The metabolism of [14C] cymoxanil in the rat

A rat, given a single oral dose of [¹⁴C] cymoxanil, 1-(2-cyano-2-methoxyimino-[2-¹⁴C]-acetyl)-3-ethylurea, eliminated 91% of the radioactivity within 72 h. The urine contained 71%, the faeces 11%, and the expired air about 7% of the radiolabel; no ¹⁴C residue was found in the internal organs. Greater than 70% of the radioactivity in the urine was identified. The major metabolite was characterised as glycine, both free and conjugated, as hippuric acid and phenylaceturic acid [N-(phenylacetyl)-glycine], and probably in the form of polypeptides of low molecular weight. The other metabolites identified included 2-cyano-2-methoxyiminoacetic acid, 2-cyano-2-hydroxyiminoacetic acid and 1-ethylimidazolidine-2, 4, 5-trione. The minor metabolites included succinic acid and 2-oxoglutaric acid which indicated reincorporation of metabolic ¹⁴C. Cymoxanil, as such, was not detected in the urine.     

Mercapturic acid formation in the metabolism of propachlor,CDAA, and fluorodifen in the rat

When [¹⁴C]F₃-fluorodifen (2,4′-dinitro-4-trifluoromethyl diphenylether), carbonyl-[¹⁴C]CDAA (N,N-diallyl-2-chloroacetamide), and carbonyl-¹⁴C-propachlor (2-chloro-N-isopropylacetanilide) were fed to rats, 57 to 86% of the ¹⁴C was excreted via the urine within 48 hr. Although very little radioactivity was excreted in the feces of CDAA-treated rats, 15–22% of the ¹⁴C was excreted in the feces of propachlor- of fluorodifentreated rats and an average of 8% of the ¹⁴C remained in these rats 48 hr after treatment. Oxidation of the ¹⁴C label to [¹⁴C]O₂ was not a major process in the metabolism of these herbicides. The only major radioactive metabolite present in the 24-h urine of fluorodifen-treated rats, 2-nitro-4-trifluoromethylphenyl mercapturic acid, accounted for 41% of the administered dose of ¹⁴C. In the metabolism of CDAA, the corresponding mercapturic acid accounted for 76% of the dose; it was the only major metabolite present in the 24-h urine. In contrast, three major metabolites were detected in the 24-h urine of propachlortreated rats, and the mercapturic acid accounted for only 20% of the dose. The mercapturic acid of each herbicide was identified by mass spectrometry.     

The metabolism of benodanil in the rat

The metabolism of benodanil (2-iodobenzanilide) was studied in rats following an oral dose of 150 mg benodanil kg^?1 body weight. The major 24-h urinary metabolite was found to be the 4′-hydroxy derivative, both free (≈ 5%) and as the glucuronide (≈ 4%) and sulphate (≈ 4%) conjugates. Over a 6-day period, about 16% of the administered dose was excreted in the urine and about 80% in the faeces. After dosing with [¹⁴C]- benodanil, blood radioactivity levels were highest 30 min after dosing, with small broader peaks at 4 and 7 h, while biliary activity levels rose slowly to a maximum about 10–12 h after the dose, some 16% being excreted in 24 h as the glucuronide conjugate of the 4′-hydroxy derivative.     

超高效液相色谱-串联质谱法测定浙贝母中6种农药残留

建立了QuEChERS-超高效液相色谱-串联质谱 (UPLC-MS/MS) 同时测定浙贝母鲜样和干样中吡虫啉、啶菌齅唑、氟唑菌酰胺、嘧菌环胺、吡唑醚菌酯和阿维菌素共6种农药残留量的方法。样品用V(乙腈) : V(水) = 4 : 1混合溶液提取,经C₁₈ 50 mg + PSA 50 mg + MgSO₄ 150 mg净化,采用UPLC-MS/MS电喷雾离子化正离子扫描和多反应监测模式 (MRM) 测定,基质匹配标准溶液外标法定量。结果表明:在0.001~0.2 mg/L 范围内,6种农药的质量浓度与相应的峰面积间呈良好的线性关系,相关系数均大于0.994。6种农药在浙贝母鲜样中的定量限 (LOQ) 为0.01 mg/kg,检出限 (LOD) 为2×10–5~3×10–4 mg/kg,在干样中的LOQ 为0.05 mg/kg,LOD 为1×10–4~1×10–3 mg/kg。在0.01、0.5 和 2 mg/kg 添加水平下,6种农药在浙贝母鲜样中的平均回收率均在80%~109%之间,相对标准偏差 (RSD) 在0.95%~13%之间 (n = 5);在0.05、0.5 和 2 mg/kg 添加水平下,6种农药在浙贝母干样中的平均回收率均在77%~101%之间,RSD在0.89%~7.5%之间 (n = 5)。经实际样品检测验证,该方法快速、简便、可靠、高效,适用于同时检测浙贝母中吡虫啉、啶菌齅唑、氟唑菌酰胺、嘧菌环胺、吡唑醚菌酯和阿维菌素等农药的残留。     

The metabolism of cis-2,5-dimethylpyrrolidine-1-carboxanilide in rodents

The metabolism of cis-2,5-dimethylpyrrolidine-1-carboxanilide was studied in rats, rabbits, guinea-pigs and mice. The major metabolite in all species was cis-4′-hydroxy-2,5-dimethylpyrrolidine-1-carboxanilide, both free and as glucuronide and sulphate conjugates. About 95% of the compound was absorbed from the gut; over a 3-day period, about 50% of the administered dose was excreted in urine and about 27% in faeces.     

Resistance Risk Assessment of Cereal Eyespot, Tapesia Yallundae and Tapesia Acuformis, to the Anilinopyrimidine Fungicide, Cyprodinil

Eyespot pathogens, Tapesia yallundae and Tapesia acuformis, were isolated from two trial sites in the UK over several years. Both sites were treated with 2 applications per year of cyprodinil (a new anilinopyrimidine fungicide), prochloraz and a mixture of cyprodinil with prochloraz. One trial site was exposed to cyprodinil for 3 years, and the second for a total of 11 years, including 5 years before the trial was initiated. Control of eyespot and sensitivity to cyprodinil were monitored. During the first 3 years of the trial, disease control with all fungicide treatments ranged from 43% to 82%. At the site, where the trial was extended for a further 3 years, control then began to decline but no practical resistance was detected. The decline in control by both fungicides suggests that factors other than reduced sensitivity might be involved. Field isolates of both T. yallundae and T. acuformis with reduced sensitivity to cyprodinil were found predominantly in plots treated with cyprodinil. A reduction in sensitivity to cyprodinil was identified in the population from cyprodinil-treated plots in two years out of six, and in the population from mixture plots in the final year. No obvious trends could be identified and in-vivo studies showed control of most isolates with reduced sensitivity could be regained by increasing the dose to one tenth of the recommended field rate. Analysis of progeny from sexual crosses involving a sensitive isolate and a field isolate with an ED₅₀ value higher than the baseline sensitivity range indicated that a single gene controlled the reduction in sensitivity to cyprodinil in one T. yallundae isolate. There is clearly a resistance risk in eyespot to cyprodinil. The reduction in sensitivity is monogenic in inheritance and at a significant level in some isolates, but any shift in sensitivity in field populations has so far been gradual.     

The metabolism of the herbicide flamprop-methyl in rats and some comparative data for dogs,mice and rabbits

[¹⁴C]Flamprop-methyl administered orally to rats (3-4 mg kg^?1 body weight) was excreted mostly via the faeces (78.7 and 61.6% in males and females, respectively). Elimination was rapid and 90% of the dose of ¹⁴C was excreted in faeces and urine 0-48 h after dosing. The distribution of ¹⁴C between faeces and urine was different in males and females. No expired [¹⁴C]carbon dioxide was detected and less than 2% of the dose remained in the animals 4 days after dosing. The predominant metabolic pathway was hydrolysis of the ester bond to afford the carboxylic acid which was excreted unchanged and as its glucuronide conjugate. Aromatic hydroxylation occurred at the para- and meta-positions of the N-benzoyl ring. N-(3)-Chloro- 4-fluorophenyl-N-(3,4-dihydroxybenzoyl)-DL -alaninate was also formed. This hydroxylated form of flamprop-methyl was partially O-methylated at the 3-hydroxy group. Flamprop-methyl was also metabolised and eliminated rapidly by dogs, mice and rabbits. The last of these three species afforded very little aromatic hydroxylation and also differed from the others in that the metabolites were eliminated mostly in the urine. Aromatic hydroxylation lay in the order: male rat = female rat > dog= mouse>rabbit (female).     

A Reliable Method for Testing the Sensitivity of Botryotinia fuckeliana to Anilinopyrimidines In Vitro

Cyprodinil is a representative of the new class of broad-spectrum anilinopyrimidine fungicides. The effect of cyprodinil on mycelial growth of Botryotinia fuckeliana on solid agar medium depends on the composition of the medium and on the age of the mycelium to be used for the bioassay. An in-vitro method was developed to study the sensitivity distribution to cyprodinil in two wild-type populations of B. fuckeliana from fruits of strawberry with grey mould. To validate the applicability of the method, sensitivities to cyprodinil, mepanipyrim and pyrimethanil were monitored in populations of B. fuckeliana from grapes with grey mould from different vineyards, including one trial vineyard where reduced performance of cyprodinil had been encountered. The monitoring procedure was based on the inhibition of the mycelial growth on a synthetic medium containing L -asparagine (asp-agar) amended with the active ingredients. The mycelium was grown on asp-agar discs, starting from a spore suspension, for 17 h prior to the beginning of the test. This procedure proved to be efficient. The two wild-type populations from different sampling sites showed similar distributions of the sensitivity to cyprodinil. Some isolates from the trial site with reduced performance of anilinopyrimidines showed reduced sensitivities to cyprodinil, mepanipyrim and pyrimethanil, demonstrating cross-resistance between these anilinopyrimidines.     

The metabolism of the carbamate insecticide bendiocarb in the rat and in man

The metabolism of the carbamate insecticide bendiocarb (2,2-dimethylbenzo-1, 3-dioxol-4-yl methylcarbamate) has been investigated in male and female rats and in a male human volunteer using radiolabelled material. The compound was rapidly and extensively absorbed and completely metabolised following oral administration. In man, absorption was complete, >99% of the dose being excreted in the urine within 22 h. In the rat, > 86% of the radiolabel was excreted in the urine within the first 24 h. Faecal excretion from the rat was minor (3–8% of dose) and a small amount of the compound (1–3%) was metabolised and excreted as [¹⁴C]carbon dioxide. The major metabolic pathway in both species involved cleavage of the carbamate ester group to yield the phenol,2,2-dimethylbenzo-1, 3-dioxol-4-ol (I). This metabolite, occurring as sulphate and glucuronide conjugates, accounted for more than 95% of the dose excreted by the human volunteer. In man, small amounts of conjugates of 2, 2-dimethylbenzo-1, 3-dioxol-4-yl N-(hydroxymethyl)carbamate (II) were also found in early samples. In the rat, the metabolism was more complex with the formation of small amounts of conjugates of II and several minor metabolites, thought to be ring-hydroxylated derivatives of bendiocarb and I.     

Comparative effects of three isoxazole-urea herbicidal derivatives on the metabolism of enzymatically isolated soybean leaf cells*

The effects of the herbicide isouron and of its plant degradation products designated as metabolite l {N-[5-(1,1-dimethylethyl)-3-isoxazolyl]-N-methylurea} and metabolite 2 {N-[5-(1,1-dimethylethyl)-3-isoxazolyl]-urea} on the metabolism of enzymatically isolated leaf cells of soybean [Glycine max (L.) Merr., cv. Essex] were compared under laboratory conditions. Photosynthesis, protein synthesis, ribonucleic acid synthesis, and lipid synthesis were assayed by the incorporation of NaH¹⁴CO₃, [¹⁴C]-leucine, [¹⁴C]-uracil, and [¹⁴C]-acetate, respectively, into the isolated cells. 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 the three herbicides. The urea derivative of isouron (metabolite 2) was the least active of the three compounds. The activity of the mono-methylated derivative of isouron (metabolite 1) was comparable to that of isouron and the sensitivity of the four processes to both chemicals decreased in the order: photosynthesis > ribonucleic acid synthesis > lipid synthesis > protein synthesis. The concentration of isouron that caused a 50% inhibition of photosynthesis of the isolated soybean leaf cells was calculated at 0.51 μM. The effects of isouron and metabolite 1 on photosynthesis, lipid and RNA synthesis appeared to be independent of incubation lime as maximal inhibition occurred within 30 min. Inhibition of protein synthesis by both chemicals was time-dependent, increasing in magnitude with concomitant increases in incubation time.     

Metabolism and fate of triazophos in rats

The excretion patterns and tissue residues were determined after single and repeated oral dosing of rats with triazophos-¹⁴C Within 4 days after a single oral dose 76.3 % of the ¹⁴C was excreted in the urine and 21.0% in the faeces. After daily application for 12 days 69.5–83.4% of the label was eliminated in urine and 30.9–18.1 % in the faeces. Following prolonged application, however, elimination is distinctly slower. Distribution of radioactive residues in organs and tissue in both test series showed no appreciable or critical concentrations of radioactivity, with the exception of the gastrointestinal tract (contents and walls). Unchanged triazophos and l-phenyl-1,2,4-triazol-3-ol-3-¹⁴C were excreted in the faeces. Renewed release of other metabolites into the gastrointestinal tract apparently does not take place. The following metabolites are detected in the urine: urea-¹⁴C (approx. 85% of the radioactivity excreted with the urine); and three compounds as conjugates with glucuronic acid, i.e. 1-phenyl-l,2,4-triazol-3-ol-3-¹⁴C (approx. 3%), l-phenylsemicarbazide-3-¹⁴C (approx. 5%), and semicarbazide-¹⁴C (approx. 5%). Two further metabolites, so far unidentified, occurred in small quantities.     

Metabolism in rats of 3-phenoxybenzyl alcohol and 3-phenoxybenzoic acid glucoside conjugates formed in plants

Upon single oral administration to rats, the mono-, di- and tri-glucose conjugates of [¹⁴C]-3-phenoxybenzyl alcohol ( I ) or the mono-glucose conjugate of [¹⁴C]-3-phenoxybenzoic acid ( II ) were rapidly hydrolysed and extensively eliminated in the urine mostly as the sulphate conjugate of 3-(4-hydroxyphenoxy)benzoic acid ( X ). The faecal elimination was a minor route, whereas the biliary excretion was about 42% of the dose and the glucuronide conjugates of I , II and X were common major metabolites. The biliary glucuronides were cleaved in the small intestine to the respective aglycones, which were reabsorbed, metabolised further, and excreted in the urine as the sulphate conjugate of X . Although small amounts of the mono-, di-and tri-glucosides were found in the 0.5-h blood and liver samples following oral administration of the tri-glucoside of I , they were not detected in the urine, bile or faeces. Similarly the sulphate conjugate was one of the major urinary metabolites of germ-free rats, dosed with the ¹⁴C-glucosides via the oral or the intraperitoneal route, although they were excreted unchanged in certain amounts in the urine and faeces. The glucose conjugates were cleaved in vitro by gut microflora and in various rat tissues, including blood, liver, small intestine and small intestinal mucosa. The tissue enzymes showed a different substrate specificity in hydrolysis of the glucosides. However, they were not cleaved in gastric juice, bile, pancreatic juice or urine.     

The metabolic fate in rats of the pyrethroid insecticide WL85871, a mixture of two isomers of cypermethrin

The metabolism of the pyrethroid insecticide WL85871, labelled in the alcohol moiety, has been studied in male and female Wistar rats at a dose of ca 2 mg kg^?1. The compound was rapidly broken down and the radioactivity was mainly eliminated in the urine as the sulphate conjugate of 3-(4-hydroxyphenoxy)benzoic acid (40% of the dose). Some hydroxylation occurred before ester cleavage. Approximately 20% of the ingested compound was not absorbed and was eliminated unchanged in the faeces. There was no evidence for any racemisation of the chiral centres of WL85871 either in the intestine, the faeces or in fat. The small proportion of the dose stored in adipose tissue was eliminated with biphasic kinetics (t½ values, 2–3 days and 17–26 days). The t½ values for skin were, respectively, 2 days and 40 days. As the residue in fat depleted between 3 and 40 days, an increasing proportion (from 28% to 48%) was present as a lipophilic metabolite of WL85871, or of 3-phenoxybenzoic acid, probably a mixture of 3-phenoxybenzoyl diacyl glycerols.     

Animal metabolism of propham (isopropyl carbanilate): The fate of residues in alfalfa when consumed by the rat and sheep

Alfalfa was root-treated with [¹⁴C]propham (isopropyl carbanilate[¹⁴C-phenyl(U)]) for 7 days and then harvested and freeze-dried. Rats and sheep were orally given either ¹⁴C-labeled alfalfa roots ([¹⁴C]root) or ¹⁴C-labeled alfalfa shoots ([¹⁴C]shoot). When the [¹⁴C]root was given, 6.5–11.0% of the ¹⁴C was excreted in the urine and 84.6–89.4% was excreted in the feces within 96 h after treatment. Less than 3% of the ¹⁴C remained in the carcass (total body—gastrointestinal tract and contents) 96 h after treatment. When [¹⁴C]shoot was given, 53.2–55.2% of the ¹⁴C was excreted in the urine, 32.1–43.4% was excreted in the feces, and the carcass contained 0.2–1.1% of the ¹⁴C 96 h after treatment. When the insoluble fraction (not extracted by a mixture of CHCl₃, CH₃OH, and H₂O) of both alfalfa roots and shoots was fed to rats, more than 86% of the ¹⁴C was excreted in the feces and less than 3% remained in the carcass 96 h after treatment. The major radiolabeled metabolites in the urine of the sheep fed ¹⁴C shoot were purified by chromatography and identified as the sulfate ester and the glucuronic acid conjugates of isopropyl 4-hydroxycarbanilate. Metabolites in the urine of the sheep treated with [¹⁴C]root were tentatively identified as conjugated forms of isopropyl 4-hydroxycarbanilate, isopropyl 2-hydroxycarbanilate, and 4-hydroxyaniline. The combined urine of rats dosed with [¹⁴C]shoot and [¹⁴C]root contained metabolites tentatively identified as conjugated forms of isopropyl 4-hydroxycarbanilate, isopropyl 2-hydroxycarbanilate, and 4-hydroxyaniline.     

Acifluorfen metabolism in soybean: Diphenylether bond cleavage and the formation of homoglutathione, cysteine, and glucose conjugates

Metabolism of the substituted diphenylether herbicide, acifluorfen [sodium 5-(2-chloro-4-trifluoromethylphenoxy)-2-nitrobenzoate], was studied in excised leaf tissues of soybean [Glycine max (L.) Merr. ‘Evans’]. Studies with [chlorophenyl-¹⁴C]- and [nitrophenyl-¹⁴C]acifluorfen showed that the diphenylether bond was rapidly cleaved. From 85 to 95% of the absorbed [¹⁴C]acifluorfen was metabolized in less than 24 hr. Major polar metabolites were isolated and purified by solvent partitioning, adsorption, thin layer, and high-performance liquid chromatography. The major [chlorophenyl-¹⁴C]-labeled metabolite was identified as a malonyl-β- -glucoside (I) of 2-chloro-4-trifluoromethylphenol. Major [nitrophenyl-¹⁴C]-labeled metabolites were identified as a homoglutathione conjugate [S-(3-carboxy-4-nitrophenyl) γ-glutamyl-cysteinyl-β-alanine] (II), and a cysteine conjugate [S-(3-carboxy-4-nitrophenyl)cysteine] (III).     

Residues and fate of endosulfan on field-grown pepper and tomato

Endosulfan (Thiodan 3 EC), a mixture of α- and β-isomers, was sprayed on 92-day-old field-grown pepper and tomato at the recommended rate of 0·61 kg AI ha^-1. Plant tissue samples were collected at 1 h to 14 days after application and analysed to determine the content and dissipation rate of endosulfan isomers (α- and β-endosulfan) and the major metabolite, endosulfan sulfate. Analysis of samples was accomplished using gas chromatography-mass selective detection (GC-MSD). The results indicated the formation of endosulfan sulfate as a residue component on the plant tissues and also the relatively higher persistence of the β-isomer as compared to the α-isomer on pepper fruits. The initial total residues (α- and β-endosulfan isomers plus endosulfan sulfate) were higher on leaves than on fruits. On pepper fruits, the α-isomer, which is the more toxic to mammals, dissipated faster than the less toxic β-isomer. Total residues (α- and β-endosulfan isomers plus the sulfate metabolite) on tomato leaves revealed longer persistence (t_1/2 4·6 days) compared to the total residues detected on pepper leaves (t_1/2 2·0 days) 3–14 days following spraying. Persistence of the β-isomer on pepper fruits was high 3–14 days following spraying compared to on tomato fruits. This long persistence increases risk of exposure of the consumer. In addition, the longer persistence of the total residues on tomato foliage should be considered of importance for timing the safe entry of tomato harvesters due to the high mammalian toxicity of endosulfan. © 1998 Society of Chemical Industry     

The metabolism of chlorotoluron in the rat

The metabolic fate of ¹⁴C-labeled chlorotoluron, i.e., 1-(3-chloro-4-methyl[⁴C]-phenyl)-3,3-dimethyl urea, was followed in rats. After a single oral dose the radioactivity was preferably excreted with the urine. Nine of the eleven urinary metabolites isolated, were identified by spectroscopic and derivatization techniques, whereas the structure of the remaining two metabolites was only partially elucidated. N-Demethylation and stepwise oxidation of the ring methyl group to hydroxymethyl and carboxyl derivatives were found as the major metabolic mechanisms. Both mechanisms proceeded simultaneously so that the isolated metabolites showed all combinations of N-demethylation and ring methyl group oxidation in their structures. One of these metabolites was an N-formyl derivative, being probably an intermediate product of demethylation. In the urine of rats fed doses of [¹⁴C]chlorotoluron higher than 50 mg/kg three additional metabolites with different degrees of N-dealkylation were found, the ring methyl group of which was transformed to a methylthio methyl group. The metabolites identified in the faeces were of the same type as those found in the urine. Based on the structures of the metabolites elucidated, a metabolic pathway of chlorotoluron in the rat is presented.     

The metabolism in the rat of the herbicidally active isomer (R)- flamprop-methyl in comparison with the racemic form

A single dose (4 mg kg^?1) of ¹⁴ C-labelled (R)-flamprop-methyl to rat was rapidly metabolised and 90% of the dose was eliminated in urine and faeces within 48 h. Four days after dosing, tissue residues were 0–1 μg equivalents g^?1 tissue or much less, with the exception of kidney (0–22 μg g^?1). There was a statistically significant sex difference in the routes of elimination; this may be attributed to differences in the biliary elimination of the major metabolite, flamprop acid, or its glucuronide conjugate. The fate of racemic flamprop-methyl was very similar to that of the (R)-isomer. The major metabolic routes were hydrolysis of the esters to the corresponding acids, hydroxylation of the benzoyl aromatic rings and conjugation. The flamprop acid derived from the (R)-flamprop-methyl was found to be partially converted to the (S)-form (R:S ratio, 87:13). This reaction is discussed in the context of other such biological racemisations recently reported.     

Metabolism of amitrole in apple: III. Model systems

Excised shoots from apple trees and cell suspension cultures were used as model systems to study the metabolism of [3,5-¹⁴C]amitrole in Malus domestica Borkh. Significant differences in the metabolism of the compound applied were observed with excised shoots, cultured cells and whole apple trees. The major metabolite in excised shoots was aminotriazolylalanine which occurred both in the free form and as conjugates. The major metabolite from whole plants. triazolylalanine, was detected in shoots in minor amounts only. In cell suspension cultures, the type of metabolism strongly depended on the concentration of amitrole when initially applied. At 10 ^?3 m or lower, mainly aminotriazolylalanine was formed. Depending on the concentration of the active ingredient, this metabolite predominantly occurred in free form or as glycosides. At concentrations above 5 × 10^?4 M a new metabolite, 3,5-dihydroxytriazole, was detected which was the only metabolite found at 5 × 10^?3M. Significant amounts of nonmetabolized amitrole remained in the medium.     

The metabolism of the pyrethroid insecticide cypermethrin in rats; excreted metabolites

The metabolism of the pyrethroid insecticide cypermethrin has been studied in rats using three forms of ¹⁴C-labelling (benzyl-, cyclopropyl- and cyano-) and separate cis- and trans- isomers. The proportion of the dose absorbed from the intestines (50–70% at 2–3 mg kg^?1) is rapidly metabolised and eliminated. The major reaction is cleavage of the ester bond to afford the constituent cis- and trans- acids which are conjugated with glucuronic acid and eliminated in the urine. The 3-phenoxybenzyl portion of the molecule is probably released as the α-hydroxynitrile, which is converted via the aldehyde into 3-phenoxybenzoic acid. This compound is then largely hydroxylated and eliminated as a sulphate conjugate. The cyanide ion is metabolised via predictable routes, for instance, as thiocyanate. Cypermethrin is hydroxylated to some extent before hydrolysis. Most of this hydroxylation occurs at the methyl group trans to the cyclopropane carboxyl group, and at the 4-position of the phenoxy group. cis- Cypermethrin is slightly more stable than the trans-isomer.