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At least 19 recordsLinked to original sources
PubMed2006

Effect of a mixture of iprobenfos and malathion on the development of malathion resistance in the mosquito Culex pipiens pallens Coq.

A malathion-resistant (RM) strain of Culex pipiens pallens Coq was obtained by successively selecting a field population with malathion in the laboratory. The synergistic effect of iprobenfos on malathion toxicity and alpha-naphthyl acetate (alpha-NA) esterase assay revealed that malathion resistance in the RM strain was associated with increased alpha-NA esterase activity and the synergism was mainly due to the inhibition by iprobenfos of this activity. There was no difference in alpha-NA esterase activity between the larvae and female adults in the susceptible (S) strain, but the activity in the adults was 13-fold higher than in the larvae of the RM strain. To understand the effect of the application of a mixture of iprobenfos and malathion on the evolution of malathion resistance, an artificial strain (Syn) was generated by mixing the RM and S strains with 0.1 frequency of the malathion-resistant individuals. The offspring of the Syn strain were divided into two sub-strains, Rm and Rm+ibp, which were successively treated with, respectively, malathion alone and malathion + iprobenfos (1:2) at LC70. In the mixture, the fungicide iprobenfos acted as a synergist of malathion. After treatment for 10 generations, the resistance level to malathion was 317.4-fold for the Rm sub-strain, whereas for the Rm+ibp sub-strain it was only 38.9-fold, compared with the Syn strain. Similar results were obtained by measurement of alpha-NA esterase activity from both larvae and female adults. The alpha-NA esterase activities in larvae and female adults at F10 generation were 2.6- and 10.9-fold from the Rm+ibp sub-strain and 5.7- and 98.5-fold from the Rm sub-strain, respectively, compared with the Syn strain. The above results suggested that iprobenfos, although it cannot completely stop or prevent the onset of malathion resistance, could dramatically delay its evolution.

Animals↗
PubMed1982

Dimethylphosphorothioates. Reaction with malathion and effect on malathion toxicity.

Five dimethylphosphorothioates were tested for their toxicity to rats, potentiation of malathion toxicity in rats, inhibition of carboxylesterase in vitro, and reaction with malathion in vitro. The compounds were: potassium salts of (CH3S)2P(O)O-(I), (CH3O)(CH3S)P(O)S-(II), (CH3O)2P(O)S-(III), (CH3O)2P(S)S-(IV), and (CH3O)(CH3S)P(O)O-(V). The dimethylphosphorothioates are not toxic to rats (up to 1 g/kg, orally), they do not potentiate malathion toxicity in rats, and do not inhibit carboxylesterase activity in vitro (up to 1 mM concentrations). However, when the S-acid diesters (II, III, IV) are incubated with malathion for serveral days at room temperature or for several hours at 50 degrees C they become methylated forming the trimethylphosphorothioates OSS-trimethyl phosphorodithioate, OOS-trimethyl phosphorothioate and OOS-trimethyl phosphorodithioate respectively, which potentiate malathion toxicity. Furthermore, these same acid diesters increase the rate of isomerization of malathion into OS-dimethyl-S-(1,2-dicarbethoxyethyl) phosphorodithioate (isomalathion) particularly, diester IV. The formation of the trimethylphosphorothioates and isomalathion from the interaction of the S-acid diesters with malathion was determined by thin layer chromatography (TLC), gas chromatography and mass spectrometry and could be detected by in vitro inhibition of carboxylesterase. TLC methods can detect 1 mg of the trimethylphosphorothioates and isomalathion per gram malathion.

Animals↗
PubMed1997

Genotoxicity of malathion in human lymphocytes assessed using the micronucleus assay in vitro and in vivo: a study of malathion-exposed workers.

The aerial application of malathion, a widely used organophosphate insecticide, has raised public concerns about potential adverse health effects. We therefore studied micronucleus formation in human lymphocytes as a biomarker of genotoxicity both in vitro and in vivo. Lymphocytes were cultured either as whole blood or after Ficoll isolation and treated with malathion in doses from 5 to 100 micrograms/ml for 48 h. A significant increase in micronucleated cells (47.5/1000 versus 16.0/1000 in DMSO control, p < 0.001) was found in isolated lymphocytes at high dose levels (75-100 micrograms/ml), concurrent with cytotoxicity and a strong inhibition of proliferation (p < 0.001). Many of the treated cells also possessed multiple micronuclei. Antikinetochore-antibody staining revealed that the majority of malathion-induced micronuclei were kinetochore-negative. A significant dose-response was also observed in whole blood cultures, although the increase in micronucleated cells was lower than in isolated lymphocyte cultures (p = 0.03). When the same technique was applied to lymphocytes of 38 intermittently malathion-exposed workers involved in the Mediterranean Fruit Fly Eradication Program in California, no change in either proliferation or micronucleus level was observed compared with an unexposed control group. We conclude that malathion has a relatively low potential to cause chromosome damage in vitro, and corresponding doses are much higher than ones that even professional applicators are likely to be exposed to in vivo. The potential risk of chromosome damage for malathion exposure in vivo is therefore relatively low. More studies are needed to assess the possibility of interaction of malathion with other pesticides through combined exposure.

Alcohol Drinking↗
PubMed2001

Fitness consequences of malathion-specific resistance in red flour beetle (Coleoptera: Tenebrionidae) and selection for resistance in the absence of malathion.

Malathion resistance in the red flour beetle, Tribolium castaneum (Herbst), is a worldwide problem and is very stable once it becomes widespread in natural populations. In the absence of insecticide the proportion of resistant phenotypes may rapidly decline but the development of resistance does not always involve reduced fitness. Malathion-specific resistance in T. castaneum seems not to involve any loss of fitness in laboratory or field conditions. Susceptible beetles were in competition with resistant beetles at different initial frequencies and modifications of susceptible gene frequency were estimated in these laboratory populations over 10 generations. A significant decrease in susceptible gene frequency was observed in Tribolium populations over time. The selection coefficient of the susceptible allele was estimated and the fitness of susceptible alleles in all tests was observed to range from 0.89 to 0.93 compared with the fitness of resistant genotypes, which was assumed to be 1. Data provided evidence that the resistant strains exhibited fitness advantages in the absence of malathion. We also compared the biotic potential (fecundity and developmental time) of the susceptible strain, the homozygous malathion-specific resistant strain, and their hybrids. Malathion-specific resistant strains showed an 8 -23% increase in biotic potential relative to the susceptible strain. These findings are consistent with those of malathion-specific resistance in T. castaneum; the fitness of the insects seems independent of the genetic background and the fitness of the resistant insects is not affected by this resistance mechanism.

Animals↗
PubMed2001

Malathion resistance and prevalence of the malathion carboxylesterase mechanism in populations of mosquito vectors of disease in Sri Lanka.

OBJECTIVE: To determine the levels of malathion resistance and prevalence of the malathion carboxylesterase mechanism among mosquitoes in Sri Lanka. METHODS: Bioassays were carried out using WHO-recommended methods on samples of the following Sri Lankan mosquito vectors: Culex quinquefasciatus, C. tritaeniorhynchus, C gelidus, Anopheles culicifacies B, A. subpictus, Aedes aegypti and A. albopictus. FINDINGS Malathion-specific carboxylesterase mechanisms were found in A. culicifaies and A. subpictus, both giving high rates of insecticide metabolism. In contrast, malathion resistance in C. quinquefasciatus and C. tritaeniorhynchus is linked to broad-spectrum resistance to organophosphorus compounds due to elevated levels of esterases that sequester malaoxon, but are unable to metabolize malathion. CONCLUSIONS: Resistance among the Anophelesspp. must have occurred as a direct result of antimalarial activities, since malathion use in Sri Lanka is limited to public health treatments. In contrast, resistance among Culex spp. has resulted from large-scale use of the organophosphorus insecticide group as larvicides for filariasis control and on rice paddy, where C tritaeniorhynchus predominantly breeds, for agricultural purposes.

Animals↗
PubMed1984

The joint action of malathion and IBP against malathion-resistant and -susceptible strains of Anopheles stephensi.

Malathion resistance in an Anopheles stephensi strain from Pakistan is dependent on a single gene, which results in increased degradation of malathion to the monocarboxylic acid. Mixtures of malathion and the fungicide IBP (O, O-bis(1-methylethyl) S-phenylmethyl phosphorothioate) were tested against this resistant strain and a laboratory susceptible strain. The mixtures were more toxic to both the resistant and susceptible insects than either IBP or malathion alone. The high degree of synergism with the mixtures against the susceptible strain would not be expected if IBP were simply competing with malathion for a common carboxylesterase detoxification enzyme. The reason for the high degree of synergism in the susceptible strain is unknown.

Anopheles↗
PubMed1997

Effects of oral administration of malathion on the course of disease in MRL-lpr mice.

Malathion administration at non-cholinergical doses was shown to elevate macrophage, proliferative and humoral immune responses. This study examined the effects of malathion on autoimmunity, autoantibody formation, macrophage function and mitogenic responses in MRL-lpr mice (genetically predisposed to autoimmune disease) and MRL-+/+ mice. Malathion, 33-300mg/kg, was administered by gavage once per week, beginning at 6 weeks of age. At 300mg/kg in MRL-lpr mice, malathion administration accelerated the appearance of significant (>100mg/l) levels of urinary protein by approximately 3 weeks and increased the maximum level of protein detected. Increased urinary protein was delayed at lower doses of malathion, but was elevated compared to vehicle control. This increase in urinary protein was not observed in the group of MRL-+/+ mice. The popliteal and axillary lymph nodes (LN) were larger in malathion-treated (>33mg/kg) than in control mice at 19 weeks of age. Within the same time-frame in MRL-+/+ mice, malathion did not affect and increased the size of the axillary and popliteal LN, respectively. Rheumatoid factor (RF) and anti-DNA (dsDNA) antibodies in the serum were not elevated in any group of MRL-+/+ mice by 19 weeks of age. However, in the MRL-lpr mice, weekly malathion treatment (>33mg/kg) elevated the level of serum RF at 12 and 19 weeks of age. Malathion treatment (>100mg/kg) also increased the level of anti-dsDNA antibodies in the serum of MRL-lpr mice at 19 weeks of age. Malathion treatment increased the number of inflamed glomeruli. Histopathological analysis of various organs showed no effect on vasculitis after malathion treatment. Acute administration of 300mg/kg malathion to 6-week-old mice elevated the secretion of nitric oxide by peritoneal macrophages, but did not affect the secretion of tumor necrosis factor. In addition, the basal and mitogen-induced proliferation of splenocytes of malathion-treated MRL-lpr mice were elevated, but the stimulation index was unchanged.

Administration, Oral↗
PubMed1990

Modulation of respiratory burst activity and mitogenic response of human peripheral blood mononuclear cells and murine splenocytes and peritoneal cells by malathion.

Previous studies showed that acute administration of noncholinergic doses of malathion in vivo elevated the humoral immune and mitogenic responses but did not alter the generation of the cytotoxic T lymphocyte (CTL) response to alloantigen of splenocytes from treated mice. However, in vitro exposure to malathion suppressed the generation of a CTL response. In this study, the effects of in vivo and in vitro (with and without an NADPH-regenerating liver enzyme system) exposure to malathion on the mitogenic responses of murine splenocytes or respiratory burst activity of peritoneal cells were examined. The effect of in vitro exposure to malathion on the ability of human peripheral blood mononuclear cells (PBMC) to perform these functions was also examined. In vivo exposure to malathion significantly elevated proliferative responses of murine splenocytes to mitogens. Cell separation and reconstitution studies indicated that adherent splenocytes from treated mice could elevate the proliferative responses of nonadherent splenocytes from control mice. Alternatively, in vitro exposure of murine splenocytes or human PBMC to malathion or malathion metabolized by a liver enzyme system suppressed or did not change, respectively, the proliferative responses to mitogens. In addition, cell separation and reconstitution experiments indicated that in vitro exposure to malathion affected nonadherent splenocytes and PBMC. In vivo exposure to malathion also elevated the production of hydrogen peroxide, following stimulation with phorbol myristate acetate, by murine peritoneal cells. In vivo exposure of murine peritoneal cells to malathion suppressed or elevated the respiratory burst activity following exposure to malathion or malathion metabolized by a liver enzyme system, respectively. Exposure of human PBMC to metabolized malathion in vitro enhanced their ability to produce hydrogen peroxide.

Animals↗
PubMed2005

Biodegradation and detoxification of organophosphate insecticide, malathion by Fusarium oxysporum f. sp. pisi cutinase.

Efficiencies of two lypolytic enzymes (fungal cutinase and yeast esterase) in malathion degradation were investigated. Surprisingly, degradation rate of malathion by fungal cutinase was very high, i.e. almost 60% of initial malathion (500 mg l(-1)) was decomposed within 0.5 h, and nearly 50% of the degraded malathion disappeared within initial 15 min. With the yeast esterase, despite the same concentration, more than 65% of malathion remained even after 2-day treatment. During enzymatic degradation of malathion, two malathion-derived compounds were detected, and time-course changes in composition were also monitored. In the degradation by both fungal cutinase and yeast esterase, two additional organic chemicals were produced from malathion: malathion monoacid (MMA) and malathion diacid (MDA) by ester hydrolysis. Final chemical composition after 2 d was significantly dependent on the enzyme used. Fungal cutinase produced MDA as a major degradation compound. However in the malathion degradation by yeast esterase, an isomer of MMA was produced in abundance in addition to MDA. Toxic effects of malathion and its final degradation products were investigated using various recombinant bioluminescent bacteria. As a result, the degradation products (including MMA) by esterase severely caused membrane damage and inhibition of protein synthesis in bacterial cells, while in the fungal cutinase processes, malathion was significantly degraded to non-toxic MDA after the extended period (2 days).

Biodegradation, Environmental↗
PubMed2003

Effect of ULV malathion use in boll weevil (Coleoptera: Curculionidae) eradication on resistance in the tarnished plant bug (Heteroptera: Miridae).

Tarnished plant bugs, Lygus lineolaris (Palisot de Beauvois), from regions 1, 2, and 3 of the boll weevil, Anthonomous grandis Boheman, eradication program in Mississippi were collected from wild hosts and tested for malathion resistance during the spring and fall of 2000 and 2001. Plant bugs were also tested in region 1 in late-July and October of 1999, just before and after multiple applications of ultra-low-volume (ULV) malathion were used for reproduction-diapause control of boll weevils in August and September. Regions 1 (north Delta), 2 (south Delta), and 3 (hills) began boll weevil eradication in 1999, 1998, and 1997, respectively. A glass-vial bioassay was used to determine resistance in plant bugs to malathion by comparing LC50 values against an LC50 value obtained for susceptible plant bugs. Comparison of the LC50 value obtained for plant bugs at a location in the spring was also made with the LC50 value obtained in the fall at the same location. After multiple applications of malathion made for reproduction-diapause boll weevil control in region 1 in August and September, malathion resistance increased by 4.9-, 6.5-, and 20.8-fold in plant bug populations from the three test locations. Results from testing bugs from all three eradication regions were similar. Malathion resistance usually increased significantly from spring to fall and then declined significantly from fall to spring of the next year. Despite reduced use of malathion in all three eradication regions for boll weevils in 2001, resistance to malathion in plant bugs still increased significantly from spring to fall at all test locations in regions 1 and 2 (the Delta). Malathion resistance did not increase significantly in plant bug populations in region 3 (the hills) in 2001 from spring to fall at three of four test locations in this year. Possible causes for the higher malathion resistance found in plant bugs in the Delta are discussed. Overall test results showed that the use of malathion in boll weevil eradication in cotton probably contributed to increases in resistance to malathion in plant bug populations in the eradication areas. However, the expression of this resistance was usually rapidly lost by spring of the following year. Boll weevil eradication did not seem to produce a permanent increase in the expression of malathion resistance in tarnished plant bug populations found in the eradication regions.

Animals↗