Effect of the herbicide prometryne [2,4-bis(isopropylamino)-6-(methlthio)-s-triazine] on mitochondria (original) (raw)
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Effects of the herbicide pendimethalin on mitochondrial functions
Biologia (3), 2006
Two main functions of rat liver mitochondria namely the respiration rate and generation of membrane potential, were analysed simultaneously to evaluate the toxicity of the dinitroaniline herbicide pendimethalin. The chromatography grade pendimethalin enhanced the mitochondrial respiration in a concentration-dependent manner and markedly decreased the membrane potential starting from 8.2×10-5 M up to 5.47×10-4 M (23-154 mg/ml). A higher toxicity of technical grade pendimethalin (Stomp-a mixture of pure ingredient and adjuvant(s)) was observed at lower concentrations of the pure ingredient (pendimethalin) than those of the single chromatography grade chemical. These data indicate that: 1) pure and technical grade pendimethalin preparations act as uncouplers of oxidative phosphorylation in mitochondria (enhance respiration and diminish membrane potential), 2) these effects are weaker but comparable (of the same concentration order) to those of 2,4-dinitrophenol, and 3) technical grade pendimethalin is more toxic to oxidative phosphorylation in mitochondria than pure chemical pendimethalin (active ingredient) itself. These data clearly disclaim the statement presented in the manual "Recognition and Management of Pesticides Poisonings" (US EPA 1999) that pendimethalin does not act as an uncoupler of oxidative phosphorylation.
Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
Journal of Biochemical and Molecular Toxicology, 2001
Paraquat herbicide is toxic to animals, including humans, via putative toxicity mechanisms associated to microsomal and mitochondrial redox systems. It is also believed to act in plants by generating highly reactive oxygen free radicals from electrons of photosystem I on exposure to light. Paraquat also acts on non-chlorophyllous plant tissues, where mitochondria are candidate targets, as in animal tissues. Therefore, we compared the interaction of paraquat with the mitochondrial bioenergetics of potato tuber, using rat liver mitochondria as a reference. Paraquat depressed succinate-dependent mitochondrial ∆ψ, with simultaneous stimulation of state 4 O 2 consumption. It also induced a slow time-dependent effect for respiration of succinate, exogenous NADH, and N, N, N , Ntetramethyl-p-phenylenediamine (TMPD)/ascorbate, which was more pronounced in rat than in potato mitochondria. However, with potato tuber mitochondria, the ∆ψ promoted by complex-I-dependent respiration is insensitive to this effect, indicating a protection against paraquat radical afforded by complex I redox activity, which was just the reverse of to the findings for rat liver mitochondria. The experimental set up with the tetraphenyl phosphonium (TPP +)-electrode also indivated production of the paraquat radical in mitochondria, also suggesting its accessibility to the outside space. The different activities of protective
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.
Comparative effects of herbicide dicamba and related compound on plant mitochondrial bioenergetics
Journal of Biochemical and Molecular Toxicology, 2003
The herbicide dicamba (3,6-dichloro-2methoxybenzoic acid) was evaluated for its effects on bioenergetic activities of potato tuber mitochondria to elucidate putative mechanisms of action and to compare its toxicity with 2-chlorobenzoic acid. Dicamba (4 mol/mg mitochondrial protein) induces a limited stimulation of state 4 respiration of ca. 10%, and the above concentrations significantly inhibit respiration, whereas 2-chlorobenzoic acid maximally stimulates state 4 respiration (ca. 50%) at about 25 mol/mg mitochondrial protein. As opposed to these limited effects on state 4 respiration, transmembrane electrical potential is strongly decreased by dicamba and 2chlorobenzoic acid. Dicamba (25 mol/mg mitochondrial protein) collapses, almost completely, ∆ψ; similar concentrations of 2-chlorobenzoic acid promote ∆ψ drops of about 50%. Proton permeabilization partially contributes to ∆ψ collapse since swelling in Kacetate medium is stimulated, with dicamba promoting a stronger stimulation. The ∆ψ decrease induced by dicamba is not exclusively the result of a stimulation on the proton leak through the mitochondrial inner membrane, since there was no correspondence between the ∆ψ decrease and the change on the O 2 consumption on state 4 respiration; on the contrary, for concentrations above 8 mol/mg mitochondrial protein a strong inhibition was observed. Both compounds inhibit the activity of respiratory complexes II and III but complex IV is not significantly affected. Complex I seems to be sensitive to these xenobiotics. In conclusion, dicamba is a stronger mitochondrial respiratory chain inhibitor and uncoupler as compared to 2-chlorobenzoic acid. Apparently, the differences in the lipophilicity are related to the different activities on mitochondrial bioenergetics.
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.
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.
Journal of Agricultural and Food Chemistry, 2011
A study was carried out to compare the effects of treating wheat (Triticum aestivum) and Italian ryegrass (Lolium multiflorum) with atrazine and fluorodifen. The herbicides interfered with photosynthesis and dark respiration, depending on the species. Atrazine decreased photosynthesis in both species and dark respiration in wheat, while fluorodifen caused decrements of photosynthetic activity of wheat. Antioxidant enzymes, such as ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), and glutathione reductase (GR), were generally more active in untreated and treated wheat with respect to Italian ryegrass, which explains why oxidative damage, expressed as malondialdehyde (MDA) content, was only found in ryegrass. Investigations on the activity of herbicide-detoxifying enzyme, glutathione S-transferase (GST), and on the accumulation and persistence of the herbicides in the plants showed higher detoxification rates in wheat than in the grass.