The herbicide flamprop-M-methyl has a new antimicrotubule mechanism of action

BACKGROUND: The herbicidal mode of action of flamprop‐M‐methyl [methyl N‐benzoyl‐N‐(3‐chloro‐4‐fluorophenyl)‐D ‐alaninate] was investigated. RESULTS: For initial characterization, a series of bioassays was used, which indicated a mode of action similar to that of mitotic disrupter herbicides. Cytochemical fluorescence studies, which included monoclonal antibodies against polymerized tubulin, were applied to elucidate effects on mitosis and microtubule assembly in maize roots. When seedlings were root treated with 50 µM of flamprop‐M‐methyl, cell division activity in meristematic root tip cells ceased within 4 h. The compound severely disturbed the orientation of spindle and phragmoblast microtubules, leading to defective spindle and phragmoblast structures. Cortical microtubules were only slightly affected. In late anaphase and early telophase cells, phragmoblast microtubules were disorganized in multiple arrays that hampered regular cell plate deposition in cytokinesis. Microtubules of the spindle apparatus were found attached to chromosomal kinetochores, but did not show regular organization associated with a zone of microtubule‐organizing centres at the opposite ends of the cell. On account of this loss of spindle organization, chromosomes remained in a condensed state of prometaphase or metaphase. Unlike known microtubule disrupter herbicides, flamprop‐M‐methyl and its biologically active metabolite flamprop did not inhibit soybean tubulin polymerization to microtubules in vitro at 50 µM . In contrast, soybean plants responded sensitively to the compounds. CONCLUSION: The results indicate that flamprop‐M‐methyl is a mitotic disrupter herbicide with a new antimicrotubule mechanism of action that affects orientation of spindle and phragmoblast microtubules, possibly by minus‐end microtubule disassembly. Copyright © 2008 Society of Chemical Industry     

Herbicidal cyanoacrylates with antimicrotubule mechanism of action

The herbicidal mode of action of the new synthetic cyanoacrylates ethyl (2Z)-3-amino-2-cyano-4-ethylhex-2-enoate (CA1) and its isopropyl ester derivative CA2 was investigated. For initial characterization, a series of bioassays was used indicating a mode of action similar to that of mitotic disrupter herbicides such as the dinitroaniline pendimethalin. Cytochemical fluorescence studies including monoclonal antibodies against polymerized and depolymerized tubulin and a cellulose-binding domain of a bacterial cellulase conjugated to a fluorescent dye were applied to elucidate effects on cell division processes including mitosis and microtubule and cell wall formation in maize roots. When seedlings were root treated with 10 microM of CA1 or CA2, cell division activity in meristematic root tip cells decreased within 4 h. The chromosomes proceeded to a condensed state of prometaphase, but were unable to progress further in the mitotic cycle. The compounds caused a complete loss of microtubular structures, including preprophase, spindle, phragmoplast and cortical microtubules. Concomitantly, in the cytoplasm, an increase in labelling of free tubulin was observed. This suggests that the herbicides disrupt polymerization and microtubule stability, whereas tubulin synthesis or degradation appeared not to be affected. In addition, cellulose labelling in cell walls of root tip cells was not influenced. The effects of CA1 and CA2 were comparable with those caused by pendimethalin. In transgenic Arabidopsis plants expressing a green fluorescent protein-microtubule-associated protein4 fusion protein, labelled arrays of cortical microtubules in living epidermal cells of hypocotyls collapsed within 160 min after exposure to 10 microM CA1 or pendimethalin. Moreover, a dinitroaniline-resistant biotype of goosegrass (Eleusine indica (L) Gaertn) with a point mutation in alpha-tubulin showed cross-resistance against CA1 and CA2. The results strongly indicate that the cyanoacrylates are a new chemical class of herbicide which possess the same antimicrotubule mechanism of action as dinitroanilines, probably including interaction with the same binding site in alpha-tubulin.     

Carrot microtubules are dinitroaniline resistant. I. Cytological and cross-resistance studies

Treatment of both tolerant and susceptible species with dinitroaniline herbicides results in root swelling typical of mitotic disrupters, however, no root swelling was observed in carrots treated with saturated solutions of all the dinitroaniline herbicides tested, with the exception of oryzalin treatments at ≥ 10^?5 M. These levels of treatment are 100–1000 times the levels that caused root-tip swelling, even in tolerant plants. This properly classifies carrot as dinitroaniline-resistant rather than merely tolerant. Cross-resistance was noted to the structurally related mitotic disrupter, hexanitrodiphenylamine, and to the structurally unrelated herbicide, amiprophos-methyl. No resistance was noted to a number of other mitotic-disrupting herbicides. Both immunofluorescence and electron microscopy indicate that the microtubules of carrot roots were unaffected by dinitroaniline treatment. All organized microtubule configurations (cortical, pre-prophase bands, spindle, and phragmoplast) were observed in the treated material.     

Quinclorac does not inhibit cellulose (cell wall) biosynthesis in sensitive barnyard grass and maize roots

The effect of the auxin herbicide quinclorac on cellulose, callose, and (1→3),(1→4)β-glucan deposition in newly produced cell walls of meristematic root tip cells was examined in maize and barnyard grass. Particularly, the developing cell plate of dividing cells was investigated as a site of de novo cellulose biosynthesis. A cellulose-binding domain of a bacterial cellulase and monoclonal antibodies against the hemicellulose constituents were used for specific labelling in fluorescence microscopic examination. Root-treatment of plants with 100 μM quinclorac in maize and 10 μM quinclorac in barnyard grass decreased cell division activity in root tips and root elongation. Quinclorac did not induce the swelling of root tips into a club shape and a glassy appearance of tissue, which are typical symptoms for the action of cellulose biosynthesis inhibitors such as dichlobenil. During 24 h of treatment, no effects of quinclorac on cellulose deposition at the cell plates and parental walls of meristematic root cells were found. In contrast, 10 μM dichlobenil inhibited cellulose deposition in cell plate formation within 4 h of treatment. Concerning the hemicellulose constituents, increased staining for callose in areas of cell plates and parental cell walls was observed 24 h after treatment with 10 μM quinclorac. Concomitantly, (1→3),(1→4)β-glucan deposition in cell walls decreased. The latter may be an indirect effect of quinclorac through a stimulated production of cyanide from ethylene biosynthesis. In contrast with previous reports, no evidence that quinclorac, directly or indirectly inhibits cellulose biosynthesis in roots of susceptible grasses was found.     

Cytological studies of dinitroaniline-resistant Eleusine

Ultrastructural studies of primary roots (goosegrass) from dinitroaniline-resistant (R) and susceptible (S) biotypes of Eleusine indica (L). Gaertnr. establish a possible cytological basis for trifluralin resistance. Although the S biotype has a normal ultrastructure when grown in water, exposure to trifluralin solutions (between 10⁻⁸ and 10⁻⁵M) for 24 h results in a swelling of the root tip, typical of herbicides that affect microtubule production. The loss of spindle microtubules in the S biotype results in a mitosis arrested at prometaphase and the loss of cortical microtubules results in the formation of isodiametric cells in the zone of elongation. Nuclear membranes reform around the chromosomes in arrested prometaphase, producing abnormal, polymorphic nuclei. The mitotic index is increased in the S biotype after trifluralin treatment because many of the cells are arrested in prometaphase. The root tips of R biotypes are not swollen by even 10⁻⁵M trifluralin treatment. Trifluralin does not markedly affect cell division in the R biotype nor are the mitotic irregularities noted in the S biotype after treatment. However, even when the R biotype is not exposed to trifluralin, the microtubules are less abundant than in the S biotype and frequently cell walls are oriented abnormally or are incompletely formed. The level of resistance exhibited by the R biotype, the apparent difference in microtubule number and function between the two biotypes, and the lack of effect on the microtubules at high trifluralin concentrations indicate a site-of-action mutation.     

Mitotic disruption by a novel pyrimidine herbicide, NS-245852, in oat (Avena sativa L.) roots

The effects of a novel pyrimidine herbicide, NS-245852 [2-chloro-6-fluorophenyl-4-(trifluoromethyl)thieno[2,3-d]pyrimidine-2-yl-ketone], on mitosis in oat ( Avena sativa L. cv. Zenshin) root tips were investigated by using light and immunofluorescence microscopy. The root growth was strongly inhibited at 10⁻⁷ mol L⁻¹ of NS-245852, and swollen root tips were induced at 5 × 10⁻⁸ mol L⁻¹. As observed by the use of light microscopy, the herbicide produced disrupted mitosis and large polynucleate cells in the meristematic root tissue. These symptoms were similar to those of mitotic disrupter herbicides. The immunofluorescence microscopy studies of the root tip cells treated for 30 min revealed that spindle fibers and the preprophase band were reduced, although kinetochore fibers and the phragmoplast were not affected. Kinetochore fibers remained as small fluorescence spots, and the phragmoplast disappeared after a 3 h treatment. No microtubule arrays were observed by a longer treatment (longer than 3 h). Among the microtubule arrays, spindle fibers and the preprophase band were found to be the most sensitive to the herbicide, whereas kinetochore fibers were the most resistant. The phragmoplast was intermediate. Thus, the primary action of NS-245852 is the inhibition of polymerization of tubulin into microtubules.     

Comparison of trifluralin,oryzalin, pronamide,propham, and colchicine treatments on microtubules

The mode of action of trifluralin (α,α,α-trifluoro-2,6-dinitro-N,N-dipropyl-p-toluidine), oryzalin (3,5-dinitro-N⁴,N⁴-dipropylsulfanilamide), pronamide(N-(1,1-dimethylpropynyl) 3,5-dichlorobenzamide), and propham (isopropyl carbanilate) on purified microtubules from pig brains and on the ultrastructure of wheat (Triticum aestivum L. “Mediterranean,” C. I. 5303) and corn (Zea mays L. “yellow dent, U. S. 13”) roots was compared with that known for colchicine. Colchicine disrupts the in vivo cortical and spindle microtubules of root cells. Like colchicine, the herbicides trifluralin, oryzalin, and pronamide caused the loss of both cortical and spindle microtubules of root cells. The rate of microtubule disappearance depended on the type of herbicide and length of exposure of roots to the herbicide. Unlike colchicine, cortical microtubules were present in propham-treated roots but they were disoriented within the cell.In vitro polymerization studies with pig brain microtubules (Sus scrofa) showed that the herbicides failed to inhibit the assembly of purified microtubular protein into microtubules and that radioactively labeled herbicides did not bind to the microtubular protein. Colchicine inhibited the polymerization of microtubular protein and readily bound to the microtubular subunits. These results indicate that the mode of action of the herbicides is not similar to that of colchicine and that the loss of microtubules from root tip cells treated with trifluralin, oryzalin, and pronamide may be caused by these herbicides interfering with synthesis of microtubular protein or metabolism of endoplasmic reticulum membranes involved in microtubule assembly. The mode of action of propham appears to be on the microtubular organizing centers rather than on microtubules per se.     

Probing mode of action in plant cell cycle by the herbicide endothall, a protein phosphatase inhibitor

The mode of action of endothall, an herbicide which was reported to inhibit plant protein phosphatases 1 (PP1) and 2A (PP2A), was investigated. For initial characterization, a series of bioassays was used for comprehensive physiological profiling of endothall effects which suggested a phytotoxic mode of action similar to mitotic disrupter herbicides. Unlike known microtubule disrupters, endothall did not inhibit soybean tubulin polymerization in vitro. As shown in meristematic corn root tips, endothall distorted the orientation of cell division plane and microtubule spindle structures which led to cell cycle arrest in prometaphase. In tobacco BY-2 cells, malformed spindles together with prometaphase arrest of nuclei and abnormal perinuclear microtubule patterns were detected as early as 4 h of endothall treatment. These effects were also observed after treatment with other protein phosphatase inhibitors, cantharidin and okadaic acid, which phenocopied the mitotic changes described in tonneau1 (ton1) and tonneau2 (ton2) Arabidopsis mutants. These mutants are defective in TONNEAU2 (TON2) protein, a regulatory subunit of PP2A, which governs cell division plane and microtubule orientation. Therefore, PP2A/TON2 phosphatase complex is suggested to be an in planta molecular target of endothall. However, in BY-2 cells, additional effects of endothall, including inhibition of S-phase initiation and DNA synthesis, detected by 5-ethynyl-2′-deoxyuridine (EdU) incorporation, and condensed nuclei arrested in late mitosis were observed which were not reported in Arabidopsiston1 and ton2 mutants. This result indicates that two additional checkpoints in cell cycle were blocked by endothall which are probably not associated with TON2-pathway inhibition. Possibly, inhibition of PP1 and/or other PP2A protein phosphatases are involved in the regulation of these cell cycle phenomena.     

The possible role of quinate in the mode of action of glyphosate and acetolactate synthase inhibitors

BACKGROUND: The herbicide glyphosate inhibits the biosynthesis of aromatic amino acids by blocking the shikimate pathway. Imazethapyr and chlorsulfuron are two herbicides that act by inhibiting branched‐chain amino acid biosynthesis. These herbicides stimulate secondary metabolism derived from the aromatic amino acids. The aim of this study was to test if they cause any cross‐effect in the amino acid content and if they have similar effects on the shikimate pathway. RESULTS: The herbicides inhibiting two different amino acid biosynthesis pathways showed a common pattern in general content of free amino acids. There was a general increase in total free amino acid content, with a transient decrease in the proportion of amino acids whose pathways were specifically inhibited. Afterwards, an increase in these inhibited amino acids was detected; this was probably related to proteolysis. All herbicides caused quinate accumulation. Exogenous application of quinate arrested growth, decreased net photosynthesis and stomatal conductance and was ultimately lethal, similarly to glyphosate and imazethapyr. CONCLUSIONS: Quinate accumulation was a common effect of the two different classes of herbicide. Moreover, exogenous quinate application had phytotoxic effects, showing that this plant metabolite can trigger the toxic effects of the herbicides. This ability to mimic the herbicide effects suggests a possible link between the mode of action of these herbicides and the potential role of quinate as a natural herbicide. Copyright © 2009 Society of Chemical Industry     

Einfluß von Diclofop-methyl auf Wachstum und Entwicklung der Keimlinge von Zea mays L.*

Effect of diclofop-methyl on the growth und development of Zea mays L. seedlings Diclofop-mcthyl, a diphenoxypropionic acid herbicide, had no effect on the germination of maize (Zea mays) seed. Prc-ger-minated maize embryos showed inhibited radicle growth when treated with the herbicide, but those of beans were considerably less sensitive. The inhibitory effect of the herbicide on maize radicle growth was reversed when the embryos were transferred to herbicide-free medium within 24 h of treatment. The higher concentrations of diclofop-methyl tested (≥10^?6 M) induced necrosis on the second day of treatment, which first appeared in the meristematic and elongation zone of the root tip and then via the rest of the root to the grain. The herbicide increased the fresh and dry weight as well as the dry matter content of the radicle tips of Zea mays. These effects were attributed in an accumulation of cell wall material in the herbicide-treated root lips. In the presence of hydroxyurea, a selective inhibitor of cell division, the effect of diclofop-melhyl on radicle elongation was reduced but did not cease complelely. From these results it can be concluded that diclofop-methyl interferes with the processes that effect both cell division and cell elongation.     

Pronamide disrupts mitosis in a unique manner

Pronamide (3,5-dichloro(N-1,1-dimethyl-2-propynyl)benzamide) has traditionally been grouped with mitotic disrupters, such as colchicine or trifluralin, that inhibit polymerization of tubulin into microtubules. Many of the effects of pronamide (c-metaphases, polymorphic nuclei, isodiametric cells, abnormal xylem development, swollen root tips) are similar to these well-studied mitotic disrupters. However, immunofluorescence microscopy studies using anti-tubulin sera revealed that, unlike other mitotic disrupters, pronamide-treated cells have greatly shortened microtubules that are located only at the kinetochore region. These structures detected by immunofluorescence studies were determined by electron microscopy to be microtubules. Because these short kinetochore microtubules did not allow for mitosis to proceed normally, the nuclear envelope reforms around the chromosomes leading to polymorphic nuclei. Frequently, other cytoplasmic organelles normally excluded in the zone occupied by the chromosomes and spindle during mitosis were retained within the reformed nuclei. These data indicate that, although the net effect of pronamide is similar to those of colchicine and trifluralin, pronamide acts by a different mechanism.     

Interactions between the root pathogen Rhizoctonia solani AG-8 and acetolactate-synthase-inhibiting herbicides in barley

BACKGROUND: The widespread acceptance of reduced‐tillage farming in cereal cropping systems in the Pacific Northwest of the United States has resulted in increased use of herbicides for weed control. However, soil residual concentrations of widely used imidazalone herbicides limit the cultivation of barley, which is more sensitive than wheat. In addition, increased severity of the root rot disease caused by Rhizoctonia solani is associated with reduction in tillage. Many crops exhibit altered disease responses after application of registered herbicides. In this study, the injury symptoms in barley caused by sublethal rates of two acetolactate synthase (ALS)‐inhibiting herbicides, imazamox and propoxycarbazone‐sodium, were assessed in factorial combinations with a range of inoculum concentrations of the root rot pathogen Rhizoctonia solani AG‐8. RESULTS: Both herbicides and pathogen had negative impacts on plant growth parameters such as root and shoot dry weight, shoot height and first leaf length, and interactions between pathogen and herbicide were detected. CONCLUSIONS: The results suggested that sublethal rates of herbicides and R. solani could alter severity of injury symptoms, possibly owing to the herbicide predisposing the plant to the pathogen. Copyright © 2012 Society of Chemical Industry     

加拿大一枝黄花防除化学药剂的筛选及其应用效能

为获得防除加拿大一枝黄花的有效药剂,揭示化学防治的主要特征,采用单一药剂、单一药剂+助剂、混合药剂及触杀型+内吸型药剂4种药剂处理方式进行田间药效试验。结果表明,25%环嗪酮可溶液剂7 500mL/hm~2、41%草甘膦异丙铵盐水剂6 000mL/hm~2+有机硅300g/hm~2、20%氯氟吡氧乙酸乳油750mL/hm~2+20%草铵膦水剂8 740mL/hm~2、41%草甘膦异丙铵盐水剂6 000mL/hm~2+20%草铵膦水剂8 740mL/hm~2对加拿大一枝黄花的防效显著。施药35d后,株防效均达到100.00%,地上部分鲜重防效分别达到80.2%、90.4%、83.0%和88.9%。除25%环嗪酮可溶液剂致植株根腐效果不佳外,其余3种药剂组合地下部分鲜重防效均达到70%以上,可作为加拿大一枝黄花防除的典型药剂进行推广。组合药剂喷施方式表明,内吸型和触杀型药剂喷施顺序不同,对加拿大一枝黄花的防除效果存在明显差异。以单一药剂最大剂量防除加拿大一枝黄花的效果显示,喷施大剂量单一药剂不一定能明显提高防治效果。     

Determination of genotoxic effects of chlorfenvinphos and fenbuconazole in Allium cepa root cells by mitotic activity, chromosome aberration, DNA content, and comet assay

Genotoxic effects of Chlorfenvinphos and fenbuconazole were examined by using mitotic index, mitotic phase, chromosomal abnormalities, 2C DNA content and Comet assay on the root meristem cells of Allium cepa. The roots were treated with 10, 20, 40, 60, 80, and 100 ppm concentrations for 24 and 48 h. The results indicated that Chlorfenvinphos and fenbuconazole significantly decreased the mitotic index in all treatments when compared with their controls. The percentages of mitotic phases have changed. Chlorfenvinphos and fenbuconazole significantly increased the abnormal cell frequency at all concentrations and treatment periods when compared with their controls. Different abnormal mitotic figures were observed in all mitotic phases. Among these abnormalities were stickiness, anaphase bridges, c-mitosis, laggards, and micronucleus. These pesticides remarkably depressed the 2C DNA content in the root meristems of A. cepa. The genotoxicity of chlorfenvinphos and fenbuconazole in A. cepa root cells was analyzed using comet assay, which allows the detection of single strand breaks. In all concentrations, chlorfenvinphos and fenbuconazole induced a significant increase in DNA damage. Additionally, it was also researched to determine if there is a relation between the amount of DNA and the DNA damage and a regression analyses was conducted. When the data that was accumulated via comet analysis from A. cepa root tip cells that are treated with type chlorfenvinphos and fenbuconazole, was compared to the data that was acquired as the result of the measurement of 2C DNA amount, a relation with negative correlation was found, (respectively, r = −0.80 and r = −0.82). This relation factor is statistically important and strong (p < 0.05).     

代谢酶抑制剂PX对除草剂防除稗草的增效作用

为解决除草剂防除困难的问题,采用室内盆栽试验测定了PX、PM和Mn²⁺三种代谢酶抑制剂对精喹禾灵、莠去津、烟嘧磺隆、硝磺草酮和烯禾啶防除稗草Echinochloa crus-galli的增效作用,测定不同用量代谢酶抑制剂PX对这5种除草剂的增效作用及其与莠去津混用后稗草体内谷胱甘肽转移酶（glutathione S-transferase,GST）和细胞色素 P450（cytochrome P450,CYP450）活性的变化。结果显示,在3种代谢酶抑制剂中,代谢酶抑制剂PX对精喹禾灵、莠去津、烟嘧磺隆、硝磺草酮和烯禾啶5种除草剂的增效作用最显著。不同用量代谢酶抑制剂PX对不同除草剂的增效作用不同,其中75 g (a.i.)/hm²代谢酶抑制剂PX对莠去津的增效最佳,株防除效果和鲜重防除效果分别增加了35.33个百分点和37.33个百分点。莠去津与代谢酶抑制剂PX混用后,稗草体内GST和CYP450活性均较对照显著降低。表明除草剂与代谢酶抑制剂PX混用能增加除草剂对稗草的防除效果,可以达到减施除草剂的目的。     

Thaxtomin A: evidence for a plant cell wall target

Thaxtomins are unique 4-nitroindol-3-yl containing dioxopiperazines that cause dramatic plant cell hypertrophy and seedling stunting. This family of phytotoxins is produced by Streptomyces species that cause diseases of root and tuber crops; its members are essential for pathogenicity. The symptoms produced by thaxtomin A suggest several potential plant cell targets including the plasma membrane, various components of the cytoskeleton and the cell wall. Dramatic increases in cell volume in onion seedling hypocotyls, radish seedling hypocotyls and tobacco suspension cultures, in response to 0.05–1.0 μM thaxtomin A, suggested that this phytotoxin is interacting with one or more conserved plant cell targets. Onion root tip cells treated with thaxtomin A concentrations at or below that which inhibited onion root growth were binucleate or had abnormal cell plates. Thaxtomin A (1.0–3.0 μM) inhibited normal cell elongation of tobacco protoplasts in a manner that suggested an effect on primary cell wall development. In summary, these data suggest that thaxtomin A alters, either directly or indirectly, the deposition or composition of monocot and dicot plant cell walls in ways that affect the wall integrity and the ability of the cell to progress normally through cytokinesis.     

Perspective: root exudation of herbicides as a novel mode of herbicide resistance in weeds

The evolution of resistance to herbicides in weeds has become a great challenge for global agricultural production. Weeds have evolved resistance to herbicides through many different physiological mechanisms. Some weed species are known to secrete herbicide molecules from roots into the rhizosphere upon being treated. However, root exudation of herbicides as a mechanism of resistance has only recently been identified in two weed species. Root exudation pathways have been investigated in Arabidopsis, and this work suggested that ATP‐binding cassette (ABC) and multidrug and toxic compound extrusion (MATE) transporters play a role in the secretion of primary and secondary plant products from roots. We hypothesize that the mechanisms involved in root exudation of herbicides that result in resistance are mediated by overactive or overexpressed transporters, probably similar to those found for the exudation of primary and secondary compounds from roots. Elucidating the molecular and physiological basis of root exudation in herbicide‐resistant weeds would improve our understanding of the pathways involved in herbicide root secretion mediated by transporters in plants. © 2020 Society of Chemical Industry     

The influence of the herbicide mefenacet on cell division and cell enlargement in plants

The herbicide mefenacet has recently been developed for pre–emergence control of graminaceous and some dicotyledonous weeds in rice. Whereas mefenacet is known to inhibit root growth, its effect on the components of growth, cell division and cell enlargement, have not been determined. The purpose of this study was to evaluate the influence of mefenacet on growth, cell enlargement and cell division in Chlamydomonas (a green alga) and oats. Cell division in Chlamydomonas was completely inhibited and cell enlargement was inhibited by an average of 18% during the first cell cycle period when cells were treated with 6–7 μM mefenacet. The rate of oat root growth in sand culture between 12 and 24 h after initiation of treatment was reduced 90% at 10 μM mefenacet. Cell enlargement of oat coleoptile sections in culture solution was inhibited 25% at 10 μM. Mefenacet inhibited mitotic entry rather than disrupted the mitotic sequence. Cell division in oat roots was inhibited 54% by 10 μM mefenacet. This shows cell division inhibition occurs in G₁, S, or G₂ of the cell cycle. The action of mefenacet is most like that of the chloroacetamides among the herbicide classes known to inhibit growth.     

除草剂对作物产生药害的原因及治理对策

本文论述了我国除草剂使用过程中作物产生药害的主要原因和除草剂药害的治理对策。提出:除草剂使用不合理,除草剂和作物本身的因素,异常的环境条件是药害产生的主要原因。杜绝假冒伪劣及不合格产品,加强除草剂试验、示范、推广工作,深化除草剂应用技术研究,加强农民用药技术水平培训是除草剂安全使用应解决的问题。     

Ultrastructural changes in leaf and needle segments treated with herbicides containing picloram

The herbicide Tordon 50D (picloram+2,4-D) affected the integrity of the nucleus and cell membranes in Pinus radiata needle segments and caused the swelling of internal chloro plast membranes and the eventual disintegration of the chloroplasts. Tordon 22K (picloram) only affected chloro plast structure. Both herbicides had similar adverse effects on cell membranes and chloroplasts of Eucalyptus viminalis.