Nitro free radical formation of diphenyl ether herbicides is not necessary for their toxic action

The diphenyl ether herbicides MC 15608 {5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-chloromethylbenzoate} and MC 10878 {5-[2-chloro-4-(trifluoromethyl)phenoxy]methyl benzoate} are structurally similar to acifluorfen-methyl (methyl ester of 5-[2-chloro-4-(trifluoromethyl)phenoxy]-nitrobenzoic acid), except that the NO₂ is replaced by a Cl and H, respectively. These diphenyl ether herbicides required light for herbicide toxicity to the green unicellular alga Chlamydomonas eugametos and three major weeds (Xanthium pennsylvanicum, Abutilon theophrasti, and Ipomoea sp.). Acifluorfen-methyl and MC 15608 toxicity in Chlamydomonas decreased in an atmosphere of nitrogen, and in the presence of the free radical scavengers α-tocopherol and ethanol. Therefore, the mechanism of toxic action of these three different diphenyl ether herbicides is similar and appears to involve some type of free radical reaction. As confirmed by cyclic voltammetry studies, MC 15608 and MC 10878, unlike AFM, cannot readily accept electrons to become free radicals. Therefore, initiation of free radical reactions in polyunsaturated fatty acids of membranes does not necessarily involve direct reduction and reoxidation of the diphenyl ether molecule.     

Mitochondrial involvement in the mode of action of acifluorfen

The herbicidal action of acifluorfen {5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoic acid} was studied with greened and expanded discs from cotyledons of cucumber (Cucumis sativus L.). Discs were floated on various treatment solutions for 20 hr in darkness before exposure to 400 μE m^?2 sec^?1 of white light. Herbicide damage, as measured by electrolyte leakage, began in the light after a 1- to 2-hr lag period. Cytochemical methods at the ultrastructural level indicated that acifluorfen caused marked increases in production of superoxide radical and hydrogen peroxide in the mitochondrion, but not in the plastid. The mitochondrial inhibitors antimycin A, rotenone, CCCP, and DNP antagonized the action of acifluorfen, lengthening the lag period and reducing the rate of electrolyte leakage. Ethanol, α-tocopherol, N-[2-(2-oxo-1-imidazolidinyl)ethyl]-N′-phenylurea, and copper-penicillin also lengthened the lag phase and slowed the rate of damage, indicating that acifluorfen damage involves toxic oxygen species. PS II-inhibiting levels of DCMU, atrazine, or bentazon did not affect acifluorfen-induced ion leakage. Yellow tissue produced by treatment with tentoxin was supersensitive to acifluorfen, but white tissue produced by treatment with norflurazon was relatively insensitive. These data indicate that, after an initial carotenoid-acifluorfen interaction, the mitochondrion is involved in production of toxic oxygen species and that this process is closely tied to the mechanism of action of this herbicide.     

Photoreceptors and respiratory electron flow involvement in the activity of acifluorfen-methyl and LS 82-556 on nonchlorophyllous soybean cells

The diphenyl ether acifluorfen-methyl [AFM; methyl 5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoate] and the pyridine derivative LS 82-556 [(S)-3-N-(methylbenzyl)carbamoyl-5-propionyl-2,6-lutidine] induce light-dependent polyunsaturated fatty acid peroxidation, leading to general membrane disruption. Although devoid of functional chloroplasts, cultured soybean cells are sensitive to AFM and LS 82-556 only in the light. The possible involvement of carotenoids and respiratory electron flow was examined by monitoring ethane evolution, fluorescein release, and dry weight/fresh weight ratio alteration. Herbicide effects on cells exposed to white light or blue light (380–540 nm) remain unchanged when the cells are deprived of carotenoids by treatment with norflurazon [4-chloro-5-(methylamino)-2-(α,α,α-trifluoro-m-tolyl)-3(2H)-pyridazinone]. Treatment with antimycin A reduced sensitivity to AFM and LS 82-556. In nonchlorophyllous cells, chromophores, other than carotenoids, absorbing between 380 and 540 nm are involved as photoreceptors. Furthermore, respiratory electron flow also participates in the toxic process.     

三氟羧草醚类似物的合成及除草活性

以2,5-二羟基苯甲酸甲酯和三氟羧草醚为起始原料,设计合成了3个系列20个新的三氟羧草醚类似物,通过核磁共振氢谱、碳谱对其结构进行了表征。分别采用小杯法和室内盆栽法测定了目标化合物的除草活性。结果表明,化合物 III-02 [5-(2-氯-4-三氟甲基苯氧基)-2-硝基苯甲酸-(6-甲基苯并噻唑-2-基)酯]对单子叶杂草的除草活性明显高于对照药剂三氟羧草醚,其对稗草Echinochloa crusgalli和马唐Digitaria sanguinalis根茎生长的EC₅₀值分别为2.03、0.93 μg/mL和1.49、0.52 μg/mL;在有效成分100 g/hm2的施药剂量下,化合物 III-02 对单子叶杂草稗草、马唐及狗尾草Setaria viridis的防治效果均在85%以上,明显高于三氟羧草醚,对阔叶杂草马齿苋Portulaca oleracea、反枝苋Amaranthus retroflexus及苘麻Abutilon theophrasti的防治效果可达100%。初步构效关系表明,2-硝基苯甲酰衍生物的除草活性明显优于其2-甲氧基衍生物,三氟羧草醚苯甲酸酯衍生物对单子叶杂草的除草活性明显高于其苯甲酰胺衍生物。     

Diphenyl ether-chloroplast interactions

The diphenyl ethers acifluorfen (sodium-5-[2-chloro-4-(trifluoromethyl)-phenoxyl]-2-nitrobenzoate), acifluorfen-methyl (methyl-5-[2-chloro-4-(trifluoromethyl)-phenoxyl]-2-nitrobenzoate), and oxyfluorfen (2-chloro-1-[3-ethoxy-4-nitrophenoxy]-4-(trifluoromethyl)benzene have an absolute light requirement for herbicidal activity. CO₂-dependent O₂ evolution was inhibited in leaf disks obtained from 5-week-old spinach plants as a result of incubation in the light in the presence of each of the three diphenyl ethers. I₅₀'s were determined for inhibition by the diphenyl ethers of CO₂-dependent O₂ evolution in intact chloroplasts obtained from three species of varying susceptibilities (spinach, coffeeweed, and pea). Rankings obtained correlated well with relative susceptibilities and with relative effectiveness of the three compounds tested. Coupled and uncoupled photosynthetic electron transport in susceptible species were unaffected by the three compounds at concentrations in the I₅₀ range. Exposure to herbicidally inactive isomeric analogs of oxyfluorfen and acifluorfen did not affect photosynthesis in leaf disks but was effective in inhibiting photosynthesis in isolated chloroplasts. Photosynthetic abilities of intact tissue were not affected by herbicide treatment in red light. Red light was, however, as effective as white light in mediating the inhibition of photosynthesis in isolated intact chloroplasts by diphenyl ethers. The existence of two photoreceptors for diphenyl ether action, one located at the chloroplast envelope and a second outside of the chloroplast, is suggested as a possible basis for these findings.     

Phytotoxicity of m-phenoxybenzamides: Inhibition of cell-free phytoene desaturation

Inhibition of carotenoid biosynthesis by herbicidal m-phenoxybenzamide derivatives has been investigated in a cell-free carotenogenic system from Aphanocapsa. Their target is the phytoenedesaturase reaction. Double-reciprocal plots of β-carotene biosynthesis (from ¹⁴C-labeled geranylgeranyl pyrophosphate) showed that 3-(2,5-dimethylphenoxy)-N-ethylbenzamide was a noncompetitive inhibitor of the phytoene-desaturase complex. The K_i value for cell-free inhibition of β-carotene formation was almost identical to the I₅₀ value of intact cells. Furthermore, the influence of certain substituents on herbicidal activity has been investigated. Inhibition increased with the length of the unbranched N-alkyl chains. In addition, substituents at the phenoxy group with higher lipophilicities showed greater inhibitory activities. The presence of a phenoxy or trifluoromethyl moiety at position 3 is essential.     

Pyrazole phenyl ether herbicides inhibit protoporphyrinogen oxidase

Two isomeric pairs of pyrazole phenyl ether herbicides [AH 2.429, 4-chloro-1-methyl-5-(4-nitrophenoxy)-3-(trifluoromethyl)-1H-pyrazole; AH 2.430, 4-chloro-1-methyl-3-(4-nitrophenoxy)-5-(trifluoromethyl)-1H-pyrazole; AH 2.431, 5-((4-chloro-1-methyl-5-(trifluoromethyl)-1H-pyrazol-3-yl)oxy)-2-nitrobenzoic acid; and AH 2.432, 5-((4-chloro-1-methyl-3-(trifluoromethyl)-1H-pyrazol-5-yl)oxy)-2-nitrobenzoic acid were evaluated for herbicidal activity in both intact plants and in tissue sections. Their capacity to induce accumulation of porphyrins in tissue sections and to inhibit protoporphyrinogen oxidase (Protox) in vitro were determined. In whole plant tests, the order of herbicidal activity was AH 2.430 AH 2.431 > AH 2.429 > AH 2.432. AH 2.430 consistently caused light-dependent membrane leakage in both green and far-red light grown cucumber cotyledon and barley primary leaf tissue sections after incubation for 20 hr in darkness in 0.1 mM solutions. The same treatment caused marked increases in protoporphyrin IX (PPIX) content during the 20-hr dark incubation. AH 2.429 and 2.431 were less effective and not effective in all tissues in causing herbicidal damage and PPIX accumulation. AH 2.432 was ineffective in tissue section assays. Mg-PPIX levels were not significantly affected by any of the compounds. Protochlorophyllide levels were decreased by AH 2.430 and 2.431 in barley and increased by AH 2.429, 2.431, and 2.432 in cucumber. A positive relationship was found between herbicidal activity and the amount of PPIX that was caused to accumulate by each compound. All of the compounds inhibited Protox activity. Positive correlations were found between herbicidal activity in planta over a 300-fold range and in vitro Protox inhibition and the amount of PPIX caused to accumulate in vivo. These data support the view that the pyrazole phenyl ethers exert their herbicidal activity entirely through inhibition of Protox.     

Potassium uptake in atrazine-treated roots of sensitive and resistan plants

The action of atrazine and its biodegradation products on the membrane transport of potassium in roots was evaluated in both sensitive and resistant plants. Excised roots of maize and oat showed inhibition of potassium uptake efficiency in the presence of 1.4 × 10^?4M atrazine and 1.4 × 10^?4M deethylated atrazine. Other biodegradation products such as 2-chloro-4-amino-6-ethylamino-1,3,5-triazine,2-chloro-4,6-,bisamino-1,3,5-triazine, and 2-chloro-4-amino-1,3,5-triazine showed no inhibitory effect on the K⁺ uptake capacity. Two maize hybrids showing different uptake efficiency were inhibited differently by atrazine. We suggest that atrazine and deethylated atrazine inhibited the K⁺ transport interacting directly with the plant cell membranes without discerning between resistant and sensitive plants.     

Analysis of soils for diclofop-methyl and diclofop

A method is described for the analysis of soils for residues of the herbicide diclofop-methyl, methyl (RS)-2-[4-(2,4-dichlorophenoxy)phenoxy]propionate, and its breakdown product diclofop, (RS)-2-[4-(2,4-dichlorophenoxy)phenoxy]propionic acid. Diclofop-methyl undergoes hydrolysis in the soil to diclofop, which also has herbicidal activity. A procedure, using a 1% phosphoric acid solution for extraction purposes, has been developed and gives good recoveries of both diclofop-methyl and diclofop at the 0.5 and 0.05 mg kg^?1 levels. After methylation, gas-liquid chromatography with electron-capture detection is used to determine total residue concentrations.     

Synthesis and herbicidal activities of novel 3-(substituted benzyloxy or phenoxy)-6-methyl-4-(3-trifluoromethylphenyl)pyridazine derivatives

BACKGROUND: 4‐(3‐Trifluoromethylphenyl)pyridazine represents a new series of compounds with bleaching and herbicidal activities. RESULTS: A total of 43 novel 3‐(substituted benzyloxy or phenoxy)‐6‐methyl‐4‐(3‐trifluoromethylphenyl)pyridazine derivatives were synthesised, and their bleaching and herbicidal activities were evaluated through Spirodela polyrrhiza and greenhouse tests. Some compounds exhibited excellent herbicidal activities, even at a dose of 7.5 g ha^?1. CONCLUSION: The results showed that a substituted phenoxy group at the 3‐position of the pyridazine ring and the electron‐withdrawing group at the para ‐position on the benzene ring were essential for high herbicidal activity. Copyright © 2011 Society of Chemical Industry     

Potential involvement of alkoxyl and hydroxyl radicals in the peroxidative action of oxyfluorfen

The potential involvement of hydroxyl and alkoxyl radicals in the peroxidative action of the p-nitro diphenyl ether herbicides acifluorfen (5-[2-chloro-4-(trifluoromethyl)phenoxyl]-2-nitrobenzoic acid), acifluorfen-methyl (methyl ester of acifluorfen), nitrofen [2,4-dichloro-1-(4-nitrophenoxy)benzene], nitrofluorfen [2-chloro-1-(4-nitrophenoxy)-4-(trifluoromethyl)benzene], and oxyfluorfen [2-chloro-1-(3-ethoxy-4-nitrophenoxy)-4-(trifluoromethyl)benzene] was evaluated under laboratory conditions. Methional was added to illuminated thylakoids from peas (Pisum sativum L., cv Little Marvel) and its oxidation to ethylene was used as an indicator of hydroxyl and alkoxyl radical production. Oxyfluorfen stimulated the rate of methional oxidation by 138% at 10 μM and 175% at 1 mM. This oxyfluorfen-induced stimulation of the rate of methional oxidation was dependent on light, photosynthetic electron transport, and hydrogen peroxide since it was not observed under dark conditions or in the presence of DCMU and catalase. Addition of Fe-EDTA, a catalyst of the Fenton reaction, stimulated the oxyfluorfen-induced enhancement of methional oxidation sixfold, suggesting that hydroxyl radicals are synthesized through a Fenton reaction. Acifluorfen, nitrofen, and nitrofluorfen inhibited the rate of methional oxidation whereas acifluorfen-methyl had no effect on the rate of methional oxidation, even at high concentrations (1 mM). Nitrofluorfen at 1 mM was the only p-nitro diphenyl ether herbicide tested to inhibit photosynthetic electron transport of pea thylakoids. In experiments with pea leaf disks, acifluorfen at low concentrations stimulated the rate of methional oxidation, whereas acifluorfen-methyl, nitrofen, and nitrofluorfen had no effect. These data indicate that hydroxyl and alkoxyl radicals could be involved in the mechanism of cellular damage caused by oxyfluorfen but they are not important for the activity of the diphenyl ether herbicides acifluorfen, acifluorfen-methyl, nitrofen, and nitrofluorfen.     

Control of Sorghum halepense (L.) Pers. in cotton with post-emergence herbicides and trifluralin

A field experiment was conducted in 1981 and 1982 to evaluate five post-emergence herbicides applied alone or following a preplant incorporated application of trifluralin for the control of Sorghum halepense (L.) Pers. in cotton (Gossypium hirsutum). One application of the methyl ester of haloxyfop [methyl 2- (4- ((3-chloro-5-trifluoromethyl)-2-pyridinyl)oxy)phenoxy)pro-panoate], trifluralin plus the ethyl ester of DPX-Y6202 [ethyl[2-[-4-(6-chloro-2-quinoxalinyl)oxy]phenoxy]propionate], the butyl ester of fluazifop and trifluralin plus haloxyfop resulted in over 90% control of S. halepense just prior to harvest in 1981 and 1982. Sorghum halepense control was similar whether the post-emergence herbicides were applied alone or following preplant incorporated trifluralin at 0.8 kg ha^?1. La lutte contre Sorghum halepense (L.) Pers. en culture de cotonnier moyennant des herbicides de post-levée et la trifluraline Une expérience a été installée en plein champ en 1981 et 1982 dans le but d'évaluer cinq herbicides de post-levée, appliqués seuls ou suite à la trifluraline incorporée avant le semis, dans la lutte contre Sorghum halepense (L.) Pers. en culture de cotonnier (Gossypium hirsutum). Une seule application de l'haloxyfop ester de méthyle [méthyle 2-(4-((3-chloro-5- (trifluorométhyle)-2-pyridinyle) oxy)phénoxy)propanoate], de trifluraline + DPX-Y6202 ester d'éthyle (éthyle[2-[4-(6-chloro-2-quinoxalinyle)oxy]phénoxy)propionate), de l'ester butylique du fluazifop et de trifluraline + haloxyfop a permis en 1981 et 1982 une bonne maîtrise (90%) de S. halepense juste avant la récolte. La maîtrise de Sorghum halepenseétait semblable, que les herbicides de postlevée aient été précédés ou non d'une application de trifluraline à 0,8 kg ha^?1 incorporée avant le semis. Bekämpfung von Sorghum halepense (L.) Pers. in Baumwolle mit Nachauflaufherbiziden und Trifluralin In den Jahren 1981 und 1982 wurden Feldversuche zur Bekämpfung von Sorghum halepense (L.) Pers. in Baumwolle (Gossypium hirsutum) mit fünf Nachauflaufherbiziden durchgeführt. Die Herbizide wurden allein oder nach einer vor der Baumwollsaat erfolgten Einarbeitung von Trifluralin appliziert. Eine Applikation des Methylesters von Haloxyfop [Methyl-2-(4-((3-chloro-5-(trifluormethyl)-2-pyridinyl)oxy)phenoxy)propanoat]. Von Trifluralin + Aethylester von DPX-Y 6202 [Aethyl[2-[-4-(6-chlor-2-quinoxalinyl)oxy)phenoxy)propionat], des Butylesters von Fluazifop und Trifluralin + Haloxyfop ergaben in beiden Jahren kurz vor der Ernte eine über 90 ige Kontrolle von S. halepense. Der Bekämpfungserfolg war ähnlich, gleichgültig ob die Herbizide allein oder nach der Einarbeitung von Trifluralin (0,8 kg ha^?1) appliziert worden waren.     

Localizing the action of two thiadiazolyl herbicidal derivatives

Enzymatically isolated leaf cells from navy beans (Phaseolus vulgaris L., cv. “Tuscola”) were used to study the effect of buthidazole (3-[5-(1,1-dimethylethyl)-1,3,4-thiadiazol-2-yl]-4-hydroxy-1-methyl-2-imidazolidinone) and tebuthiuron (N-[5-(1,1-dimethylethyl)-1,3,4-thiadiazol-2-yl]-N,N′-dimethylurea) on photosynthesis, protein, ribonucleic acid (RNA), and lipid synthesis. The incorporation of NaH¹⁴CO₃, [¹⁴C]leucine, [¹⁴C]uracil, and [¹⁴C]acetic acid as substrates for the respective metabolic process was measured. Time-course and concentration studies included incubation periods of 30, 60, and 120 min and concentrations of 0.1, 1, 10, and 100 μM of both herbicides. Photosynthesis was very sensitive to both buthidazole and tebuthiuron and was inhibited in 30 min by 0.1 μM concentrations. RNA and lipid syntheses were inhibited 50 and 87%, respectively, by buthidazole and 42 and 64%, respectively, by tebuthiuron after 120 min at 100 μM concentration. Protein synthesis was not affected by any herbicide at any concentration or any exposure time period. The inhibitory effects of buthidazole and tebuthiuron on RNA and lipid syntheses may be involved in the ultimate herbicidal action of these herbicidal chemicals.     

Effects of various classes of herbicides on four species of algae

Chlorella pyrenoidosa, Chlorococcum sp., Lyngbya sp., and Anabaena variabilis were cultured in Bold's basal medium. They were treated with 0.1, 1.0, and 10 μM concentrations of 2-chloro-2′, 6′-diethyl-N-(methoxymethyl)acetanilide (alachlor), 2-chloro-4-(ethylamino)-6-(tert-butyl-amino)-s-triazine (terbuthylazine), 2-sec-butyl-4,6-dinitrophenol (dinoseb), 1,1-dimethyl-3-(α,α,α-trifluoro-2,6-dinitro-N-propyl-p-toluidine) (profluralin), 2, 4-bis(isopropylamino)-6-(methylthio)-s-triazine (prometryne), and (2,4-dichlorophenoxy)acetic acid (2,4-D). Growth of all algal species tested was markedly reduced by the triazines. Alachlor, dinoseb, and fluometuron inhibited growth of some algae at higher concentrations while 2,4-D and profluralin did not inhibit growth at the concentrations tested. Photosynthesis was greatly inhibited by the triazines, even at the 0.1 μM concentration. Fluometuron was very toxic to the blue-green algae but had less effect on the green algae tested. Lyngbya was most susceptible to photosynthesis reduction by the herbicides. The concentrations of herbicides tested had little effect on respiration of the algae species. It appears that effects on algal growth were due primarily to inhibition of photosynthesis rather than to other metabolic processes.     

Physiological effects of methyl 2-[4(2,4-dichlorophenoxy)phenoxy] propanoate on oat,wild oat,and wheat

Methyl 2-[4-(2,4-dichlorophenoxy)phenoxy]propanoate (dichlofop-methyl) is a selective herbicide for wild oat (Avena fatua L.) control in wheat (Triticum aestivum L.). Dichlofop-methyl inhibited IAA-stimulated elongation of oat and wheat coleoptile segments by 51 and 13%, respectively, at 10 μM concentrations. Dichlofop-methyl alone had no auxin activity at concentrations of 0.1, 1.0, and 10 μM. The inhibitory effect of dichlofop-methyl was overcome partially by increasing the IAA concentration or by application of 3,6-dichloro-o-anisic acid (dicamba), a herbicide with weak auxin activity. The de-esterified free acid metabolite, 2-[4-(2,4-dichlorophenoxy)phenoxy]-propionic acid (dichlofop), at 10 μM inhibited auxin-stimulated oat coleoptile elongation by 23%, but it did not affect wheat coleoptile elongation at the same concentration. Both dichlofop-methyl and dichlofop inhibited root growth in excised shoots and seedlings of wild oat but had no effect on wheat. Dichlofop was a more effective inhibitor of root growth than dichlofop-methyl. The results suggest that dichlofop-methyl functions as a strong auxin antagonist, while the metabolite, dichlofop, inhibits root growth and development by another mechanism. The herbicidal effect of dichlofop-methyl may be the net effect of two biologically active forms of the compound each with a different mode of action acting at different sites within a susceptible plant.     

An evaluation of the herbicidal and plant growth regulatory activity of a novel class of carbohydrate-derived 6,8-dioxabicyclo[3.2.1]octanes

Thirty-five carbohydrate-derived dioxabicyclo[3.2.l]octane derivatives have been tested for herbicidal and plant growth regulatory (PGR) activity in an Arabidopsis thaliana assay. Nine of these were herbicidal at concentrations of ? 16 μg ml^?1 in the growth medium. Three compounds, viz, 1,6-anhydro-3-deoxy-4-O-(2,6-dichlorobenzyl)-2-O-methyl-β-D-ribo-hexopyranose(I), its 4-O-benzyl analogue (II), and l,6-anhydro-2-azido-4-O-benzyl-2,3-dideoxy-β-D-ribo-hexopyranose (III) were very active herbicides, killing plants by the rosette stage at 1 μg ml^?1 or less. At lower rates, the herbicides acted as growth regulators, reducing growth rates of shoots and roots as well as flowering and seed-pod development. A further 14 compounds exerted PGR effects only, while 12 compounds were virtually inactive at 16 μg ml^?1, the highest rate tested. The ability of the active compounds to reduce seed viability on mature plants at sublethal concentrations was demonstrated in four cases.     

吡啶衍生物研究(Ⅺ):2-仲丁胺基-5-(2-氯吡啶-4-基)-1,3,4-噻二唑对映异构体的合成及除草活性

2-仲丁胺基-5-(2-氯吡啶-4-基)-1,3,4-噻二唑(BCPT)是早期发现的一个具有良好除草活性的外消旋先导化合物,报道了使用R/S-仲丁胺为原料分别合成BCPT的两个对映异构体的方法。初步生测结果显示,3种噻二唑化合物(外消旋体和两个对映异构体)对稗草的根和茎均表现出较强的抑制作用,其中S-(+)对映异构体对茎的抑制作用强于R-(-)对映异构体和外消旋体,但对根的生长抑制作用三者间没有显著差异。     

新型含吡唑杂环邻氨基苯甲酰胺类化合物的合成与杀螨活性

以氯虫苯甲酰胺和氟虫腈的结构为基础,通过活性亚结构拼接的方法,设计合成了24个新型含吡唑杂环邻氨基苯甲酰胺类化合物,其结构经1H NM R、IR及APCI-M S表征。初步生物活性测试结果表明:化合物5-溴-N-[4-氯-2-甲基-6-(甲氨基甲酰基)苯基]-1-1-[2,6-二氯-4-(三氟甲基)苯基]-4-三氟甲基亚磺酰基-1H-吡唑-3-甲酰胺(5k)和5-溴-N-[4-溴-2-甲基-6-(甲氨基甲酰基)苯基]-1-[2,6-二氯-4-(三氟甲基)苯基]-4-三氟甲基亚磺酰基-1H-吡唑-3-甲酰胺(5l)在500 mg/L下对朱砂叶螨Tetranychus cinnabarinus的致死率为100%,但在100 mg/L下其致死率则分别降至30%和50%。所得结果可为邻氨基苯甲酰胺类化合物构效关系研究提供参考。     

Inhibition of two acetylcholinesterases by the 4-nitrophenyl esters of methyl-, ethyl-, and isopropyl(phenyl)phosphinic acid

The inhibition of eel acetylcholinesterase and bovine erythrocyte acetylcholinesterase by the 4-nitrophenyl esters of methyl-, ethyl-, and isopropyl(phenyl)phosphinic acid (MPP, EPP, and IPP, respectively) was investigated at pH 6.90 in 0.067 M phosphate buffer (25.0°C) using stopped-flow instrumentation and automated data processing. Our evaluation of the dissociation constant, K_d, the unimolecular bonding rate constant, k₂, and the bimolecular reaction constant, k_i, are the first reported values for these constants for a homologous series of this class of organophosphorus compounds. The largest k₁ value (29,428 M^?1 sec^?1) was observed for the reaction of eel acetylcholinesterase with 4-nitrophenyl methyl(phenyl)phosphinate. The smallest k_i value (9.6 M^?1 sec^?1) was observed for the reaction of bovine erythrocyte acetylcholinesterase with 4-nitrophenyl isopropyl(phenyl)phosphinate.     

嘌呤氧基苯氧丙酸酯的合成及除草活性

以4,6-二氯-5-硝基嘧啶为起始原料,经过还原胺化、取代、醚化等一系列反应,得到11个未见文献报道的嘌呤氧基苯氧丙酸酯类化合物1a~1k,其结构经1H NM R和M S确认。初步生物活性测定表明:在200 mg/L下,所有目标化合物均表现出一定的除草活性,其中化合物1f((R)-2-(4-((9-(4-氯苯)-8-(三氟甲基-9H-嘌呤-6-基)氧)苯氧)丙酸丁酯)和1h((R)-2-(4-((9-(4-氯苯)-8-(三氟甲基-9H-嘌呤-6-基)氧)苯氧)丙酸乙酯)对靶标的抑制率几乎都达到100%。