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PubMed1996

Effects of fertilizer on insecticides adsorption and biodegradation in crop soils.

Recent organic fertilizer treatments (cow manure, pig slurry, composts, or green manure) simultaneously increase insecticide adsorption onto soil and the insecticide soil persistence, indicating a mechanism of slow release of insecticide into soil by the organic matter. This occurred in sugar beet crops with aldicarb, thiofanox and imidacloprid; also, in leek, cauliflower and brussels sprouts crops with chlorpyrifos and chlorfenvinphos. In contrast, organic fertilizer treatments applied once or repeatedly in the past, have no significant influence on adsorption or persistence of insecticides; the same is observed for the old soil organic matter, when its soil concentrations change in limited ranges

Adsorption↗
PubMed1995

A comparison of trimedoxime, obidoxime, pralidoxime and HI-6 in the treatment of oral organophosphorus insecticide poisoning in the rat.

This study summarizes the results of examination of acute oral toxicity of 26 organophosphorus insecticides in rats. The effectiveness of trimedoxime, obidoxime, pralidoxime and HI-6, given with atropine and diazepam, was tested in the treatment of poisoning with 2 LD50 of the insecticides. It was shown that the oximes were potent antidotes in poisoning with phosphate insecticides. Obidoxime, pralidoxime and HI-6 had low effectiveness in the treatment of poisoning with phosphonates and phosphorothiolates. However, none of the oximes was an effective antidote in poisoning with dimethoate and pyridafenthion. Trimedoxime was the most effective oxime in the treatment of insecticide poisoning, being successful especially at the lowest tested doses.

Administration, Oral↗
PubMed2006

Effects of triazine herbicides on organophosphate insecticide toxicity in Hyalella azteca.

The frequent use of pesticides in agricultural and commercial settings has led some researchers to devote their attention to studying the effects of mixtures of these compounds as they co-occur in the environment. Recent studies have demonstrated the potentiating effects of triazine herbicides, such as atrazine and its analogs, to the toxicity of a variety of organophosphate (OP) insecticides. One such OP insecticide, chlorpyrifos, has been the topic of much concern because of its prevalence in the environment. This study focused on examining the effects of 10 select triazine herbicides at concentrations of 1 mumole/L (approximately 200 mug/L) to chlorpyrifos with Hyalella azteca. The compounds selected include atrazine, three of its degradation products, and six other herbicide active ingredients. Toxicity tests were performed using a two-way analysis of variance matrix design with effect levels determined by way of probit analysis. Atrazine was found to have the greatest acutely lethal effect to H. azteca, followed by its closest degradation product, deethylatrazine. Two of the six atrazine analogs, simazine and cyanazine, also showed significant effects to the insecticide's toxicity. Synergistic ratios (SRs) were calculated to compare the effect magnitudes for each of the herbicides. The highest ratio obtained was with atrazine (SR = 1.42). A majority of the past studies involving mixtures of triazines and OPs have examined the potentiation effects of active-use triazine herbicides on Chironomus species. However, compared with the acute effects previously obtained for Chironomus species, H. azteca show a higher tolerance to the presence of the triazine herbicides, even at levels often considered as being at the high end of environmentally relevant concentrations. When coupled with past studies from our laboratory, this research helps to provide a better understanding of the toxic effects of herbicide-insecticide interactions.

Amphipoda↗
PubMed2003

Regulation of uteroglobin/Clara cell protein expression after acute lung exposure to an organophosphoreted insecticide.

Uteroglobin (UG) or Clara cell protein (CC16), the main secretory product of bronchiolar Clara cells, plays an important protective role in the respiratory tract against inflammatory processes. In the lung, protein secretion is regulated by glucocorticoids, but also proinflammatory cytokines, such as interferon-gamma (IFN-gamma) and TNF-alpha, have been found to modulate the expression of this peptide. We have previously demonstrated that the acute exposure to an organophosphoreted insecticide induces an enhanced production of UG/CC16 by Clara cells. In the present report, we worked with intact and adrenalectomised (ADX) animals to study the mechanism involved in the UG/CC16 increase caused by the insecticide and the role played by a glucocorticoid (dexamethasone; DEX). In intact rats we found that DEX treatment could not reproduce such an increase of UG/CC16 synthesis with pharmacological doses. In ADX rats, even though glucocorticoid deprivation provoked a strong inhibition of UG/CC16 synthesis, the exposure to the organophosphoreted insecticide stimulated the synthesis of the protein, shown by the great accumulation of secretory granules in the cytoplasm of Clara cells and the increase of UG/CC16 detected by immunocytochemistry and western blot. These results imply that glucocorticoids are not essential to trigger the increase of UG/CC16 in response to an injury, and they also suggest an involvement of other molecules associated with inflammation. In coincidence with these observations, we have found that IFN-gamma, a proinflammatory cytokine, increased after insecticide exposition in both groups, intact and ADX, mainly in ADX rats. The stimulation of UG/CC16 synthesis occurring during inflammatory processes of the respiratory tract caused by acute inhalation of a toxicant appears to be functional without the intervention of glucocorticoids and mediated by IFN-gamma as a mechanism for local control of the inflammatory response.

Adrenalectomy↗
PubMed2003

Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.

AIM: Pesticides are widely used throughout the world, in agriculture to protect crops and in public health to control diseases transmitted by vectors or intermediate hosts. After the prohibition of organochlorines such as DDT, today, mainly pyrethroids and organophosphorus insecticides are used. Whereas many studies have been published on background exposure of the population to organochlorines, data on internal exposure of the population to pyrethroids and organophosphorus insecticides are scarce. Here, we report on internal exposure of children and young people, in an urban area in Germany, to pyrethroids and organophosphorus acids, assessed by the analysis of urinary levels of their corresponding specific metabolites. METHODS: Approximately 673 children and adolescents took part in this voluntary investigation, including 331 children <6 years of age. Their parents stated that they and their children had never used pyrethroids or organophosphorus acids in their homes or for medical reasons. We analysed their spot urine samples for six metabolites of organophosphorus insecticides [dimethyl-phosphate (DMP), diethyl-phosphate (DEP), dimethyl-thiophosphate (DMTP), diethyl-thiophosphate (DETP), dimethyl-dithiophosphate (DMDTP) and diethyl-dithiophosphate (DEDTP)] and for four metabolites of pyrethroids [cis-3-(2,2-dibromo-vinyl)-2,2-dimethyl-cyclopropane carboxylic acid (Br2CA), cis-3-(2,2-dichloro-vinyl)-2,2-dimethyl-cyclopropane carboxylic acid (cis-Cl2-CA ), trans-3-(2,2-dichloro-vinyl)-2,2-dimethyl-cyclopropane carboxylic acid (trans-Cl2-CA) and 4-fluoro-3-phenoxy-benzoic acid (F-PBA)] using gas chromatographic methods with mass-selective detection. The limit of detection was 0.1-0.2 microg/l for pyrethroid metabolites and 1 microg/l for metabolites of organophosphorus acids; in DMP it was 5 microg/l. RESULTS: The 95th percentiles of the urinary metabolite concentrations were, in microgrammes per litre, DMP 158, DMTP 180, DMDTP 12, DEP 17, DETP 8, DEDTP <1; Br2CA 0.30, cis-Cl2-CA 0.44, trans-Cl2-CA 1.22, F-PBA 0.30. There were no correlations between urinary metabolite levels and the age of the children. CONCLUSION: Current background levels of internal exposure to pyrethroids and organophosphorus insecticides in children and adolescents in Germany are shown. Exposure to these substances in the general population is thought to occur mainly via residues in the diet. The level of background internal pyrethroid exposure in the children is orders of magnitude lower than the corresponding acceptable daily intake (ADI) values published, but the level of internal organophosphate exposure may reach and even exceed ADI values. This observation demands further investigation.

Adolescent↗
PubMed2002

Structure-toxicity relationships study of a series of organophosphorus insecticides.

Structure-toxicity relationships were studied for a set of 47 insecticides by means of multiple linear regression (MLR) and artificial neural network (ANN). A model with three descriptors, including shape surface [S(R2)], hydrogen-bonding acceptors [HBA(R2)] and molar refraction [MR(R1)], showed good statistics both in the regression (r = 0.875, s = 0.417 and q2 = 0.675) and artificial neural network model with a configuration of [3-5-1] (r = 0.966, s = 0.200 and q2 = 0.647). The statistics for the prediction on toxicity [log LD50 (lethal dose 50, oral, rat)] in the test set of 20 organophosphorus insecticides derivatives is (r = 0.849, s = 0.435) and (r = 0.748, s = 0.576) for MLR and ANN respectively. The model descriptors indicate the importance of molar refraction and shape contributions toward toxicity of organophosphorus insecticides derivatives used in this study. This information is pertinent to the further design of new insecticides.

Animals↗
PubMed1992

Determination of organophosphorous and carbamate insecticides by flow injection analysis.

A flow injection system, incorporating an acetylcholinesterase (AChE) single bead string reactor (SBSR), for the determination of some organophosphorous (azinphos-ethyl, azinphos-methyl, bromophos-methyl, dichlorovos, fenitrothion, malathion, paraoxon, parathion-ethyl and parathion-methyl) and carbamate insecticides (carbofuran and carbaryl) is presented. The detector is a simple pH electrode with a wall-jet entry. Variations in enzyme activity due to inhibition are measured from pH changes when the substrate (acetylcholine) is injected before and after the passage of the solution containing the insecticide. The percentage inhibition of enzyme activity is correlated to the insecticide concentration. Several parameters influencing the performance of the system are studied and discussed. The detection limits of the insecticides ranged from 0.5 to 275 ppb. The determination of these compounds was conducted in Hepes buffer and a synthetic sea water preparation. The enzyme reactor can be regenerated after inhibition with a dilute solution of 2-PAM and be reused for analysis. The immobilized enzyme did not lose any activity up to 12 weeks when stored at 4 degrees C.

Acetylcholine↗
PubMed1989

Activation and degradation of the phosphorothionate insecticides parathion and EPN by rat brain.

Cytochrome P-450-dependent monooxygenases are known to activate phosphorothionate insecticides to their oxon (phosphate) analogs by oxidative desulfuration. These activations produced potent anticholinesterases, decreasing the I50 values to rat brain acetylcholinesterase almost 1000-fold (from the 10(-5) M range to the 10(-8) M range). Since the usual cause of death in mammals from organophosphorus insecticide poisoning is respiratory failure resulting, in part, from a failure of the respiratory control center of the brain, we investigated the ability of rat brain to activate and subsequently degrade two phosphorothionate insecticides, parathion (diethyl 4-nitrophenyl phosphorothioate) and EPN (ethyl 4-nitrophenyl phenylphosphonothioate). Microsomes from specific regions (cerebral cortex, corpus striatum, cerebellum, and medulla/pons) of the brains of male and female rats and from liver were incubated with the phosphorothionate and an NADPH-generating system. Oxon production was quantified indirectly by the amount of inhibition resulting in an exogenous source of acetylcholinesterase added to the incubation mixture as an oxon trap. The microsomal activation specific activity was low for brain when compared to liver [0.23 to 0.44 and 5.1 to 12.0 nmol.min-1.(g tissue)-1 respectively]. The mitochondrial fraction of the brain possessed an activation activity for parathion similar to that of microsomes [about 0.35 nmol.min-1.(g tissue)-1 for each fraction], but mitochondrial activity was slightly greater than microsomal activity for EPN activation [0.53 to 0.58 and 0.23 to 0.47 nmole.min-1.(g tissue)-1]. Whole homogenates were tested for their ability to degrade paraoxon and EPN-oxon (ethyl 4-nitrophenyl phenylphosphonate), quantitated by 4-nitrophenol production. Specific activity for oxon degradation in liver was greater than that in brain [31 to 74 and 1.1 to 10.7 nmole.min-1.(g tissue)-1 respectively]. Overall, the brain and liver had about 1.5- to 12-fold higher specific activities for degradation than activation depending on the compound used. These findings demonstrate that the brain possesses both phosphorothionate activation and oxon degradation abilities, both of which may be significant during exposures to organophosphorus insecticides.

Acetylcholinesterase↗
PubMed1977

Nitrosated methylcarbamate insecticides: effect on the DNA of human cells.

Normal human skin cells were treated with six insecticide esters of N-methylcarbamic acid or their N-nitroso derivatives. The DNA of the cells was sedimented in alkaline sucrose gradients at various times after treatment. The insecticides used were aldicarb, baygon, BUX-TEN, carbofuran, landrin, and methomyl. Numerous single-strand breaks were apparent in the DNA of all the nitroso derivative-treated cells but not in the DNA of those treated with the parent insecticides. Since the effect of the nitroso derivatives on the DNA could be observed for at least 20 h after removal of the chemical from the cultures, the DNA repairing events normally occurring in human cells after damage initiated by these chemical agents was not repaired as UV-type DNA damage or ionizing-type DNA damage in human cells. These observations suggest that the human cellular DNA in vivo is irreversibly altered by nitrosated N-methyl carbamate insecticides resulting in numerous alkali-sensitive bonds.

Carbamates↗
PubMedDate not supplied

A comparison of the efficacy of insecticide-treated and untreated bed nets in preventing malaria in Gambian children.

An evaluation of the Gambian national insecticide bed net programme, which has introduced insecticide treatment of bed nets into all primary health care (PHC) villages in The Gambia, provided an opportunity to compare the individual risk of malaria in children who slept under untreated or insecticide-treated bed nets. 2300 children 1-4 years old were selected for a survey at the end of the 1992 rainy season, 1500 from PHC villages and 800 from non-PHC villages. All malariometric indices were lower, and the mean packed cell volume was higher, in children who slept regularly under treated or untreated bed nets than in those who did not use a net. This study suggested that untreated bed nets provide some individual protection against malaria, although not as efficiently as that provided by insecticide-treated bed nets which were particularly effective at preventing infections accompanied by high parasitaemia.

Bedding and Linens↗
PubMed1986

Effect of commercial formulation of four organophosphorus insecticides on the LH-induced germinal vesicle breakdown in the oocytes of a freshwater teleost, Mystus vittatus (Bloch)--a preliminary in vitro study.

Effect of commercial formulation of four organophosphorus insecticides such as malathion, phosdrin (mevinphos), birlane (chlorfenvinphos), and gardona (tetrachlorvinphos) on LH-induced in vitro germinal vesicle breakdown (GVBD) in the oocytes of Mystus vittatus was investigated using three concentrations for each insecticide. All of these insecticides could significantly inhibit the LH-induced GVBD in all of their concentrations except two lower concentrations of birlane. A probable mechanism of inhibition of reproduction by these insecticides is discussed in the light of present findings.

Animals↗
PubMed1992

Nerve membrane Na+ channels as targets of insecticides.

The mechanisms of action of neuroactive insecticides on the nervous system has been studied for many years. It is now well established that severe neurological symptoms of poisoning with pyrethroids and DDT in mammals and insects are the result of modification of Na+ channel activity. Toshio Narahashi discusses the history, approaches and results of the studies leading to this conclusion. Advanced electrophysiological experiments using voltage clamp and patch clamp, together with ligand-binding and ionic flux experiments, have unveiled unique actions of pyrethroids and DDT of keeping the Na+ channel in the open state for an extremely long period, sometimes as long as several seconds. This modification of Na+ channel properties leads to hyperactivity of the nervous system. These insecticides have also been shown to suppress GABA and glutamate receptor-channel complexes and voltage-activated Ca2+ channels, but the toxicological significance of these actions remains to be seen. The results of these studies provide clues for developing newer insecticides with higher selectivity between mammals and insects and for coping with the problem of insecticide resistance.

Animals↗
PubMed1992

Combined effects of selected insecticides on humoral immune response in mice.

Biological effects data with single insecticides are far more abundant than with mixtures. These data cannot be used directly to predict the effects of insecticide mixtures. Three insecticides of different chemical classes: organochlorine; dieldrin, organophosphate; malathion, and carbamate; carbofuran, previously evaluated for their immunotoxic potential, were selected for studies of combined acute exposure in C57B1/6 inbred mice. The humoral response to sheep red blood cells (SRBC) and the functional activities of peritoneal macrophages, such as phagocytosis of fluorescent beads and presentation of a single protein antigen, avidin, were examined after in vivo exposure of mice to different combinations of the selected pesticides and compared with the vehicle controls. Regarding exposure to single substances, the data confirmed the immunosuppressive potential of dieldrin and carbofuran and the immunopotentiating effect of malathion. Following the acute concomitant exposure to dieldrin/carbofuran mixture, however, values for the parameters of antigen presentation, primary IgM antibody response to SRBC antigen, and macrophage phagocytosis, returned to control or above-control values, indicating a lack of any synergistic or additive effects of the chemicals on the immune response. Thus, it was concluded the dieldrin/carbofuran mixture had an antagonistic effect on the humoral response to SRBC and the macrophage phagocytic activity, in comparison with the action of administration of each of the insecticides alone.

Animals↗
PubMed1987

Potentiations of N-methylcarbamate toxicities by organophosphorus insecticides in male mice.

A N-methylcarbamate insecticide, 2-sec-butylphenyl N-methylcarbamate (BPMC), is markedly potentiated by low-dose treatments of P = S type organophosphorus insecticides. As a mechanism of this potentiation, the increase of plasma BPMC concentrations due to the inhibited metabolic degradation has been suggested. In this study, acute toxicities of five N-methylcarbamates structurally related to BPMC were studied after low-dose treatments of three P = S type organophosphorus insecticides (cyanophos, fenitrothion, and malathion) and one P = O type organophosphorus insecticide (dichlorvos), and the role of plasma concentrations of N-methylcarbamates in the potentiations was examined. Acute toxicities of five N-methylcarbamates were potentiated by the treatments of the P = S types, among which the potentiation of BPMC was strongest. BPMC toxicity was not potentiated by the treatment of the P = O type. Plasma concentrations of BPMC were increased by the treatments of the P = S types, but not by the treatment of the P = O type. The acute toxicity and plasma concentrations of BPMC were increased by SKF 525-A (an inhibitor of mixed-function oxidase). These results suggest that the increase of plasma BPMC concentrations may be related to the potentiation of BPMC toxicity. The treatment of fenitrothion increased plasma concentrations of other N-methylcarbamates more than those of BPMC, although the potentiation of BPMC toxicity was strongest. SKF 525-A and fenitrothion treatments increased plasma BPMC concentrations to a similar degree, but the potentiation of BPMC toxicity by SKF 525-A was significantly less than that by fenitrothion. Thus, some other mechanism(s) may be responsible for the potentiations of the N-methylcarbamate toxicities.

Animals↗
PubMed1989

Effect of diphenhydramine on organophosphorus insecticide toxicity in mice.

Male mice were treated orally with the organophosphorus insecticides fenamiphos and dichlorvos at 10 and 150 mg/kg, respectively. The insecticides produced signs of toxicosis characteristic of cholinesterase inhibition, and induced death in all treated mice. Pretreatment of mice with diphenhydramine HCl (20 and 30 mg/kg, subcutaneously) 15 min before either insecticide significantly (P less than 0.05) reduced the incidence of toxic manifestations (excessive salivation, Straub tail, and whole body tremor), delayed the onset of death, and increased the percentage of survivors. Doses of diphenhydramine less than 20 mg/kg were not so effective. The data indicated a protective property of diphenhydramine against organophosphorus insecticide-induced toxicosis.

Animals↗
PubMed1982

Pharmacology of insecticide-induced release of hyperlipaemic hormone in the locust, Locusta migratoria.

1. The mechanism of insecticide-induced release of hyperlipaemic hormone from the glandular lobe of the isolated corpora cardiaca (CC) of locusts has been studied using pharmacological agents. 2. Treatment of isolated CC with various insecticides induces the release of hyperlipaemic hormone as judged by bioassay. 3. Reserpinisation of CC (25 micrograms/locust) or treatment of isolated CC with the alpha-adrenergic-receptor blocker phentolamine had no effect on the action of DDT or bioresmethrin, but partially blocked the action of dieldrin and chlorfenvinphos. 4. Treatment of isolated CC with the postsynaptic cholinergic blocker hexamethonium bromide abolished the effect of dieldrin and chlorfenvinphos, but did not block the action of DDT or bioresmethrin. 5. The effects of all the insecticides tested in this study were completely blocked by treatment of the CC with 10(-6) M tetrodotoxin. 6. The results indicate that DDT and bioresmethrin may act directly on the glandular cells via a sodium-dependent mechanism. The results with dieldrin and chlorfenvinphos suggest the presence of two distinct cholinergic pathways, one of which acts via the pre-synaptic aminergic terminals which control the glandular cells, whereas the other acts elsewhere in the CC. Sodium channels are also involved in the ultimate expression of these two insecticides.

Animals↗
PubMed1991

Solid phase extraction method for rapid isolation and clean-up of some synthetic pyrethroid insecticides from human urine and plasma.

A simple and rapid method for the isolation of seven synthetic pyrethroid insecticides (methothrin, fenpropathrin, cyhalothrin, permethrin, cypermethrin, fenvalerate, deltamethrin) with a solid phase extraction (SPE), utilizing Sep-Pak C18 cartridges, from human urine and plasma is presented. The detection of the insecticides was performed using a wide bore capillary gas chromatograph (GC) with flame ionization detection (FID). The insecticide-containing samples mixed with 70% methanol were directly applied to the cartridges and eluted with 2 ml chloroform. The recoveries using the cartridges were between 90-102% for urine and 81-93% for plasma. Mixing samples with 70% methanol prior to extraction, seems very useful for the screening of synthetic pyrethroid insecticides.

Chromatography, Gas↗
PubMed1987

Effect of mosquito killer insecticides on freshwater mussels.

The effect of four insecticides (Fyfanon, K-Othrin, Unitox 7 and Unitox 20) was investigated on the freshwater mussels Anodonta cygnea L., Anodonta anatina L. and Unio pictorum L. The studies were performed in hard water (total salinity of 310 mg/l). The LC50 values for 24, 48, 72, 96 hr and 7 days were determined with a static test at 22 degrees C. All the three mussel species proved to be extremely tolerant against the insecticides tested. The effect of sublethal concentrations of these insecticides on the periodic activity of the mussels was also analyzed, comparing the changes of the active and resting periods. In a concentration of 0.1 microliter/l, all the four insecticides affected the periodic activity of U. pictorum, whereas in A. anatina three of them (Fyfanon, K-Othrin and Unitox 7) and in A. cygnea two of them (K-Othrin and Unitox 7) evoked alterations. This concentration is lower by three to five orders than those of the LC50 values of 96 hr.

Animals↗