
Wild Oat ◽  
Leaf Chlorosis ◽  
Acceptor Activity ◽  
Proton Uptake

Experiments were conducted with isolated protoplasts of wild oat (Avena fatuaL. # AVEFA) and isolated chloroplasts of wild oat and wheat (Triticum aestivumL.), to determine if the methyl sulfate salt of difenzoquat (1,2-dimethyl-3,5-diphenyl-1H-pyrazolium) might influence photoreactions in these species. Difenzoquat did not affect CO2fixation, uncoupled electron transport, or proton uptake. At concentrations of 0.5 mM and 1 mM, difenzoquat caused a slight, but statistically significant, inhibition of photophosphorylation. Experiments assaying coupled electron transport indicated that inhibition of photophosphorylation occurred not through uncoupling, but by an energy-transfer inhibition. This same effect was observed in isolated mitocondria of both species, with about 50% inhibition of state 3 respiration rates occurring with 10 μM difenzoquat. However, no important differentials were observed in the relative susceptibilities of wheat and wild oat mitochondria. Difenzoquat also functioned as a weak autooxidizing electron acceptor in photosynthetic electron transport. Therefore, difenzoquat-induced leaf chlorosis and necrosis may result from a bipyridilium-type electron acceptor activity if sufficient herbicide is absorbed.

scholarly journals Cardiolipin promotes electron transport between ubiquinone and complex I to rescue PINK1 deficiency

2017 ◽  
Vol 216 (3) ◽  
pp. 695-708 ◽  
Author(s):  
Melissa Vos ◽  
Ann Geens ◽  
Claudia Böhm ◽  
Liesbeth Deaulmerie ◽  
Jef Swerts ◽  
...  
Keyword(s):  
Electron Transport ◽  
Complex I ◽  
Fatty Acid Synthase ◽  
Induced Pluripotent Stem Cell ◽  
Mitochondrial Inner Membrane ◽  
Mitochondrial Defects ◽  
Mouse Cells ◽  
Induced Pluripotent ◽  
Specific Lipid ◽  
Pharmacologic Inhibition

PINK1 is mutated in Parkinson’s disease (PD), and mutations cause mitochondrial defects that include inefficient electron transport between complex I and ubiquinone. Neurodegeneration is also connected to changes in lipid homeostasis, but how these are related to PINK1-induced mitochondrial dysfunction is unknown. Based on an unbiased genetic screen, we found that partial genetic and pharmacological inhibition of fatty acid synthase (FASN) suppresses toxicity induced by PINK1 deficiency in flies, mouse cells, patient-derived fibroblasts, and induced pluripotent stem cell–derived dopaminergic neurons. Lower FASN activity in PINK1 mutants decreases palmitate levels and increases the levels of cardiolipin (CL), a mitochondrial inner membrane–specific lipid. Direct supplementation of CL to isolated mitochondria not only rescues the PINK1-induced complex I defects but also rescues the inefficient electron transfer between complex I and ubiquinone in specific mutants. Our data indicate that genetic or pharmacologic inhibition of FASN to increase CL levels bypasses the enzymatic defects at complex I in a PD model.

New inhibitors of Complex I of the mitochondrial electron transport chain with activity as pesticides

1994 ◽  
Vol 22 (1) ◽  
pp. 230-233 ◽  
Author(s):  
Robert M. Hollingworth ◽  
Kabeer I. Ahammadsahib ◽  
G. Gadelhak ◽  
J. L. McLaughlin
Keyword(s):  
Electron Transport ◽  
Complex I ◽  
Electron Transport Chain ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain
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