Comparative effects of herbicide dicamba and related compound on plant mitochondrial bioenergetics (original) (raw)
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Plant physiology, 1994
The herbicide bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) was tested on mitochondria from etiolated pea (Pisum sativum L. cv Alaska) stems. This compound when used at micromolar concentrations ([almost equal to]20 [mu]M) inhibited malate- and succinate-dependent respiration by intact mitochondria but not oxidation of exogenously added NADH. Bromoxynil did not affect the activities of the succinic and the internal NADH dehydrogenases. Analyses of the effects induced by this herbicide on the membrane potential, [delta]pH, matrix Ca2+ movements, and dicarboxylate transport demonstrated that bromoxynil is likely to act as an inhibitor of the dicarboxylate carrier. In addition, bromoxynil caused a mild membrane uncoupling at concentrations [greater than or equal to]20 [mu]M. No effect on the ATPase activity was observed.
Dibutylchloromethyltin chloride, a potent inhibitor of electron transport in plant mitochondria
Journal of Bioenergetics and Biomembranes, 1980
Dibutylchloromethyl tin chloride (DBCT) inhibits coupled and uncoupled respiration of mitochondria from potato tubers, cauliflower florets and etiolated mung bean hypocotyls with succinate and L-malate but not with external NADH or TMPD/ascorbate as substrates. Using potato and cauliflower mitochondria, DBCT at 200 pmole/mg of protein gives complete inhibition only in KCl-based media and at pH 6.8. DBCT has no effect on the internal pH of mung bean mitochondria, but does cause a decrease in the membrane potential. Electron transport through the alternative oxidase is not inhibited, neither is the ATP-synthase system. DBCT appears to interact with the functionally-distinct pool of ubiquinone associated with the oxidation of succinate and L-malate. 309
Physiologia Plantarum, 2007
The reduction of dehydroascorbate (DHA) was investigated in plant mitochondria. Mitochondria isolated from Bright Yellow-2 tobacco cells were incubated with 1 mM of DHA, and the ascorbate generation was followed by high-performance liquid chromatography. Mitochondria showed clear ability to reduce DHA and to maintain a significant level of ascorbate. Ascorbate generation could be stimulated by the respiratory substrate succinate. The complex I substrate malate and the complex I inhibitor rotenone had no effect on the ascorbate generation from DHA. Similarly, the complex III inhibitor antimycin A, the alternative oxidase inhibitor salicylhydroxamic acid, and the uncoupling agent 2,4-dinitrophenol were ineffective on mitochondrial ascorbate generation both in the absence and in the presence of succinate. However, the competitive succinate dehydrogenase inhibitor malonate almost completely abolished the succinate-dependent increase in ascorbate production. The complex IV inhibitor KCN strongly stimulated ascorbate accumulation. These results together suggest that the mitochondrial respiratory chain of plant cells -presumably complex II -plays important role in the regeneration of ascorbate from its oxidized form, DHA.
Plant Physiology, 1962
The herbicidal actioIn of 2,4-dichlorophenoxyacetic acid (2,4-D) has been the subject of many investigations in the years sinice this compound was first demonstrated to be a plant toxicant. Almost as many possible mechanismiis for this toxicityhave been suggested. These includle depletioni of respiratory substrate, abnormal cellular proliferation, the production of toxic substances in response to 2,4-D application, changes in nitrogen mletabolismii or ioIn uptake and nietablolismi. interference with the level of endogenous auxin, andl abnormlal plhosphatase activity (4, 7, 9). While any of these imight be responsible for the death of plants, contrary evidence mnay be adduced for each of thenm, and it has becomle commnon to think of the herbicidal action of 2,4-D as a complex of many responses with nIo oIne response aloine producing the toxic effect. A possible explaniationi for the phytotoxic effect of 2,4-D imiay lie in its ability to uncouple phosphorylahere will provide a confirmation of the previous reports of uncoupling (lue to 2,4-D and some additional information on aspects of this effect which have not previously been reportedl.
Mitochondrial bioenergetics is affected by the herbicide paraquat
Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1995
The potential toxicity of the herbicide paraquat (1,1-dimethyl-4,4'-bipyridylium dichloride) was tested in bioenergetic functions of isolated rat liver mitochondria. Paraquat increases the rate of State 4 respiration, doubling at 10 mM, indicating uncoupling effects. Additionally, State 3 respiration is depressed by about 15%, at 10 mM paraquat, whereas uncoupled respiration in the presence of CCCP is depressed by about 30%. Furthermore, paraquat partially inhibits the ATPase activity through a direct effect on this enzyme complex. However, at high concentrations (5-10 mM), the ATPase activity is stimulated, probably as consequence of the described uncoupling effect. Depression of respiratory activity is mediated through partial inhibitions of mitochondrial complexes III and IV. Paraquat depresses A~ as a function of herbicide concentration. In addition, the depolarization induced by ADP is decreased and repolarization is biphasic suggesting a double effect. Repolarization resumes at a level consistently higher than the initial level before ADP addition, for paraquat concentrations up to 10 mM. This particular effect is clear at 1 mM paraquat and tends to fade out with increasing concentrations of the herbicide.
Current Topics of the Inhibitors of Mitochondrial Complex I
A Structural Perspective on Respiratory Complex I, 2012
Acetogenins isolated from Annonaceous plants are very potent inhibitors of bovine heart mitochondrial complex I and unique in chemical structure among a wide variety of inhibitors of the enzyme. The structure-activity studies of numerous acetogenins revealed that the inhibitors exhibit potent inhibition only when the two pharmacophores (i.e. the g-lactone and the hydroxylated THF moieties) are directly linked by the alkyl spacer and cooperatively bind to the two putative binding sites. Regardless of marked changes in the conformation and/or the length of the spacer region, the spacer dynamically regulates the cooperative binding of the two pharmacophores to the sites. Through structural modi fi cation of acetogenins, we developed new types of inhibitors termed D lac-acetogenins and piperazine-type inhibitors, whose inhibitory effects on complex I signi fi cantly differ from those of traditional inhibitors. In particular, examination of the inhibition mechanism of D lac-acetogenins provided valuable insights into the terminal electron transfer step of complex I including a mechanism of the generation of superoxide in the presence of inhibitor. Using a photoaf fi nity labeling technique, the binding sites of the new inhibitors (D lac-acetogenin and piperazine) as well as traditional inhibitors (acetogenin and quinazoline) were identi fi ed at sub-subunit level. The photoaf fi nity labeling studies clearly indicated that the 49 kDa and ND1 subunits construct a large inhibitor binding pocket in bovine complex I.
Biochemical Pharmacology, 1986
~IMBOA (2,4-dihydroxy-7-methoxy-l,4-benzoxazin-3-one~ is the main hydroxamic acid isolated from maize extracts. It inhibited reversibly ATP synthesis, Pi-ATP exchange reaction and ATPase activity in submitochondrial particles from bovine heart. Half-maximal effects were obtained with 4, 2, and 6 mM DIMBOA respectively. At higher concentrations it also inhibited mitochondrial electron transport (IS0 = 11 mM). Irreversible inactivation of mitochondrial electron transport, P,-ATP exchange reaction and 8-anilino-l-naphthalene sulfonate energy-dependent fluorescence enhancement was also observed. These effects of DIMBOA on energy-linked mitochondrial reactions may explain the inhibitory action of DIMBOA on several aerobic organisms.