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PubMed1969

Antiviral and antitumor antibiotics. XX. Effects of rotenone, deguelin, and related compounds on animal and plant viruses.

Rotenoids and related compounds were investigated for their effects on animal and plant viruses. Of 35 compounds examined, rotenone, rotenone norketone, acetylrotenone, acetylrotenone norketone, deguelin, deguelic acid, dehydrodeguelin, and isotubanol norketone, all used at low concentrations, suppressed the growth of Newcastle disease and herpes simplex viruses as determined by the agar diffusion, plaque inhibition method. Most of the compounds likewise decreased the number of necrotic spots on tobacco mosaic virus-infected leaf discs. Only derrisic acid completely inhibited the local lesion formation at subphytotoxic concentrations. Correlation of antiviral activity with respiratory inhibition of these compounds is discussed.

Animals↗
PubMed1988

Acetaldehyde oxidation in rat liver mitochondria, action of Mg2+, ATP and rotenone on acetaldehyde oxidation in intact mitochondria, and on some purified aldehyde dehydrogenase isozymes.

In intact rat liver mitochondria acetaldehyde is oxidized by three functionally distinct dehydrogenase systems. Two of these reduce intramitochondrial nicotinamide adenine dinucleotide (NAD): one is operative with micromolar acetaldehyde concentrations and is stimulated by Mg2+, the other is operative with millimolar acetaldehyde concentrations and is stimulated by adenosine 5'-triphosphate (ATP). The third system reduces added NAD and is stimulated by rotenone. Connected to these systems, three aldehyde dehydrogenase isozymes (ALDH) have been purified: a low-Km ALDH activated by Mg2+, a high-Km ALDH activated by ATP and Mg2+, a high-Km ALDH activated by rotenone. The properties of some isozymes are affected by detergents. Thus, deoxycholate augments the stimulation of low-Km isozyme by Mg2+ and confers sensitivity to Mg2+ and ATP on one of the high-Km isozymes. A fourth isozyme has been purified. Its affinity for acetaldehyde is so low that it is very unlikely that acetaldehyde is the physiological substrate.

Acetaldehyde↗
PubMed2004

Antimycin A treatment decreases respiratory internal rotenone-insensitive NADH oxidation capacity in potato leaves.

BACKGROUND: The plant respiratory chain contains several energy-dissipating enzymes, these being type II NAD(P)H dehydrogenases and the alternative oxidase, not present in mammals. The physiological functions of type II NAD(P)H dehydrogenases are largely unclear and little is known about their responses to stress. In this investigation, potato plants (Solanum tuberosum L., cv. Desiree) were sprayed with antimycin A, an inhibitor of the cytochrome pathway. Enzyme capacities of NAD(P)H dehydrogenases (EC 1.6.5.3) and the alternative oxidase were then analysed in isolated leaf mitochondria. RESULTS: We report a specific decrease in internal rotenone-insensitive NADH dehydrogenase capacity in mitochondria from antimycin A-treated leaves. External NADPH dehydrogenase and alternative oxidase capacities remained unaffected by the treatment. Western blotting revealed no change in protein abundance for two characterised NAD(P)H dehydrogenase homologues, NDA1 and NDB1, nor for two subunits of complex I. The alternative oxidase was at most only slightly increased. Transcript levels of nda1, as well as an expressed sequence tag derived from a previously uninvestigated closely related potato homologue, remained unchanged by the treatment. As compared to the daily rhythm-regulated nda1, the novel homologue displayed steady transcript levels over the time investigated. CONCLUSIONS: The internal rotenone-insensitive NADH oxidation decreases after antimycin A treatment of potato leaves. However, the decrease is not due to changes in expression of known nda genes. One consequence of the lower NADH dehydrogenase capacity may be a stabilisation of the respiratory chain reduction level, should the overall capacity of the cytochrome and the alternative pathway be restricted.

Antimycin A↗
PubMed2004

High resolution electrospray and electrospray tandem mass spectra of rotenone and its isoxazoline cycloadducts.

An evaluation of the gas-phase ion chemistry of rotenone (1) by electrospray ionisation (ESI) mass spectrometry (MS) and tandem mass spectrometry (MS2) is presented, aiming at providing tools for its determination in natural and biological matrices. The behaviour of its cycloadducts with benzonitrile-N-oxide (2) and 2,4,6-trimethylbenzonitrile-N-oxide (3) was also evaluated and the MS data thus obtained have provided evidence into the mechanism of formation of the key product ion at m/z 192 which can be considered a marker in the MS and MS2 spectra of rotenone and its derivatives.

Cyclization↗
PubMed1997

Specific interaction of cytokinins and their analogs with rotenone-sensitive internal NADH dehydrogenase in potato tuber mitochondria.

Effects of cytokinins were studied on rotenone-sensitive NADH dehydrogenase in mitochondria from fresh potato tubers (Solanum tuberosum), in consideration of the operation of external and rotenone-insensitive internal NADH dehydrogenases that has not been fully accounted for in previous studies. In submitochondrial particles (smp), zeatin was only weakly active, and zeatin riboside (ZR) was inactive. Inhibition rates at 400 microns of isopentenyladenine (iP) and isopentenyladenosine (iPA) were 45% and 30%, respectively, and that of BA (BA) was 64%. In intact mitochondria, the inhibition by iP and BA significantly increased, I50 being 50 and 250 microM, respectively, but that by zeatin and iPA decreased. A structure-activity study showed that hydrophobic and steric factors are important for the activity. Cytokinins inhibited the electron flow via natural quinone more strongly than that via synthetic quinone. These results suggest that among the cytokinins the species that can regulate the electron transport is iP rather than its riboside or zeatin.

Adenine↗
PubMed1999

Induction of apoptosis in AK-5 cells by rotenone involves participation of caspases.

AK-5 tumour cells undergo apoptosis after treatment with rotenone an electron transport inhibitor and oligomycin which inhibits mitochondrial ATPases. Apoptotic process involves the induction of caspases 2 and 3, whereas caspase 1 does not seem to be participating in rotenone/oligomycin induced apoptosis. DEVD which is a specific inhibitor of caspase 3, inhibited apoptosis in AK-5 cells. We have also observed a significant lowering of intracellular pH in AK-5 cells which are induced into the apoptotic process by rotenone. These results suggest an important role for mitochondrial electron transport in the induction of apoptosis in AK-5 tumour cells.

Animals↗
PubMed2004

[Ultrastructural characteristics of mitochondria during cell adaptation to rotenone].

A study was made of respiration, heat production, K+ output and ultrastructure of wheat root cells treated for 6 h with rotenone (10 microM), an inhibitor of HADH-ubiquinone oxidoreductase (Complex I). Besides, the involvement of alternative pathways for adaptation to this inhibitor was studied. After 20 min of treatment, a brightened mitochondrial matrix and mitochondria with torus shapes were observed. We propose that the outer area of mitochondria increases due to their torus shapes, and this can point to the activating of extremal NAD(P)H-dehydrogenase, which uses enternal NAD(P)H. Further on the normal ultrastructure of mitochondria was observed, which may result from activation of succinate dehydrogenase and rotenone resistant NAD(P)H-dehydrogenase. After 1 h of treatment, a decrease in respiration, heat production, K+ output and pH increase of incubation medium were observed. Starting from 2 h of incubation and up to the end of the experiment, an increase of respiration and heat production was observed, pointing to the activation of oxidative phosphorilation. Besides, re-entry of K+ and pH decrease in the incubation medium were observed. We conclude that these findings may indicate to a possible adaptation of root cells to this inhibitor. We propose that the torus shape of mitochondria may be associated with function of external NAD(P)H-dehydrogenase.

Cell Respiration↗
PubMed1980

Selective suppression of positive chemotaxis in Physarum polycephalum by treatment with rotenone or under anaerobic condition.

The chemotactic motive force of plasmodia of Physarum polycephalum was measured by the double-chamber method. The treatment of plasmodia with 0.1 mM rotenone did not affect the motility of the palsmodia but led to suppression of the chemotaxis toward all the attractants examined (glucose, galactose, c-AMP, KH2PO4). Rotenone treatment did not affect the chemotaxis against repellents (fructose, NaCl). Similar results were obtained when the chemotactic motive force was measured under an anaerobic condition (95% N2-5% CO2).

Anaerobiosis↗
PubMed1993

[Rotenone-sensitive oxidation of NADH and F0F1-ATPase activity in a homogenate of rat skeletal muscles during thermal adaptation].

A method has been developed for measuring the rates of rotenone-sensitive oxidation of NADH and oligomycin-sensitive hydrolysis of ATP in rat skeletal muscle homogenates. The method is based on the use of alamethicin which increases the permeability of the inner mitochondrial membrane for NADH and ATP. It has been shown that prolonged cold adaptation of rats (4 weeks, 4 degrees) does not change the activity of rotenone-sensitive NADH-oxidase in rat skeletal muscle homogenates which is equal to 12.4 +/- 4.4 nmol NADH/min/mg protein, but increases threefold that of F0F1-ATPase--from 31.8 +/- 7.4 up to 93.1 +/- 14.3 nmol P(i)/min/mg protein. It is suggested that prolonged cold adaptation induces structural-and-functional changes in the H(+)-ATP-synthetase complex of skeletal muscle mitochondria.

Adaptation, Physiological↗
PubMed1985

Mitochondrial translation of subunits of the rotenone-sensitive NADH:ubiquinone reductase in Neurospora crassa.

The rotenone sensitive NADH:ubiquinone was isolated from mitochondria of Neurospora crassa as a monodisperse preparation with the apparent mol. wt. in Triton solution of 0.9 X 10(6). The enzyme is composed of at least 22 subunits with apparent mol. wts. in SDS between 70 and 11 kd. Six of the subunits with the mol. wts. 70, 48, 37, 25, 22 and 18 kd were radioactively labelled in the enzyme isolated from cells which had incorporated [35S]methionine in the presence of cycloheximide. These subunits are synthesized in the mitochondria. Eleven subunits were radioactively labelled in the enzyme from cells which had incorporated [35S]methionine in the presence of chloramphenicol. These subunits are synthesized in the cytoplasm. The site of translation of the other subunits could not be established by the pulse-labelling technique. The assignment of the mitochondrially synthesized subunits to unidentified reading frames on the mitochondrial DNA is discussed.

Mitochondria↗
PubMed2005

Assay of rotenone in river water by high-throughput tandem mass spectrometry and multiple-reaction monitoring methodology.

The high-throughput analytical approach proposed for the assay of rotenone in lake and river waters presented here is based on atmospheric pressure chemical ionization (APCI) multiple-reaction monitoring (MRM) methodology whereby the analyte and internal standard solutions are directly analyzed, without any previous chromatographic separation. The very good accuracy is obtained by the critical choice of a reference compound that shows gas-phase chemistry similar to that of the analyte, by producing the same product ions selected for the MRM-based assay.

Atmosphere↗
PubMed2001

Rotenone-induced G2/M cell cycle arrest and apoptosis in a human B lymphoma cell line PW.

Concentrations of rotenone (ROT) that block electron flow through mitochondrial complex I (100 nM) did not significantly alter either cell viability or the growth of PW cells. However, 10- to 50-fold higher concentrations (1-5 microM) were found to induce a dose-dependent cell cycle arrest predominantly at the G2/M stage of the cycle and apoptosis. Apoptosis was dependent on the cell cycle arrest, since apoptosis but not the G2/M arrest was prevented with the broad spectrum caspase inhibitor zVADfmk. Biochemical features of apoptosis included mitochondrial cytochrome c release, reactive oxygen species generation, and the activation of procaspase 3. Thus, ROT inhibition of mitochondrial electron transport may be insufficient to induce apoptosis in PW cells. Instead, apoptosis in these cells occurs as a consequence of disruption of the cell cycle and is only indirectly dependent upon mitochondrial electron transport.

Amino Acid Chloromethyl Ketones↗
PubMed2004

Neurotoxicant-induced animal models of Parkinson's disease: understanding the role of rotenone, maneb and paraquat in neurodegeneration.

The etiologic basis of Parkinson's disease (PD), the second most common age-related neurodegenerative disorder, is unknown. Recent epidemiological and experimental studies indicate that exposure to environmental agents, including a number of agricultural chemicals, may contribute to the pathogenesis of this disorder. Animal models are important tools in experimental medical science for studying the pathogenesis and therapeutic intervention strategies of human diseases. Since many human disorders do not arise spontaneously in animals, characteristic functional changes have to be mimicked by neurotoxic agents. Recently, agricultural chemicals, when administrated systemically, have been shown to reproduce specific features of PD in rodents, thus opening new routes for the development of animal models for this disorder. In addition to a brief historical overview of the toxin-induced PD models, this study provides a detailed description of exiting models in which Parkinsonism is initiated via the exposure of animals to such agricultural chemicals as rotenone, paraquat, and maneb. Suggested neurotoxicity mechanisms of these chemicals are considered, and the major lessons learned from the analysis of pesticide-induced PD models are discussed.

Animals↗
PubMed1994

Translocation of two glucose transporters in heart: effects of rotenone, uncouplers, workload, palmitate, insulin and anoxia.

Our previous studies on the acute regulation of glucose transport in perfused rat hearts were extended to explore further the mechanism of regulation by anoxia; to test the effects of palmitate, a transport inhibitor; and to compare the translocation of two glucose transporter isoforms (GLUT1 and GLUT4). Following heart perfusions under various conditions, glucose transporters in intracellular membranes were quantitated by reconstitution of transport activity and by Western blotting. Rotenone stimulated glucose uptake and decreased the intracellular contents of glucose transporters. This indicates that it activates glucose transport via net outward translocation, similarly to anoxia. However, two uncouplers of oxidative phosphorylation produced little or no effect. Increased workload (which stimulates glucose transport) reduced the intracellular contents of transporters, while palmitate increased the contents, indicating that these factors cause net translocation from or to the intracellular pool, respectively. Relative changes in GLUT1 were similar to those in GLUT4 for most factors tested. A plot of changes in total intracellular transporter content vs. changes in glucose uptake was roughly linear, with a slope of -0.18. This indicates that translocation accounts for most of the changes in glucose transport, and the basal pool of intracellular transporters is five times as large as the plasma membrane pool.

Animals↗
PubMed1990

Coupling site I and the rotenone-sensitive ubisemiquinone in tightly coupled submitochondrial particles.

The rotenone-sensitive g = 2.00 low temperature EPR signal attributed to ubisemiquinone is observed in submitochondrial particles during coupled electron transfer from NADH to oxygen and from succinate to NAD+. The signal is seen only in the presence of oligomycin added to induce the respiratory control (7-9 with NADH and 3-4 with succinate) and it disappears in the presence of uncouplers (CCCP or gramicidin D). No reduction of the iron-sulfur center N-2 in the presence of 20 mM succinate and cyanide is observed, thus suggesting that N-2 is not in equilibrium with the ubiquinone pool. A hypothesis is proposed on delta mu H+ generation coupled with electron transfer between iron-sulfur center N-2 and the ubiquinone pool.

Carbonyl Cyanide m-Chlorophenyl Hydrazone↗
PubMed1991

On the mechanism of rotenone-insensitive reduction of quinones by mitochondrial NADH:ubiquinone reductase. The high affinity binding of NAD+ and NADH to the reduced enzyme form.

NADH acts as an incomplete competitive inhibitor for 5,8-dioxy-1,4-naphtoquinone during its rotenone-insensitive reduction by mitochondrial NADH:ubiquinone reductase. NAD+ and ADP-ribose act as incomplete mixed-type inhibitors. Ki of NAD+ and NADH towards quinone are about one order less than towards ferricyanide. The bimolecular rate constant of the reduction of the enzyme by NADH in the quinone reductase reaction is about 2 times less than that of ferricyanide reductase reaction. These data indicate that the reduction site of 5,8-dioxy-1,4-naphtoquinone is close to NAD+/NADH and ferricyanide binding site. It seems that during the steady-state reduction of ferricyanide and 5,8-dioxy-1,4-naphtoquinone these oxidizers react with NADH:ubiquinone reductase reduced to different extents.

Animals↗
PubMed1986

The effects of chlordane and rotenone on the alimentary tract of the field cricket.

Cricket nymphs (Acheta pennsylvanicus) were treated with the publicly available, commercial forms of 2 generically termed stomach poisons; chlordane and rotenone, and the resulting tissue changes were histologically compared against a control group. Examination utilized stained and unstained slides of the insect's fat body, alimentary tract, and malpighian tubules. The 2 dissimilar operating insecticides shared common effects such as the storage of dark bodies in the fat body, and the structural disruption of the caecal lining and the malpighian tubules. In addition, a unique effect of chlordane was shown that had not been conclusively recorded before. This insecticide demonstrated the striking ability to rapidly penetrate the internal digestive tract cuticle lining of the proventricular plates resulting in cellular damages. Concern is expressed about chronic exposures to the insecticides, especially chlordane, since it has widespread use and long persistence.

Animals↗
PubMed2004

Rotenone-sensitive mitochondrial potential in Phytomonas serpens: electrophoretic Ca(2+) accumulation.

Phytomonas sp. are flagellated trypanosomatid plant parasites that cause diseases of economic importance in plantations of coffee, oil palm, cassava and coconuts. Here we investigated Ca(2+) uptake by the vanadate-insensitive compartments using permeabilized Phytomonas serpens promastigotes. This uptake occurs at a rate of 1.13+/-0.23 nmol Ca(2+) mg x protein(-1) min(-1). It is completely abolished by the H(+) ionophore FCCP and by valinomycin and nigericin. It is also inhibited by 2 microM ruthenium red, which, at this low concentration, is known to inhibit the mitochondrial calcium uniport. Furthermore, salicylhydroxamic acid (SHAM) and propylgallate, specific inhibitors of the alternative oxidase in plant and parasite mitochondria, are also effective as inhibitors of the Ca(2+) transport. These compounds abolish the membrane potential that is monitored with safranine O. Rotenone, an inhibitor of NADH-CoQ oxidoreductase, can also dissipate 100% of the membrane potential. It is suggested that the mitochondria of P. serpens can be energized via oxidation of NADH in a pathway involving the NADH-CoQ oxidoreductase and the alternative oxidase to regenerate the ubiquinone. The electrochemical H(+) gradient can be used to promote Ca(2+) uptake by the mitochondria.

Animals↗