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At least 19 recordsLinked to original sources

PubMed1991

A simple and quick gas chromatographic method for the determination of propham and chlorpropham in potatoes.

This study describes a gas chromatographic method for the quantitative determination of residual propham and chlorpropham in potatoes. Both herbicides are extracted from the foodstuff with methylene chloride. After centrifugation and concentration, propham and chlorpropham are quantitatively determined by gas chromatography thermionic detection using a fused silica capillary column CP Sil 5CB. 2-Chloraniline is used as internal standard. Recoveries of 100 +/- 15% and 99 +/- 10% have been obtained for propham and chlorpropham in blank samples spiked at the level of 0.5, 1.0 and 5.0 mg/kg. The absolute detection limit for both compounds is 1 ng corresponding to 0.1 mg/kg. Of the 161 samples of fresh potatoes analysed using this method, 136 contained residues of these herbicides and 18 of them (11%) exceeded the maximum tolerated value of 5 mg/kg.

Carbamates↗

PubMed2001

Effects of vapours of chlorpropham and ethofumesate on wild plant species.

Effects of vapours of two herbicides on plantlets of fourteen wild higher plant species and two bryophytes were screened in fumigation experiments using foliar injury, chlorophyll fluorescence and growth as response parameters. After vaporisation of the herbicides for 48 h, concentrations in the chambers reached 77 micrograms m-3 in the chlorpropham treatments and 184 ng m-3 in the ethofumesate treatments. Despite the higher concentrations of the volatile chlorpropham (vapour pressure, VP: 1.3 mP), plants showed no foliar injury, but vapours of this herbicide caused leaf crinkling in the agriophyte Agrostemma githago. The less volatile ethofumesate (VP: 0.56 mP) caused foliar injury in all higher species, with lowest no observed effect concentrations (NOECs) of 75 ng m-3. Chlorpropham affected growth only in Agrostemma, while ethofumesate reduced growth in one third of the higher plant species. Chlorophyll fluorescence proved to be a less suitable response parameter compared to foliar injury and growth. No adverse effects were observed in mosses, probably due to the slow growth and hence small doses of herbicides taken up. The extent of foliar injury due to ethofumesate showed a weak positive relationship to relative growth rates and specific leaf area in the tested higher plant species.

Benzofurans↗

PubMedDate not supplied

Developmental toxicity of chlorpropham in mice.

The present studies were designed to evaluate the developmental toxicity of chlorpropham in mice. The first study was conducted to determine administration time, and the second study was designed to evaluate dose-response effects. Chlorpropham was administered to pregnant mice by gavage on Days 8, 8.3, 9, 9.3, 10, and 11 of gestation at a level of 3000 mg/kg bw, and the females were killed on Day 18 of gestation. The administration on Day 8.3 of gestation induced the highest percentage of external malformations with brachyury occurring among more litters than in other groups. Chlorpropham was administered to pregnant mice by gavage at a level of 0 (control), 750, 1500, and 3000 mg/kg bw on Day 8.3 of gestation, and the females were killed on Day 18 of gestation. The total resorption rate was significantly increased in the 3000 mg/kg bw group. The average fetal body weight of each sex was significantly reduced in the 3000 mg/kg treatment group. The total incidence of external malformations was significantly increased in the two highest dose groups in a dose-related manner. Again brachyury was significantly increased in the 3000 mg/kg bw group.

Abnormalities, Drug-Induced↗

PubMed2001

Residue levels of chlorpropham in individual tubers and composite samples of postharvest-treated potatoes.

Chlorpropham, a herbicide and sprout suppressant, is used on stored potatoes to prolong the storage period without deterioration of produce quality. Data for residue concentrations on an individual tuber basis are required by WHO for the estimation of the variability factor. In this study, the levels of chlorpropham in individual tubers and in composite samples were determined. The distribution of chlorpropham between the peel and the tuber flesh was examined, and the fate during the cooking process (washing, boiling, frying) was studied. The concentrations in individual tubers ranged from 1.8 to 7.6 mg/kg 10 days postapplication (mean 3.8 mg/kg, RSD 39%), from 0.7 to 4.0 mg/kg 28 days postapplication (mean 2.9 mg/kg, RSD 28%), and from 0.8 to 3.8 mg/kg 65 days postapplication (mean 2.2 mg/kg, RSD 48%). The calculated residues in composite samples 10 days postapplication ranged from 4.3 to 6.1 mg/kg (mean 4.9 mg/kg, RSD 20%). Those in samples taken 28 days postapplication ranged from 3.1 to 4.2 mg/kg (mean 3.8 mg/kg, RSD 15%). The concentrations determined in composite samples of whole tubers 65 days postapplication ranged between 2.6 and 3.2 (mean 2.9 mg/kg, RSD 11%). Peeling removed 91-98% of the total residue; washing reduced residues by 33-47%. Detectable residues were found in boiled potatoes and the boiling water, and in french fries and the frying oil. Monitoring data on commercial prefried frozen french fries are reported.

Calibration↗

PubMed1999

Reproductive and neurobehavioural toxicity study of chlorpropham in mice.

Chlorpropham was given in the diet to provide levels of 0 (control), 500, 1,000, and 2,000 mg/kg from 5 weeks of age of the F0 generation to 9 weeks of age of the F1 generation in mice, and selected reproductive and neurobehavioural parameters were measured. There were no adverse effects of chlorpropham on either litter size or litter weight and sex ratio at birth. The average body weight of offspring was significantly reduced in the middle-dose group at postnatal days (PNDs) 0 and 4 in female offspring, and was significantly increased in the middle-dose group at PND 14 in male offspring. In neurobehavioural parameters, surface righting at PND 4 was significantly affected in a dose-related manner, and negative geotaxis at PND 4 was significantly accelerated in a dose-related manner in female offspring. In male offspring, surface righting at PND 7 was significantly depressed in the middle-dose group, and olfactory orientation at PND 14 was significantly affected in the low- and middle-dose groups. The dose levels of chlorpropham in the present study produced few adverse effects in reproductive and neurobehavioural parameters in mice.

Analysis of Variance↗

PubMedDate not supplied

Reproductive and neurobehavioral effects of chlorpropham administered to mice in the diet.

Chlorpropham was given in the diet to provide levels of 0(control), 0.15, 0.30, and 0.60%, from 5 weeks of age of the F0 generation to 9 weeks of age of the F1 generation in mice, and selected reproductive and neurobehavioral parameters were measured. There were no adverse effects of chlorpropham on either litter size or litter weight and sex ratio at birth. The average body weight of offspring was significantly affected in the low-dose group of each sex and in the high-dose group of females, and was increased in the middle-dose group of males during the lactation period. In neurobehavioral parameters, surface righting at postnatal day (PND) 7 was significantly affected in male offspring in a dose-related manner. Swimming head angle at PND 4 was significantly restrained in male offspring in a dose-related manner, and olfactory orientation at PND 14 was significantly depressed in female offspring in a dose-related manner. The dose levels of chlorpropham in the present study produced some adverse effects in reproductive and neurobehavioral parameters in mice.

Animals↗

PubMed2001

Effects of chlorpropham (CIPC) on the hemopoietic system of rats.

Male F344 rats were given 0 or 3% chlorpropham in the diet and at 2, 4, 6, 8 or 13 weeks of administration, five rats in each group were examined for hematology, plasma clinical chemistry and pathology. Marked splenomegaly and hepatomegaly were observed in treated rats at 2-13 weeks of administration. Red blood cell counts, hemoglobin concentration, packed cell volume and platelet counts were significantly decreased and methemoglobin level, mean corpuscular volume and white blood cell counts were significantly increased in treated rats at 2-13 weeks of administration. The covalent binding of m-chloraniline m-CA, (the hydrolytic metabolite of chlorpropham) was observed in hemoglobin or splenic protein of treated rats, but only small amounts of free m-CA were present in blood or spleen. Congestion, hemosiderin deposits, extramedullary hemopoiesis and lymphoid atrophy in spleen and hyperplasia of hemopoietic cells in bone marrow were observed in treated rats at 2-13 weeks and fibrosis in splenic capsule were observed in treated rats at 4-13 weeks. The pathological changes in spleen rather than hematological changes progressed during administration, suggesting splenotoxicity of CIPC in rats.

Animals↗

PubMed1982

[On the determination of chlorpropham, metobromuron and chlorbromuron residues in drugs of the 2. AB-DDR (author's transl)].

A method for analyzing drugs of the 2. AB-DDR for residues of chlorpropham, metobromuron and chlorbromuron is proposed. It is based on the detection of aniline derivatives resulting from alkaline hydrolysis. Herbicide concentrations greater than 0.25 mg/kg drug may be detected and semiquantitatively estimated by thin-layer chromatography. Smaller amounts of herbicide residues are detected gas chromatographically (using an electron attachment detector) after bromination of the hydrolysis products. The limits of detection are: chlorpropham, 0.006 mg/kg drug; chlorbromuron, 0.008 mg/kg drug; and metobromuron, 0.04 mg/kg drug. For impregnated drugs, the recovery rates lie between 82 and 102%. The herbicide residues are released to infusions at a varying extent, depending on the kinds of drugs used.

Chlorpropham↗

PubMed2005

Rapid determination of aniline metabolites of chlorpropham in potatoes by micellar electrokinetic chromatography using negative-charged mixed micelles and laser-induced fluorescence detection.

A rapid, reliable method has been developed for the multi-residue analysis of aniline metabolites of chlorpropham in potato samples. The method involves the precolumn derivatization of aniline metabolites with 5-(4,6-dichloro-s-triazin-2-ylamino) fluorescein (DTAF) and their subsequent separation and determination by micellar electrokinetic capillary chromatography with laser-induced fluorescence detection (MEKC-LIF). The optimum procedure includes a derivatization step of the aniline metabolites (3-chloroaniline, 3-chloro-4-hydroxyaniline and 3-chloro-4-methoxyaniline) at 40 degrees C for 40 min and a 5-fold dilution prior to MEKC analysis, which is conducted within about 7 min using negative-charged mixed micelles (SDS/Triton X-100) in the running buffer. Under these conditions, the DTAF-anilines were readily detected at 0.3-3.1 microg/L level with a precision of 4.8-6.4%. These results indicate that negative-charged mixed surfactant MEKC-LIF is useful as a selective, rapid, and sensitive tool for the determination of these anilines and surpasses other electrophoretic alternatives based on the use of fluorescein-isothiocyanate (FITC) as label reagent. Finally, the potato matrix showed no significant effects on the derivatization and determination of these analytes, since the analytical figures of merit for the real samples were similar to those obtained in aqueous solutions, and the average recovery at fortification levels of 10-250 microg/kg was over 97%.

Aminophenols↗

PubMed1998

Metabolism and cytotoxicity of chlorpropham (CIPC) and its essential metabolites in isolated rat hepatocytes during a partial inhibition of sulphation and glucuronidation reactions: a comparative study.

The changes in metabolism and cytotoxicity of chlorpropham (CIPC) and its major metabolites, 4-hydroxychlorpropham (4-OH CIPC), 3-chloroaniline, and 3-chloroacetanilide were investigated in isolated rat hepatocyte suspensions after a partial inhibition of sulphation and glucuronidation and the two reactions combined in an attempt to assess the part of each of them in the enhanced CIPC toxicity observed in vivo after D-galactosamine treatment. With sulphation and glucuronidation effective, CIPC has a cytolytic effect and reduces intracellular ATP and K+ level while 4-OH CIPC has a weak cytolytic effect but modifies ATP and K+ level in a greater extent than CIPC. Inhibition of sulphation does not affect the cytotoxicity of CIPC or 4-OH CIPC because there is a compensatory increase in the amount of 4-OH CIPC glucuronide formed and the level of free 4-OH CIPC always remain low. In contrast, when incubations are carried out with either CIPC or 4-OH CIPC, the presence of D-galactosamine leads to a decrease of glucuronide and sulphate conjugates accompanied, respectively, by a 3.6-fold and 6. 9-fold increase of the free 4-OH CIPC level in the culture medium. This alteration of the metabolism is followed by a marked reduction of ATP synthesis with a concomitant modification of cell permeability. The cytolytic effect is due to CIPC itself, whereas the effect on energy supply was attributed to free 4-OH CIPC. The results demonstrate a combined effect of free 4-OH CIPC and D-galactosamine on intracellular ATP level that could account for the partial inhibition of sulphation. This change in the CIPC metabolism could explain the increased CIPC toxicity observed in vivo after D-galactosamine pretreatment.

Acetanilides↗

PubMed1989

Cadmium-induced alterations of chlorpropham metabolism in isolated rat hepatocytes.

In order to investigate the various steps of chlorpropham (CIPC) metabolism which could be influenced by cadmium, isolated rat hepatocytes were incubated in the presence of CIPC (0.1 mM) and of increasing Cd concentrations (0-180 microM). The results showed that Cd accumulation in hepatocytes was in good correlation to its concentration in the incubation medium. At 90 microM Cd, hydroxylation of CIPC was only slightly decreased by 30%, while CIPC hydrolysis into 3-chloraniline was unaffected by the presence of Cd. Accordingly, unchanged CIPC increased in hepatocytes. At 27 microM Cd, free 4-hydroxychlorpropham (4-OHCIPC) increased in the intracellular medium as a consequence of a strong suppression of both sulfation and glucuronidation which was related to the strong depletion of the intracellular ATP level under the combined influences of both cadmium and free 4-OHCIPC. Acetylation of 3-chloroaniline, which represents a minor pathway of CIPC metabolism, was already markedly suppressed (43%) with the lowest Cd concentration (27 microM). These in vitro results suggest that Phase II reactions are more sensitive to Cd than Phase I processes and that Cd enhanced the CIPC cytotoxicity as shown by alterations of the membrane integrity.

Acetylation↗

PubMed1989

Interaction of hexachlorocyclohexane (HCH) and chlorpropham (CIPC) in male rats.

Hexachlorocyclohexane (60.0 mg/kg/d) and chlorpropham (50.0 mg/kg/d) given to male rats daily orally for 30 d caused subtle biochemical lesions. The significant rise in the activity of alkaline phosphatase in liver and serum and of GOT and GPT in liver with substantial weight increase of liver has been suggestive of the initiation of biochemical lesions and adaptation of the organism. Very severe hepatocellular damage is forecasted if the pesticides are given for a prolonged period and in higher concentrations to animals.

Alkaline Phosphatase↗

PubMed2004

Chlorpropham-induced splenotoxicity and its recovery in rats.

To determine the reversibility of hematological and pathological changes in spleen induced by sub-chronic administration of chlorpropham (CIPC), male F344 rats were given CIPC in the diet at 0, 600, 3000 or 15,000 ppm for 13 weeks (administration period) and then were given standard (0 ppm) diet for 10 weeks (recovery period). At 0, 1, 2, 4 or 10 weeks in the recovery period, 5 rats in each groups were examined for hematology and pathology. At the end of CIPC administration, dose-dependent and significant methemoglobinemia, anemia, splenomegaly and pathological lesions indicating hemolytic anemia were observed in all the treated groups. The hematological changes, congestion of red pulp, lymphoid atrophy, increased extramedullary hematopoiesis in spleen and hematopoietic cell hyperplasia in bone marrow were diminished during the 10 weeks recovery period. However, increased hemosiderin deposition and capsular fibrosis in spleen of the treated groups remained at the end of recovery period. The results indicated that hematological changes induced by sub-chronic administration of CIPC were reversible but hemosiderin deposition and fibrosis in spleen were not reversible in the recovery period examined, suggesting the significance of splenic lesion in CIPC-toxicity.

Administration, Oral↗

PubMed2004

Chlorpropham induces mitochondrial dysfunction in rat hepatocytes.

The metabolism and action of chlorpropham (isopropyl N-(3-chlorophenyl)carbamate; CIPC, a post-harvest agent) and its metabolites were studied in freshly isolated rat hepatocytes and isolated rat hepatic mitochondria, respectively. The exposure of hepatocytes to CIPC caused a concentration (0.25-1.0 mM)- and time (0-3h)-dependent cell death accompanied by loss of cellular ATP and adenine nucleotides. CIPC at a weakly toxic level (0.5 mM) was metabolized to isopropyl N-(3-chloro-4-hydroxyphenyl)carbamate (4OH-CIPC) and subsequently to its glucuronide and sulfate conjugates (major metabolites) or alternatively to a minor metabolite 3-chloroaniline (3CA). The addition of SKF-525A (50 microM), an inhibitor of microsomal monooxygenase, enhanced the CIPC (0.5 mM)-induced cytotoxicity accompanied by loss of ATP and 4OH-CIPC and inhibited the decrease in the concentration of the parent compound. CIPC led to a strong decrease in cellular ATP content compared to its metabolites, 4OH-CIPC and 3CA. On the other hand, the exposure of isolated hepatic mitochondria to CIPC reduced State 3 respiration with a FAD-linked substrate (succinate plus rotenone) and/or with a NAD+ -linked substrate (pyruvate plus malate), whereas State 3 respiration with ascorbate plus tetramethyl-p-phenylendiamine (cytochrome oxidase-linked respiration) was not affected markedly by CIPC. Further, the addition of CIPC caused an increase in the rate of State 4 oxygen consumption, indicating an uncoupling effect, and a decrease in the rate of State 3 oxygen consumption in a concentration-dependent manner, respectively. In contrast, the addition of neither 4OH-CIPC nor 3CA markedly affected the rate of states 3 and/or 4 oxygen consumption. These results indicate that CIPC-induced cytotoxicity is mediated by the parent compound rather than by its metabolites such as 4OH-CIPC and 3CA, and that the toxicity is associated with a rapid depletion of ATP via impairment of mitochondrial function related to oxidative phosphorylation.

Adenine Nucleotides↗

PubMed2000

Subchronic toxicity of chlorpropham (CIPC) in ICR mice.

Male and female ICR mice were given 0, 1875, 7500 or 30,000 ppm of chlorpropham (CIPC) in the diet for 13 weeks. Methemoglobin levels of male and female mice in the 7500 and 30,000 ppm groups were significantly elevated. Hemoglobin concentration, packed cell volume, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration and white blood cell count of male and female mice in the 30,000 ppm group were significantly increased. Dose-dependent splenomegaly was observed in male and female mice in the 7500 and 30,000 ppm group. Congestion, increased hemosiderin deposition and increased extramedullary hematopoiesis in the spleen, hematopoietic cell hyperplasia and hemosiderin deposition in bone marrow was observed dose dependently in male and female mice in the 7500 or 30,000 ppm group. Eosinophilic granular cytoplasm of hepatocytes, sinusoidal dilatation, hemosiderin deposition, extramedullary hematopoiesis and necrosis of hepatocytes were observed in the liver of male and female mice in the 30,000 ppm group. Hemosiderin deposition was increased in the kidney of male and female mice in the 30,000 ppm group. Administration of CIPC in diet for 13 weeks caused methemoglobinemia and splenomegaly in ICR mice.

Animals↗

PubMed1997

Hemotoxicity of chlorpropham (CIPC) in F344 rats.

Chlorpropham[Isopropyl-N-(3-chlorophenyl)carbamate; CIPC] is a widely used sprout suppressant. Groups of ten male and ten female F344 rats were given 0, 7500, 15,000 or 30,000 ppm of CIPC in the diet for 13 weeks. Body weight gain of male and female rats in the 30,000 ppm-group was depressed. Spleen and liver weights of male and female rats in the treated groups were dose-dependently increased. Red blood cell count, hemoglobin concentration, hematocrit, mean corpuscular hemoglobin concentration and platelet count were decreased in male and female rats of the treated groups. Methemoglobin level, mean corpuscular volume and mean corpuscular hemoglobin were increased in male and female rats of the treated groups. Those hematological changes were dose-dependent and were marked in the 15,000 and 30,000 ppm-groups. White blood cell count of male and female rats in the 30,000 ppm-group were significantly higher than those of the control group. Congestion, increased hemosiderin deposition, increased extramedullary hemopoiesis, lymphoid atrophy and fibrosis were seen in spleen of male and female rats of all treated groups in a dose-dependent manner. Hemopoietic cell hyperplasia was marked in bone marrow of male and female rats in all treated groups. The results suggested that the erythrocyte is one of the primary targets of CIPC toxicity in rats.

Animals↗

PubMed2004

Biotransformation of chlorpropham (CIPC) in isolated rat hepatocytes and xenoestrogenic activity of CIPC and its metabolites by in vitro assays.

1: The metabolism and action of chlorpropham (isopropyl N-(3-chlorophenyl)carbamate; CIPC, a post-harvest agent) were studied in freshly isolated rat hepatocytes, and the oestrogen-like activity of CIPC and its metabolites was assessed by in vitro assays. The exposure of hepatocyte suspensions to CIPC caused concentration- (0.25-1.0 mM) and time- (0-3 h) dependent cell death, which was assessed by Trypan blue exclusion, accompanied by losses of cellular adenosine triphosphate and adenine nucleotide pools, and formation of cell bleb. 2: CIPC at a weakly toxic level (0.25 or 0.5 mM) was metabolized to isopropyl N-(3-chloro-4-hydroxyphenyl)carbamate (4OH-CIPC) and subsequently to its glucuronide and sulfate conjugates (major metabolites) or alternatively to the minor metabolites 3-chloroaniline (3CA) and 3-chloroacetanilide. CIPC (0.25 mM) added to hepatocyte suspensions was distributed equally between hepatocytes and the extracellular medium during the incubation. The glucuronide rather than the sulfate conjugate of 4OH-CIPC predominantly increased in the medium with time, while the amount of unconjugated free 4OH-CIPC in the extracellular medium increased by approximately threefold compared with the amount in the cell fraction after 0.5 h and then decreased rapidly accompanied by increases in the conjugates. This indicates that unconjugated free 4OH-CIPC produced in hepatocytes was temporarily excreted in the extracellular medium and subsequently converted to the conjugates via re-influx into hepatocytes. 3: Diethylstilbestrol (DES), bisphenol A (BPA) and 4-hydroxybenzoic acid butyl ester (butylparaben), which are known xenoestrogenic compounds, competitively displaced 17beta-oestradiol bound to the oestrogen receptor-alpha (ERalpha) in a concentration-dependent manner; IC50 values of DES, BPA, butylparaben and its derivative 3-chloro-4-hydroxybenzoic acid butyl ester (3-chloro-butylparaben) were approximately 10(-8), 10(-5), 5 x 10(-5) and 5 x 10(-4) M, respectively. In contrast, neither CIPC nor 4OH-CIPC impaired the binding of 17beta-oestradiol to ERalpha at concentrations ranging from 10(-9) to 10(-4) M, whereas at concentrations of >5 x 10(-4) M, the binding affinity of 4OH-CIPC was greater than that of CIPC. In a proliferation assay of MCF-7 cells, CIPC, 4OH-CIPC and 3CA did not increase cell numbers at concentrations ranging from 10(-9) to 10(-5) M, but these compounds at a concentration of 10(-4) M induced a considerable decrease in cell numbers relative to the control. The results suggest that even if CIPC is metabolized to 4OH-CIPC by hepatocytes, the chlorine adjacent to the 4-hydroxy group added to the intermediate as well as 3-chloro-butylparaben obstructs the appearance of oestrogen-like effects via an interaction between the intermediate and the ER.

Animals↗

PubMedDate not supplied

Comparison of an HPTLC and an HPLC procedure for the determination of chlorpropham, propham and thiabendazole residues in potatoes.

HPTLC was used to check for residues of chlorpropham, propham (sprout inhibitors) and thiabendazole (fungicide) applied to potatoes. The method used gave good precision and analytical sensitivity. The sample preparation method developed by the authors was simple and gave good recovery and selectivity as far as other components of the matrix were concerned. Comparison with liquid chromatography confirmed the validity of the results.

Carbamates↗