Search

Early detection of insecticide resistance is essential to develop resistance countermeasures and depends on accurate and rapid biological and biochemical tests to monitor resistance and detect associated mechanisms. Many such studies have measured activities of esterases, enzymes associated with resistance to ester- containing insecticides, using the model substrate, α-naphthyl acetate (α-NA). However, in the field, pests are exposed to ester-containing insecticides such as malathion, that are structurally distinct from α-NA. In the current study, malathion resistance in C. quinquefasciatus (3.2- to 10.4-fold) was highly associated with esterase activity measured with either α-NA (R2 = 0.92) or malathion (R2 = 0.90). In addition, genes encoding two esterases (i.e., EST-2 and EST-3) were over-expressed in field- collected strains, but only one (EST-3) was correlated with malathion hydrolysis (R2 = 0.94) and resistance (Rs = 0.96). These results suggest that, in the strains studied, α-NA is a valid surrogate for measuring malathion hydrolysis, and that heightened expression of an esterase gene is not necessarily associated with metabolic resistance to insecticidal esters. [Display omitted] • Resistance to malathion was detected in field- collected Culex quinquefasciatus • Malathion resistance was associated with heightened esterase activities towards a model substrate (1- naphthyl acetate) and an insecticide (malathion), and the two activities were highly correlated in the field strains. • Increased expression of genes encoding two esterases (EST-2 and EST-3) was measured in the field strains, and heightened expression of EST-3 (but not EST-2) was associated with resistance to malathion. [ABSTRACT FROM AUTHOR]

Ammannia auriculata Willd. is a noxious broadleaf weed, commonly infesting rice ecosystems across southern China. A putative resistant A. auriculata population (AHSC-5) was sampled from a rice field of Anhui Province, where bensulfuron-methyl (BM) was unable to control its occurrence. This study aimed to determine the sensitivities of the AHSC-5 population to common-use herbicides, and to investigate the underlying resistance mechanisms. The bioassays showed that the AHSC-5 population was 138.1-fold resistant to BM, compared with the susceptible population (JSGL-1). Pretreatment of malathion reduced the resistance index to 19.5. ALS sequencing revealed an Asp376Glu substitution in the AHSC-5 population, and in vitro ALS activity assays found that 50% activity inhibition (I 50) of BM in AHSC-5 was 75.4 times higher than that of JSGL-1. Moreover, the AHSC-5 population displayed cross-resistance to pyrazosulfuron-ethyl (10.6-fold), bispyribac‑sodium (3.6-fold), and imazethapyr (2.2-fold), and was in the process of evolving multiple resistance to synthetic auxin herbicides fluroxypyr (2.3-fold) and florpyrauxifen-benzyl (3.1-fold). This study proved the BM resistance in A. auriculata caused by the Asp376Glu mutation and P450-regulated metabolism. This multi-resistant population can still be controlled by penoxsulam, MCPA, bentazone, and carfentrazone-ethyl, which aids in developing targeted and effective weed management strategies. [Display omitted] • An Ammannia auriculata population evolved 138.1-fold resistance to bensulfuron-methyl. • The Asp-376-Glu mutation in AaALS1 was initially identified in A. auriculata. • Malathion significantly reduced bensulfuron-methyl resistance in A. auriculata. • A. auriculata exhibited multiple resistance to fluroxypyr and florpyrauxifen-benzyl. [ABSTRACT FROM AUTHOR]

Japanese brome (Bromus japonicus) has become one of the main weeds in wheat fields in Hebei province of China and causes a large decrease of wheat production. A total of 44 putative resistant and 2 susceptible Japanese brome populations were collected in the 2021/2022 crop season from Hebei province of China to determine resistance levels to flucarbazone‑sodium and to investigate the diversity of acetolactate synthase (ALS) mutations, as well as to confirm the cross-and multiple-resistance levels to ALS and EPSPS (5-enolpyruvate shikimate-3-phosphate synthetase) inhibitors. Whole plant bioassay results showed that 15 out of 44 populations tested or 34% were resistant to flucarbazone‑sodium. The resistance indices of Japanese brome to flucarbazone‑sodium ranged from 43 to 1977. The resistant populations were mainly distributed in Baoding and Shijiazhuang districts, and there was only one resistant population in Langfang district. Resistant Japanese brome had diverse ALS mutations, including Pro-197-Ser, -Thr, -Arg and Asp-376-Glu. The incidence of Pro-197-Ser mutation was the highest at 68%. Application of the CYP450 inhibitor malathion suggested that CYP450 was involved in metabolic resistance in a population without an ALS mutation. The population with Pro-197-Thr mutation evolved weak cross-resistance to mesosulfuron-methyl and pyroxsulam, and it is in the process of evolving multiple-resistance to glyphosate. [Display omitted] • The resistance indices of Japanese brome to flucarbazone-sodium were from 43 to 1977. • ALS mutations of Japanese brome were Pro-197-Ser, -Thr, -Arg and Asp-376-Glu. • Japanese brome evolved cross- and multiple-resistance to ALS and EPSPS inhibitors. [ABSTRACT FROM AUTHOR]

The oriental fruit fly, Bactrocera dorsalis (Hendel), an invasive insect pest infesting fruits and vegetables, possesses a remarkable capacity for environmental adaptation. The investigation of behind mechanisms of the stress adaptability in B. dorsalis holds significantly practical relevance. Previous studies on the molecular mechanism underlying stress resistance in B. dorsalis have predominantly focused on nuclear-coding genes, with limited exploration on organelle-coding genes. In this study, we assessed alterations in the mitochondrial physiological parameters of B. dorsalis under exposure to malathion, avermectin, and beta-cypermethrin at LD 50 dosages. The results showed that all three insecticides were capable of reducing mitochondrial complex IV activity and ATP content. Expression patterns of mitochondrial coding genes across different developmental stages, tissues and insecticide exposures were analyzed by RT-qPCR. The results revealed that these mitochondrial coding genes were expressed in various tissues and at different developmental stages. Particularly noteworthy, atp6 , cox2 , and cytb exhibited substantial up-regulation in response to malathion and avermectin treatment. Furthermore, RNAi-mediated knockdown of atp6 and cox2 resulted in the increased toxicity of malathion and avermectin against B. dorsalis , and cox2 silencing was also associated with the decreased complex IV activity. These findings suggest that atp6 and cox2 most likely play pivotal roles in mediating tolerance or resistance to malathion and avermectin in B. dorsalis. Our results provide novel insights into the role of mitochondrial coding genes in conferring tolerance to insecticides in B. dorsalis , with practical implications for controlling this pest in the field. [Display omitted] • Malathion, avermectin and beta-cypermethrin inhibited complex IV activity and ATP content. • B. dorsalis mitochondrial coding genes expressed at various developmental stages and tissues. • atp6 , cox2 , and cytb significantly up-regulated after malathion and avermectin treatment. • Knockdown of atp6 and cox2 remarkably increase the mortality of B. dorsalis to malathion. • Silencing of cox2 resulted in increasing mortality of B. dorsalis to avermectin. [ABSTRACT FROM AUTHOR]

Wild oat (Avena fatua L.) is a common and problematic weed in wheat fields in China. In recent years, farmers found it increasingly difficult to control A. fatua using acetyl-CoA carboxylase (ACCase)-inhibiting herbicides. The purpose of this study was to identify the molecular basis of clodinafop-propargyl resistance in A. fatua. In comparison to the S1496 population, whole dose response studies revealed that the R1623 and R1625 populations were 71.71- and 67.76-fold resistant to clodinafop-propargyl, respectively. The two resistant A. fatua populations displayed high resistance to fenoxaprop-p-ethyl (APP) and low resistance to clethodim (CHD) and pinoxaden (PPZ), but they were still sensitive to the ALS inhibitors mesosulfuron-methyl and pyroxsulam. An Ile-2041-Asn mutation was identified in both resistant individual plants. The copy number and relative expression of the ACCase gene in the resistant population were not significantly different from those in the S1496 population. Under the application of 2160 g ai ha −1 of clodinafop-propargyl, the fresh weight of the R1623 population was reduced to 74.9%; however, pretreatment with the application of the cytochrome P450 inhibitor malathion and the GST inhibitor NBD-Cl reduced the fresh weight to 50.91% and 47.16%, respectively, which proved the presence of metabolic resistance. This is the first report of an Ile-2041-Asn mutation and probable metabolic resistance in A. fatua , resulting in resistance to clodinafop-propargyl. [Display omitted] • Avena fatua L. has evolved high resistance to clodinafop-propargyl in Xinjiang, China. • An Ile-2041-Asn mutation was first identified in resistant A. fatua populations in China. • TSR and NTSR mechanisms were coexisted in resistant A. fatua. [ABSTRACT FROM AUTHOR]

Bearded sprangletop (Leptochloa fusca spp. fasicularis) is a problematic weed in California rice (Oryza sativa) production. Historically, bearded sprangletop is controlled with clomazone in California rice fields. The continuous use of clomazone and lack of crop rotation in rice fields resulted in resistance to clomazone in several bearded sprangletop. The objective of this research was to determine the clomazone mechanism of resistance of two bearded sprangletop populations in California rice by investigating clomazone absorption, translocation, and metabolism under controlled environmental conditions in two resistant (CRBS1 and CRBS2) and one susceptible (S) populations. Absorption and translocation of 14C-clomazone were similar in R and S. Clomazone metabolism, as determined by inhibition of cytochrome P450 enzymes with malathion and determining clomazone metabolites profile, was different between S and R 3 days after treatment. Bearded sprangletop pretreated with malathion was 2-fold more sensitive to clomazone than when treated with clomazone alone, suggesting that cytochrome P450-mediated clomazone metabolism might be involved in the mechanism of resistance. An HPLC-MS/MS analysis revealed differences in clomazone metabolism between R and S biotypes. Hydroxymethylclomazone was the most abundant metabolite found in R plants with three and five-fold more abundant in CRBS1 and CRBS2, respectively, when compared to S plants. 5-ketoclomazone, the known toxic metabolite of clomazone, accumulated 2-fold more in S plants than in R plants at 72 h after treatment. This research shows that clomazone is metabolized differently between R and S populations of bearded sprangletop and that P450 monooxidation is likely involved in the mechanism of resistance. Unlabelled Image • Increased metabolism of clomazone is the mechanism of resistance in bearded sprangletop. • Hydroxymethylclomazone accumulated more in clomazone resistant plants than susceptible. • 5-ketoclomazone accumulated more in susceptible than in clomazone resistant bearded sprangletop plants. [ABSTRACT FROM AUTHOR]

Glutathione S -transferases (GSTs) are one of the three detoxification enzyme families. The constitutive and inducible overexpression of GSTs genes plays an important role in insecticide resistance. Previous study showed that malathion resistance was polygenic, and elevated GSTs activity was one of the important factor participating in malathion resistance of Bactrocera dorsalis (Hendel), a serious economic pest worldwide. BdGSTd5 overexpression was inducible upon exposure to malathion. However, the involvement of BdGSTd5 in malathion resistance has not been clarified. In this study, we found that BdGSTd5 sequence harbored the conserved region of delta class GSTs, which were overexpressed in malathion resistant strain of B. dorsalis compared to malathion susceptible strain. The highest mRNA expression level of BdGSTd5 was found in 1-day-old adult, and the levels decreased with aging. The ds BdGSTd5 injection effectively silenced (73.4% reduction) the expression of BdGSTd5 and caused significant increase in susceptibility to malathion with a cumulative mortality increasing of 13.5% at 72 h post malathion treatment (p < 0.05). Cytotoxicity assay demonstrated that BdGSTd5 was capable of malathion detoxification. Molecular docking analysis further indicated the interactive potential of BdGSTd5 with malathion and its toxic oxide malaoxon. The recombinant BdGSTd5 exhibited glutathione-conjugating activity toward 1-chloro-2, 4-dinitrobenzene and malathion and malaoxon metabolic capacity with significant reduction (p < 0.05) of the peak areas by 90.0% and 73.1%, respectively. Taken together, the overexpressed BdGSTd5 contributes to malathion metabolism and resistance, which detoxify the malathion in B. dorsalis via directly depleting malathion and malaoxon. [Display omitted] • BdGSTd5 was over-expressed in MR strain of B. dorsalis. • Knockdown the expression of BdGSTd5 significantly increased the susceptibility of B. dorsalis to malathion. • The cell viability significantly increased in BdGSTd5-expressed Sf9 cell. • Recombinant BdGSTd5 protein directly deplete malathion and malaoxon in the presence of GSH. [ABSTRACT FROM AUTHOR]

Malathion, one of commonly used organophosphate insecticides, has a wide range of toxic actions in different models. However, the effect of this compound on Ca2+ homeostasis and its related cytotoxicity in glial cells is elusive. This study examined whether malathion evoked intracellular Ca2+ concentration ([Ca2+] i) rises and established the relationship between Ca2+ signaling and cytotoxicity in normal human astrocytes, rat astrocytes and human glioblastoma cells. The data show that malathion induced concentration-dependent [Ca2+] i rises in Gibco® Human Astrocytes (GHA cells), but not in DI TNC1 normal rat astrocytes and DBTRG-05MG human glioblastoma cells. In GHA cells, this Ca2+ signal response was reduced by removing extracellular Ca2+. In Ca2+-free medium, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin abolished malathion-induced [Ca2+] i rises. Conversely, incubation with malathion abolished thapsigargin-induced [Ca2+] i rises. Inhibition of phospholipase C (PLC) with U73122 also blocked malathion-induced [Ca2+] i rises. In Ca2+-containing medium, malathion-induced [Ca2+] i rises was inhibited by store-operated Ca2+ channel blockers (2-APB, econazole or SKF96365) and the protein kinase C (PKC) inhibitor GF109203X. Malathion (5–25 μM) concentration-dependently caused cytotoxicity in GHA, DI TNC1 and DBTRG-05MG cells. This cytotoxic effect was partially prevented by prechelating cytosolic Ca2+ with BAPTA-AM (a selective Ca2+ chelator) only in GHA cells. Together, in GHA but not in DI TNC1 and DBTRG-05MG cells, malathion induced [Ca2+] i rises by inducing PLC-dependent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ channels. Furthermore, malathion induced Ca2+-associated cytotoxicity, suggesting that Ca2+ chelating may have a protective effect on malathion-induced cytotoxicity in normal human astrocytes. Unlabelled Image • Effects of malathion on Ca2+ homeostasis and its related physiology were explored in glial cells. • In GHA cells, malathion induced PLC-dependent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ channels. • In GHA cells, Ca2+ chelating through BAPTA-AM has a protective potential to prevent malathion-evoked cytotoxicity. [ABSTRACT FROM AUTHOR]

Malathion is one of the most commonly used organophosphorus (OP) pesticides. It is important to regard that exposure to OP poisoning may cause anxiety and depression. Malathion toxicity induces cholinergic symptoms. Brain-derived neurotrophic factor (BDNF) is the most profusely expressed neurotrophin in the central nervous system; it promotes the survival of neurons. Regular exercise improves brain well-being and enhances recovery from brain Injuries. It is suggested that BDNF may mediate these effects. Therefore, this study was planned to assess the modulatory effects of regular exercise performance on brain BDNF level, cholinergic activity, oxidative stress and apoptosis in male and female rats subjected to neurotoxicity induced by malathion administration. Thirty-two adult male and thirty-two adult female albino rats were included in this study. The rats were divided into four equal groups (8rats). Control group, malathion treated group, exercised group, malathion exercised group. Acetylcholinesterase (AchE) activity, total antioxidant capacity (TAC), BDNF level and Caspase 3 activity were assessed. Female rats had higher baseline content of BDNF in brain homogenate than male rats. Malathion administration induced a significant decrease in BDNF level in female rats and in the total antioxidant capacity in both male and female rats. A significant elevation in caspase 3 activity was detected in the malathion treated groups, with more elevation in female rats. Swimming exercise improved BDNF level, AchE activity, and apoptosis in both male and female rats in all groups. In addition, male rats were more cholinergic system responders to regular exercise than female rats. It could be concluded that malathion induced elevation in oxidative stress and apoptosis in all rats, with reduction in BDNF level in female rats. Meanwhile, regular swimming exercise was found to improve brain health through modulation of BDNF level and cholinergic activity. It is recommended to practice regular exercise to maintain brain health. Further studies are required to clarify the involvement of sex hormones in BDNF regulation. • Malathion caused induced elevation in oxidative stress and apoptosis in all rats, and a reduction in BDNF level in the female • Regular swimming exercise was found to improve brain health through modulation of BDNF level and cholinergic activity. • It is recommended to practice regular exercise to maintain brain health. • Further studies are required to clarify the involvement of sex hormones in BDNF regulation. [ABSTRACT FROM AUTHOR]

Carduus acanthoides L. is mainly a range-land weed, but in the 2010s has begun to invade GM crop production systems in Córdoba (Argentina), where glyphosate and 2,4-D have been commonly applied. In 2020, C. acanthoides was found with multiple resistance to these two herbicides. In this study, the mechanisms that confer multiple resistance to glyphosate and 2,4-D, were characterized in one resistant (R) population of C. acanthoides in comparison to a susceptible (S) population. No differences in 14C-herbicide absorption and translocation were observed between R and S populations. In addition, 14C-glyphosate was well translocated to the shoots (∼30%) and roots (∼16%) in both R and S plants, while most of 14C-2,4-D remained restricted in the treated leaf. Glyphosate metabolism did not contribute to resistance of the R population; however, as corroborated by malathion pretreatment, the mechanism of resistance to 2,4-D was enhanced metabolism (63% of the herbicide) mediated by cytochrome P450 (Cyt-P450). No differences were found in baseline EPSPS activity, copy number, and/or gene expression between the R and S populations, but a Pro-106-Ser mutation in EPSPS was present in the R population. Multiple resistances in the R population of C. acanthoides from Argentina were governed by target site resistance (a Pro-106 mutation for glyphosate) and non-target site resistance (Cyt-P450-based metabolic resistance for 2,4-D) mechanisms. This is the first case of resistance to glyphosate and 2,4-D confirmed for this weed in the world. [Display omitted] • Resistance mechanisms to glyphosate and 2,4-D were characterized in C. acanthoides. • Absorption, translocation, or metabolism did not participate in glyphosate resistance. • Population R presented metabolic resistance to 2,4-D mediated by cytochrome P450. • Pro-106-Ser mutation conferred for the resistance to glyphosate. • TSR and NTSR mechanisms were responsible for multiple resistances in C. acanthoides. [ABSTRACT FROM AUTHOR]

Redroot amaranth (Amaranthus retroflexus L.) is a noxious weed that affects soybean production in China. Experiments were conducted to determine the molecular basis of resistance to bentazone. Whole-plant dose-response experiments showed that two populations (R1 and R2) exhibited resistance to bentazone with resistance indices of 9.01 and 6.85, respectively. Sequencing of the psbA gene revealed no amino acid substitution in the two populations. qRT–PCR analysis verified that psbA gene expression in R1 and R2 populations was increased significantly after treatment with bentazone, which was 3-fold and 5-fold higher than that in S1 and S2 populations, respectively. The P450 inhibitor malathion significantly reduced the level of resistance in the R1 and R2 populations when used prior to bentazone treatment. The R1 population exhibited multiple resistance to thifensulfuron-methyl and lactofen, caused by target site mutations (Asp-376-Glu in ALS , Arg-128-Gly in PPO2). In conclusion, increased gene expression of the psbA gene and enhanced herbicide metabolism seem to be the basis of resistance to bentazone in these A. retroflexus populations. [Display omitted] • Two Amaranthus retroflexus populations exhibited moderate resistance to bentazone. • The P450 inhibitor malathion could reverse the resistance to bentazone. • Bentazone treatment leads to overexpression of the psbA gene in resistant populations. [ABSTRACT FROM AUTHOR]

Extensive use of insecticides in many orchards has prompted resistance development in the oriental fruit fly, Bactrocera dorsalis (Hendel). In this study, a laboratory selected strain of B. dorsalis (MR) with a 21-fold higher resistance to malathion was used to examine the resistance mechanisms to this organophosphate insecticide. Carboxylesterase (CarE) was found to be involved in malathion resistance in B. dorsalis from the synergism bioassay by CarE-specific inhibitor triphenylphosphate (TPP). Molecular studies further identified a previously uncharacterized α-esterase gene, BdCarE2 , that may function in the development of malathion resistance in B. dorsalis via gene upregulation. This gene is predominantly expressed in the Malpighian tubules, a key insect tissue for detoxification. The transcript levels of BdCarE2 were also compared between the MR and a malathion-susceptible (MS) strain of B. dorsalis , and it was significantly more abundant in the MR strain. No sequence mutation or gene copy changes were detected between the two strains. Functional studies using RNA interference (RNAi)-mediated knockdown of BdCarE2 significantly increased the malathion susceptibility in the adult files. Furthermore, heterologous expression of BdCarE2 combined with cytotoxicity assay in Sf9 cells demonstrated that BdCarE2 could probably detoxify malathion. Taken together, the current study bring new molecular evidence supporting the involvement of CarE-mediated metabolism in resistance development against malathion in B. dorsalis and also provide bases on functional analysis of insect α-esterase associated with insecticide resistance. [ABSTRACT FROM AUTHOR]

The extensive use of malathion, an organophosphate pesticide, raises the possibility of its undesirable toxicity to non-target organisms. Agricultural run-off and vector control sprays are the major sources of exposure to this pesticide for aquatic organisms. Some earlier studies have reported the presence of malathion at concentrations ranging from 18.12 μg/L to 105.2 μg/L in various water samples. In this study, we have tested the hypothesis that these sub-lethal yet environmentally significant concentrations of malathion has serious toxicological implications on the fingerlings of Labeo rohita. Exposure to increasing concentration of malathion (10, 50 and 100 μg/L) was reflected in the serum concentration of the pesticide and also in the inhibition of acetylcholinesterase activity in fish brains. Increased abnormalities in liver function test coupled with a rise in the oxidative stress response were observed in gills, liver and kidney. However, the increase in antioxidant enzyme activities like superoxide dismutase and glutathione-S-transferase by malathion exposure suggested a hormetic response. Tissue injury due to malathion was evident from the morphological and nuclear anomalies in the H-E stained sections of gill, liver and kidney. Cell cycle analysis of these organs further fortified the histopathological findings. This study elucidates the sub-lethal toxicity of environmentally relevant malathion concentrations on Labeo rohita which indicates the potential health hazard posed to human beings consuming this fish. This calls for careful application of malathion in areas adjoining to inland fisheries. [ABSTRACT FROM AUTHOR]

Organophosphorus (OP) and carbamate (CM) pesticides are widely used in agriculture. These pesticides are highly toxic to humans and their residues in food pose potential threat to human health. In this comparative study, we investigated the effect of subchronic exposure of OPs (malathion, MAL) and CM (Carbosulfan, CB) on rat liver and spleen. Biochemical analysis showed that levels of hepatic enzymes (ALT, ALP, LDH and PAL) changed after exposure to the pesticides. In the liver extracts, lipid peroxidation index increased after the treatment by pesticides. Our results indicated that exposure to MAL and CB leads to alteration of liver redox status. Both pesticides induced focal inflammation and fibrosis in the liver. After subchronic administration of MAL (200 mg/kg) and CB (25 mg/kg), systemic inflammation, as depicted by the increase in IFN-δ activity in liver, was observed in both malathion and carbosulfan treated animals. In addition, the results showed that MAL significantly increased TCD4+ and TCD8+ lymphocyte number. It also decreased INF-δ and IL-4 production. However, CB induced a reduction of TCD8+ number and cytokine production in spleen cells. In conclusion, malathion and carbosulfan had significant immunomodulatory properties in the spleen with inflammation and oxidative stress induction in the liver. [ABSTRACT FROM AUTHOR]

Many cases of insecticide resistance in insect pests give resulting no-cost strains that retain the resistance genes even in the absence of the toxic stressor. Malathion (rac- diethyl 2-[(dimethoxyphosphorothioyl)sulfanyl]succinate) has been widely used against the red flour beetle, Tribolium castaneum Herbst. in stored products although no longer used. Malathion specific resistance in this pest is long lasting and widely distributed. A malathion resistant strain was challenged with a range of stressors including starvation, hyperoxia, malathion and a pathogen to determine the antioxidant responses and changes to some lifecycle parameters. Adult life span of the malathion-specific resistant strain of T. castaneum was significantly shorter than that of the susceptible. Starvation and/or high oxygen reduced adult life span of both strains. Starving, with and without 100% oxygen, gave longer lifespan for the resistant strain, but for oxygen alone there was a small extension. Under oxygen the proportional survival of the resistant strain to the adult stage was significantly higher, for both larvae and pupae, than the susceptible. The resistant strain when stressed with malathion and oxygen significantly increased catalase activity, but the susceptible did not. The resistant strain stressed with Paranosema whitei infection had significantly higher survival compared to the susceptible, and with low mortality. The malathion resistant strain of T. castaneum showed greater vigour than the susceptible in oxidative stress situations and especially where stressors were combined. The induction of the antioxidant enzyme catalase could have helped the resistant strain to withstand oxidative stresses, including insecticidal and importantly those from pathogens. These adaptations, in the absence of insecticide, seem to support the increased immunity of the insecticide resistant host to pathogens seen in other insect species, such as mosquitoes. By increasing the responses to a range of stressors the resistant strain could be considered as having enhanced fitness, compared to the susceptible. [Display omitted] • Adult longevity of malathion-specific resistant strain shorter than the susceptible. • Starvation and/or 100% oxygen reduced adult life span of both strains, less for the resistant. • Under oxygen the survival of the resistant strain to the adult stage was significantly higher. • Resistant strain stressed with malathion and oxygen induced catalase, but not the susceptible. • Resistant strain stressed with Paranosema whitei infection had low mortality. [ABSTRACT FROM AUTHOR]

Two black-grass (Alopecurus myosuroides Huds.) populations (R2105 and R1027) that were suspected to be resistant to clodinafop-propargyl, an acetyl-CoAcarboxylase (ACCase) inhibitor, were found in winter wheat fields in China. Research was carried out to investigate whether resistance to clodinafop-propargyl was present and the molecular mechanism of herbicide resistance in these two populations. Dose–response assays confirmed high level resistance to clodinafop-propargyl in both R2105 and R1027 populations, with resistance indexes 25.1 and 22.1. ACCase gene sequence comparison revealed three amino acid mutations (Trp-1999-Leu, Ile-2041-Asn, or Asp-2078-Gly) in R2105 population and Ile-2041-Asn mutation in R1027 population. Sensitivity to other herbicides assays indicated that R2105 and R1027 populations were cross resistant to fenoxaprop-P-ethyl and multiple resistant to pyroxsulam and mesosulfuron-methyl. The ALS gene sequence analysis revealed that all resistant individuals in R2105 and R1027 populations had the Trp-574-Leu mutation. Applying malathion, significantly decreased the rate of metabolism of clodinafop-propargyl in both R2105 and R1027 populations. This is the first report of multiple resistance to ACCase- and ALS-inhibiting herbicides conferred by target-site mutations and enhanced metabolism in black-grass in China. [Display omitted] • Two Alopecurus myosuroides populations were resistant to ACCase and ALS herbicides. • ACCase and ALS sequencing revealed target site mutations. • P450s inhibitor malathion could reduce clodinafop-propargyl resistance. [ABSTRACT FROM AUTHOR]

The insect-specific epsilon class of glutathione S -transferases (GSTEs) plays important roles in insecticide detoxification in insects. In our previous work, five GSTEs were identified in Locusta migratoria, and two recombinant GSTEs, rLmGSTE1 and rLmGSTE4, showed high catalytic activity when 1-chloro-2,4-dinitrobenzene (CDNB) was used as a substrate. In this work, we further investigated whether these two GSTEs could metabolize three insecticides including malathion, deltamethrin and DDT. Using ultra-high-performance liquid chromatography tandem mass spectrometry (UHPLC/MS) method, we found that rLmGSTE4, but not rLmGSTE1, can metabolize malathion and DDT. Malathion bioassays of L. migratoria after the expression of LmGSTE4 was suppressed by RNA interference (RNAi) showed increased insect mortality from 33.8% to 68.9%. However, no changes in mortality were observed in deltamethrin- or DDT-treated L. migratoria after the expression of LmGSTE4 was suppressed by RNAi. Our results provided direct evidences that LmGSTE4 participates in malathion detoxification in L. migratoria. These findings are important for understanding the mechanisms of insecticide resistance in L. migratoria and developing new strategies for managing the insect populations in the field. [Display omitted] • Two recombinant locust GSTEs, rLmGSTE1 and rLmGSTE4, were expressed in E. coli BL21(DE3). • rLmGSTE4 could metabolize malathion and DDT in vitro. • Silencing LmGSTE4 increased the susceptibility of the locust to malathion. • LmGSTE4 participates in malathion detoxification, which provides new strategies for pesticide resistance management. [ABSTRACT FROM AUTHOR]

Pediculus lice represent one of the longest and most prevalent parasitic infestations of humans. Head lice are an economic and social concern whereas body lice pose a more serious public health threat. Significant progress has been made in the study of human lice over the last 10 years, allowing for new approaches in their control. An in vitro rearing system has made it possible to maintain insecticide-susceptible and -resistant reference strains, which allowed an in depth study of pediculicide resistance, including its underlying molecular mechanisms and the detection and monitoring of resistance. The generation of inbreed strains facilitated the efficient sequencing, assembly and annotation of the genomes and transcriptomes of both lice. The use of functional genomics and reverse genetics elucidated the genetics involved in the evolution of resistance and the discovery of novel target sites for the development of new pediculicides. In this review, four new effective pediculicide products, each with different mode of action and unique chemistries, will be presented. They have been found to be safe and selective, and control resistant lice. As such, they meet the criteria necessary to be used in rotations as a sustainable resistance management strategy. [Display omitted] • Head lice are resistant to permethrin/pyrethrins due to 3 kdr -type mutations. • Also resistant to malathion due to enhanced malathion carboxylesterase activity. • Four new pediculicides products kill resistant lice. • Each has novel chemistry and different modes of action. • Their use in rotations is suggested as an effective resistance management strategy. [ABSTRACT FROM AUTHOR]

Enhanced malathion carboxylesterase (MCE) activity was previously reported to be involved in malathion resistance in the head louse Pediculus humanus capitis (Gao et al., 2006 [8]). To identify MCE, the transcriptional profiles of all five esterases that had been annotated to be catalytically active were determined and compared between the malathion-resistant (BR-HL) and malathion-susceptible (KR-HL) strains of head lice. An esterase gene, designated HLCbE3, exhibited approximately 5.4-fold higher transcription levels, whereas remaining four esterases did not exhibit a significant increase in their transcription in BR-HL, indicating that HLCbE3 may be the putative MCE. Comparison of the entire cDNA sequences of HLCbE3 revealed no sequence differences between the BR-HL and KR-HL strains and suggested that no single nucleotide polymorphism is associated with enhanced MCE activity. Two copies of the HLCbE3 gene were observed in BR-HL, implying that the over-transcription of HLCbE3 is due to the combination of a gene duplication and up-regulated transcription. Knockdown of HLCbE3 expression by RNA interference in the BR-HL strain led to increases in malathion susceptibility, confirming the identity of HLCbE3 as a MCE responsible for malathion resistance in the head louse. Phylogenetic analysis suggested that HLCbE3 is a typical dietary esterase and belongs to a clade containing various MCEs involved in malathion resistance. [ABSTRACT FROM AUTHOR]

Highlights: [•] Inhibitory effects of 10 organophosphorus pesticides on MPO activity were investigated. [•] Investigated OPs affect peroxidase activity, but do not influence chlorination activity of MPO. [•] MPO peroxidase activity was affected the most by malathion and malaoxon. [ABSTRACT FROM AUTHOR]

Highlights: [•] Pancreatic endocrine system is affected in acute poisoning with malathion. [•] Malathion impairs glucose metabolism by increasing oxidative stress markers. [•] Impairment of glucose metabolism is critical in dysfunction of insulin induced by malathion. [ABSTRACT FROM AUTHOR]

Abstract: Malathion induced oxidative stress (OS) leads to the inevitable accumulation of free radicals and eventual alteration of antioxidant enzymes in various biological systems. Lactic acid bacteria (LAB), renowned for its probiotic potentials has been clinically accepted and recommended for consumption as a dietary supplement for its anti-oxidant efficacy. But the idea of treating malathion-induced OS by LAB has been in the dark. Thus, the present study is intended to investigate the protective antioxidant potential of Lactobacillus casei against malathion-induced biochemical alterations by employing the nematode Caenorhabditis elegans as model system. C. elegans exposed to malathion and L. Casei were examined for toxicity by assessing various stress markers including, reactive oxygen species (ROS), hydrogen peroxide (H2O2), protein carbonyl content (PCC) and lipid peroxidation (LPO). In addition, the levels of antioxidative enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) also were assessed. According to the results, C. elegans exposed to malathion showed a significant increase in the accumulation of stress markers and a decrease in the levels of antioxidative enzymes, when compared to their respective controls. Interestingly, C. elegans pretreated with L. casei significantly increased the levels of SOD and GSH and, while exposing the pretreated C. elegans with malathion, the levels of antioxidative and stress marker enzymes were rescued and reduced respectively, thereby showing that the L. casei pretreatment protects the in vivo system from malathion-induced OS. Furthermore, the FT-IR spectroscopy results suggested the protective efficacy of L. casei as an antioxidant in preventing the malathion induced damage to macromolecules such as DNA, lipids and protein. Thus, the present study reports for the first time that L. casei could be a promising biotherapeutic agent against malathion induced OS. [Copyright &y& Elsevier]

Abstract: Organothiophosphorous pesticides diazinon, malathion, chlorpyrifos, azinphos-methyl and phorate, have been indirectly electrochemically oxidized in aqueous media using anodically evolved Cl2, Br2 or I2 as a pre-step for their detection via acetylcholinesterase-based test. The presence of single oxidation product, corresponding oxo-form, was confirmed by UPLC analysis, as well as its stability with respect to hydrolysis. Comparing different halogens, the best results were obtained using Br2 as the oxidant due to high reactivity of HOBr, which is formed upon chemical reaction of anodically formed Br2 with water. Limits of detection of five analyzed pesticides were lowered upon indirect electrochemical oxidation with Br2 for two orders of magnitude or more, comparing to unoxidized parental thio-forms. In fact, the lowest possible detection limits for all five pesticides using proposed analytical procedure were achieved, as being determined by detection limits of corresponding oxo forms. Comparison of here proposed electrochemical oxidation pre-step with earlier reported ones is provided and discussed. [Copyright &y& Elsevier]

Abstract: Aquatic environments get contaminated with pesticides residues that result from the application of pesticides in agricultural practices. The present study aimed to evaluate the pesticides Malathion and Deltamethrin on biological and biochemical parameters of Helisoma duryi snails. The results showed that LC10 of the two pesticides caused considerable reduction in survival rates and egg production of treated snails. Glucose concentration in hemolymph of the exposed snails showed a significant increase. On the other hand, albumin in hemolymph and glycogen contents as well as the activities of enzymes in tissues of snails including lactate dehydrogenase (LDH), succinate dehydrogenase (SDH), arginase, and ornithine aminotransferase (OAT) were significantly inhibited. Meanwhile, the activity of AMP deaminase of the exposed snails was significantly increased in the hemolymph in response to treatment. The electrophoretic pattern of total protein showed differences in number and molecular weights of protein bands. DNA concentration was investigated by measuring the intensity of the genomic bands and its showed its increase in the treated snails. It was concluded that the residues of Malathion and Deltamethrin pesticides in aquatic environments have toxic effects on non-target organism, e.g. H. duryi snails. [Copyright &y& Elsevier]

Abstract: The aim of the work was to investigate the in vitro oxidation of diazinon and malathion, organophosphorous pesticides (OPs) containing phosphorthioate group, catalyzed by enzyme myeloperoxidase (MPO). The oxidation was performed in the presence of hydrogen peroxide. The products were identified as oxon derivatives (phosphates), where the sulfur atom from thioate group was substituted by an oxygen atom. No hydrolysis products were detected after enzyme – induced oxidation. The oxidation efficiency was controlled using acethylcholinesterase (AChE) bioassay for determination of oxon derivatives concentration. The influence of OPs concentration, incubation time of OPs with MPO, as well as MPO concentration on the yield of oxo forms was investigated. Kinetic constants of MPO in oxidation of malathion and diazinon were estimated. The maximum concentration of oxo forms was achieved after 10min incubation of OPs in 50mM phosphate buffer (pH 6.0) with 100nM MPO. [Copyright &y& Elsevier]

Abstract: Organophosphate compounds are among the most widely used synthetic chemicals for controlling a wide variety of pests. Organophosphate (OP) poisoning continues to be major cause of morbidity and mortality in the third world countries. Indiscriminate use of these pesticides tends to leave residues on the objects of the environment. Present study is aimed to compare the potential of three commonly used OP pesticides, chlorpyrifos (CPF), methyl parathion (MPT) and malathion (MLT), to generate oxidative stress in rat tissues and to evaluate whether the combined exposure of these pesticides exerts synergistic or antagonistic effects. Results of the present study showed that CPF, MPT and MLT exposure to rats caused accumulation of malondialdehyde (MDA) and 4-hydroxynonanal (4HNE), the two major end products of lipid peroxidation, in liver, kidney, brain and spleen of rats. Combined exposure of these pesticides also resulted in accumulation of MDA and 4HNE in rat tissues but the increase was almost of the same order as observed in rat tissues given these pesticides singly. Exposure with CPF, MPT and MLT singly or in mixture, caused dose-dependent decrease in the activities of antioxidant enzymes namely, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx), in rat tissues when compared with control, and the decrease observed was of the same order in all the groups. Acetylcholinesterase (AChE) activity, an indicator of OP poisoning, was also decreased in rat tissues in dose-dependent manner in CPF, MPT, MLT and mixture treated group. Differential increase in the levels of cytochrome P450 (cyt P450) in hepatic and extra-hepatic tissues of rats given CPF, MPT or MLT singly or in mixture, indicate different rates of metabolism of these pesticides. Results of the present study clearly show that CPF, MPT and MLT exposure singly or in mixture, induced oxidative stress in rat tissues which may be the major contributor of the overall toxicity of the OP pesticides. Combined exposure of these pesticides does not seem to potentiate the toxicity of each other and their toxic effects are not additive. [Copyright &y& Elsevier]

Abstract: Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in brain through the generation of free radicals and alteration of the cellular antioxidant defense system independent of its anticholinesterase effects. The aim of this study was to investigate the possible protective role of rolipram as a selective phosphodiesterase (PDE) type 4 inhibitor, on toxicity of malathion, by measuring the activities of brain mitochondrial and plasma peroxynitrite (ONOO−), glutathione peroxidase (GPx), superoxide dismutase (SOD), Mn-SOD, catalase (CAT), and lipid peroxidation (LPO) in rats. Effective doses of malathion (200mg/kg/day) and rolipram (200μg/kg/day) were administered alone or in combination for 7days by intraperitoneal injection. At the end of the experiment, the brain mitochondria and plasma of the animals were separated. In the brain cells mitochondria and blood plasma, the LPO, ONOO−, and GPx were higher in the malathion group as compared with controls. Rolipram ameliorated all of malathion-induced changes. Plasma CAT decreased in malathion-treated animals while it increased in brain mitochondria comparing with controls. Co-administration of rolipram with malathion improved CAT in both brain mitochondria and plasma. Malathion and rolipram did not alter total SOD or Mn-SOD in the plasma while both caused a significant elevation in brain mitochondria. In conclusion, this model of study that we employed, in a large extent, characterized the relationships among malathion-induced neurotoxicity, mitochondrial dysfunction, and significant increase in systemic and local oxidative/nitrosative stress in plasma and brain, respectively. Intracellular cAMP-elevating agents like rolipram, may be considered beneficial for the protection or recovery of malathion-induced toxic damage in brain mitochondria and blood. [Copyright &y& Elsevier]

Abstract: The main objective of this study was to investigate the possible protective effect of pentoxifylline as a phosphodiesterase 5 inhibitor used as a cardiovascular medication on malathion-induced changes on rat mitochondrial-bound hexokinase activity. Animals in four various groups received moderate toxic dose of malathion (200mg/kg/day), effective dose of pentoxifylline (50mg/kg/day) alone and in combination, and the control group that received only vehicle. All administrations were done intraperitoneally for one week. At the end of the experiment, the brain was removed and the mitochondria were isolated. Hexokinase (HK) activity, cellular lipid peroxidation (LPO) and total antioxidant capacity (TAC) were analyzed in brain mitochondria. Malathion noticeably decreased TAC and increased HK activity and LPO in the mitochondria whereas pentoxifylline significantly restored malathion-induced changes in LPO, HK, and TAC. The results of the present study indicate that phosphodiesterase 5 inhibition remarkably protects brain mitochondria from malathion-induced changes on HK activity and oxidative stress. [Copyright &y& Elsevier]

Abstract: The main objective of this study is to investigate the 24h kinetic effect of acute administration of malathion, an organophosphorus insecticide, on glucose homeostasis in adult rats. A single dose of malathion (400mg/kg, 1/5 of LD50) was administered orally to rats, blood glucose was measured, liver and pancreas were removed to determine the level of hepatic glycogen, the activity of pancreatic acetylcholinesterase and butyrylcholinesterase, as well as the level of TBARs. Blood glucose increased in rats treated with a single dose of malathion. This effect was observed in the first hours of treatment, reached a 2.2 fold peak after 2h, and then decreased after 4h, followed by a decrease in the level of hepatic glycogen. The storage of glycogen starts from 6 to 12h of administration. A decrease in cholinesterase activities was noted. The level of TBARs increased considerably in liver and pancreas. Results of this study can be explain by a stimulation of glycogenolysis and gluconeogenesis by liver, with a temporarily loss of endocrine functions of pancreas leading to hyperglycemia. [Copyright &y& Elsevier]

Herbicide resistance is frequently reported in E. crus-galli globally with target and non-target site resistance mechanism to acetolactate synthase (ALS)-inhibiting herbicides. However, resistance to certain herbicides can result in increased sensitivity to other herbicides, a phenomenon called negative cross-resistance. The objective of this study is to identify the occurrence of negative cross-resistance (NCR) to the pro-herbicide clomazone in populations of E. crus-galli resistant to ALS inhibitors due to increased metabolization. Clomazone dose-response curves, with and without malathion, were performed in imazethapyr-resistant and -susceptible E. crus-galli biotypes. CYP s genes expression and antioxidant enzymes activity were also evaluated. The effective dose to reduce 50% (ED 50) of dry shoot weight obtained in the clomazone dose-response curves of the metabolic based imazethapyr-resistant and -susceptible biotypes groups were 22.712 and 58.745 g ha−1, respectively, resulting in a resistance factor (RF) of 0.37, indicating the occurrence of NCR. The application of malathion prior to clomazone increased the resistance factor from 0.60 to 1.05, which indicate the reversion of the NCR. Some CYP genes evaluated were expressed in a higher level, ranging from 2.6–9.1 times according to the biotype and the gene, in the imazethapyr-resistant than in -susceptible biotypes following clomazone application. Antioxidant enzyme activity was not associated with NCR. This study is the first report of NCR directly related to the mechanism of resistance increased metabolization in plants. The occurrence of NCR to clomazone in E. crus-galli can help delay the evolution of herbicide resistance. [Display omitted] • Barnyardgrass resistant to imazethapyr due to enhanced herbicide degradation have increased susceptibility to clomazone. • CYP genes, which are involved in imazethapyr resistance, are overexpressed after clomazone application. • First report of negative-cross resistance provided by the mechanism of increased herbicide metabolization in plants. [ABSTRACT FROM AUTHOR]

Abstract: The objective of the present study was to investigate the role of α tocopherol and selenium on malathion induced hepatic damage, and antioxidant defense in chicks. The chicks were divided into three groups. First group received malathion 10mg/kg BW, orally for 60 days, the second group received the same dose of malathion but was supplemented with α tocopherol and selenium for 60 days and the third group served as the control. A compromised antioxidant capacity as evidenced by increased levels of erythrocytic lipid peroxidation and decreased concentration of vitamin E and decreased activity of glutathione peroxidase was observed in chicks following the administration of malathion. An improved antioxidant status was observed in chicks of second group with α tocopherol and selenium supplementation including higher concentration of vitamin E, increased activity of glutathione peroxidase and lower levels of lipid peroxidation. Histopathological studies of liver in the chicks which received malathion exhibited, moderate to severe degenerative and necrotic changes in the hepatocytes. The correlation of decreased antioxidant status of chicks with degenerative changes in liver suggests that lipid peroxidation may be one of the important mechanism in the chronic toxicity of malathion. The results indicate that α tocopherol and selenium were effective in partially alleviating degenerative changes induced by malathion in the liver of chicks by attenuating processes leading to lipid peroxidation. [Copyright &y& Elsevier]

Abstract: We examined the effects of malathion, an organophosphorus (OP) insecticide, on glucagon, C-peptide, and insulin content or secretion from isolated rat Langerhans islets in vitro. Islets were isolated from the pancreas of rats by standard collagenase digestion, separation by centrifugation, and hand-picking technique. Then islets were cultured in medium and supplemented with various concentrations of malathion (25, 125, and 625μg/ml) for 1, 3, and 5h. In vitro exposure to malathion increased insulin and C-peptide contents at doses of 25, 125, and 625μg/ml following 5h incubation as compared to control. All doses of malathion increased glucagon content after 3 and 5h as compared to control. Increase of the glucagon content at all doses in the fifth hour was higher than that of third hour. Malathion also decreased 2.8 and 16.7mM glucose-stimulated insulin secretion at all doses after 30min as compared to control. It is concluded that malathion reduce insulin exocytose in a short time (first hour) but after a long time (e.g., 5h), the content of insulin is increased by compensating mechanisms such as resynthesize of insulin or aggregation of insulin. The present in vitro study for the first time proposes the involvement of subcellular non-cholinergic mechanisms in malathion-induced changes in Langerhans islets insulin and glucagon. [Copyright &y& Elsevier]

Abstract: The aim of this study was to examine whether Satureja khuzestanica (Lamiaceae) essential oil (SKEO) might have protective effects on toxicity of malathion, a commonly used organophosphorus (OP), by measuring the activities of hepatic cells mitochondrial glycogen phosphorylase (GP) and phosphoenolpyruvate carboxykinase (PEPCK) activities and blood levels of glucose and acetylcholinesterase (AChE) in rats. Malathion (20mg/kg/day) and SKEO (225mg/kg/day) were administered alone or in combination by intragastric intubation for 28days. Treatment by malathion increased blood glucose as measured at days 18 and 28 of treatment. Malathion inhibited erythrocyte AChE and increased hepatic cells GP and PEPCK activities. Coadministration SKEO resulted in restoration of malathion-induced changes in hepatic cells GP and PEPCK activities and levels of blood AChE and glucose. It is concluded that SKEO interferes with malathion-induced stimulation of hepatic cells glycogenolysis and gluconeogenesis through its antioxidant potential and increasing AChE activity. [Copyright &y& Elsevier]

Abstract: Hyperglycemia is observed with exposure to organophosphorus (OP) pesticides. The aim of this study was to investigate the effects of malathion on secretion of insulin from rat pancreatic islets in vitro and in vivo. Malathion was administered through food for 4weeks at concentrations of 100, 200, and 400ppm. For in vivo experiment, at the end of treatment, blood sample was obtained and plasma was separated. For in vitro experiment, the treated rats were anesthetized and underwent a laparatomy. The common bile duct was cannulated and the pancreas distended by injecting of cold collagenase V using peristaltic infusion pump. Islets were then hand picked under a stereomicroscope and cultured in the presence of various doses of glucose and KCl. Malathion at doses of 200 and 400ppm increased plasma glucose and insulin concentrations and lowered activity of erythrocyte acetylcholinesterase. The isolated islets from pretreated animals with malathion 200 and 400ppm showed lower glucose-stimulated insulin secretion while no change was observed in the presence of KCl. Light microscopic examination revealed that malathion causes patchy degenerative changes in pancreatic islets. Combination of in vivo and in vitro findings suggests that malathion induces a kind of insulin resistance that cannot overwhelm hyperglycemia. This action of malathion is mediated through disruption of islets mitochondrial function. [Copyright &y& Elsevier]

Abstract: Despite mounting concerns about amphibian population declines, information on impact of pesticides on physiological changes is meager. The present study deals the influence of an organophosphate pesticide—malathion on the lipid metabolism of Limnonectus limnocharis under laboratory conditions. Changes in the lipid metabolism were analyzed in the liver, muscle, ovary, and testis of frogs exposed to lethal (10.67mgL−1 for 1, 2, 3, and 4 days) and sub-lethal (2.13mgL−1 for 1, 5, 10, 15, 20, and 25 days) concentrations of malathion. Upon lethal concentration treatment, against the increase of fatty acids, glycerol, and lipase activities in all tested tissues, there was decrease in the total lipids content over different durations. On the other hand, exposure to sub-lethal concentration, the amount of total lipids content, free fatty acids, glycerol and lipase activity increased. Changes in the lipid metabolism due to lethal concentration of malathion exposure could depict the negative impact on the reproductive success, which would result in decline of amphibian population. [Copyright &y& Elsevier]

Abstract: Control of the tarnished plant bug, Lygus lineolaris (Palisot de Beauvois), in cotton in the mid-South relies heavily on pesticides, mainly organophosphates. Continuous and dominant use of chemical sprays has facilitated resistance development in the tarnished plant bug. A natural population in Mississippi with resistance to malathion was studied to examine whether and how glutathione S-transferases (GST) played an important role in the resistance. Bioassays were first conducted to examine synergism of two GST inhibitors. Both ethacrynic acid (EA) and diethyl maleate (DM) effectively abolished resistance and increased malathion toxicity against two resistant strains by more than 2- and 3-fold, whereas incorporation of GST inhibitors did not significantly increase malathion toxicity against a susceptible strain. GST activities were compared in vitro between malathion susceptible and resistant strains by using 1-chloro-2,4-dinitrobenzene as a GST substrate. The resistant strain had significantly higher (1.5-fold) GST activity than the susceptible strain. Up to 99%, 75%, and 85% of the GST activities were inhibited by EA, sulfobromophthalein (SBT), and DM, respectively. The GST activities tended to increase from May to October by 1.76-fold. All three inhibitors significantly suppressed the GST activity to a constant low level over the season. Further examination of GST cDNA indicated that in the coding region only one nucleotide variation was revealed between the susceptible and resistant strain. This variation did not cause a protein sequence change, and an identical amino acid sequence was predicted for both strains. Multiple sequence alignment and phylogenetic analysis showed that the 216-residue GST from the tarnished plant bug was highly similar (up to 68% of amino acid sequence identity) to the GSTs from other insects, which conferred organophosphate resistance. GST gene expression levels were examined using real-time PCR, and the results indicated that GST gene transcripts were elevated in the resistant strain by 1.3-fold. [Copyright &y& Elsevier]

Abstract: The in vitro study to examine the effect of different pesticides on the growth and survival of Gluconacetobacter diazotrophicus strain PAL5 was carried out. Monocrotophos, Lindane and Dichlorvos had the most lethal actions against Gluconacetobacter grown on LGIP medium, while Endosulphan, Chlorpyriphos, and Malathion effects were intermediate. Herbicides generally appeared to have no adverse effect on the growth and survival of Gluconacetobacter in the medium except for the concentrations exceeding recommended rates. Fungicides, except Ridomil, had a slight effect on the growth of Gluconacetobacter at recommended dose. With the various pesticides used, the cell morphology was affected to a larger extent resulting in larger number of pleomorphic cells. Further their influence on the physiological traits like nitrogenase activity, indole-3-acetic acid, gibberellin A3 production, and phosphate and zinc solubilizing activity are discussed. [Copyright &y& Elsevier]

Abstract: Head lice from Florida (SF-HL) and California (SC-HL) were resistant to permethrin compared with colonized susceptible lice from Panama (PA-HL) (5.5- and 3.4-fold, respectively) and Ecuador (EC-HL) (8.5- and 5.3-fold, respectively). Permethrin-resistant lice were cross-resistant to pyrethrum and DDT. DNA sequencing validated presence of kdr-type mutations (T929I and L932F). Permethrin resistance was synergized by piperonyl butoxide (PBO) in SC-HL. Resistance to malathion in SF-HL (1.4–2.2-fold) and SC-HL (2.1–3.6-fold) was detected. Malathion resistance in SF-HL was synergized by S,S,S-tributylphosphorotrithioate (DEF) and by PBO in SC-HL. Malathion/permethrin-resistant lice from the UK (BR-HL) were synergized by DEF but not synerziged by PBO. PBO protected BR-HL from malathion, indicating suppressed desulfuration. Abamectin resistance in SF-HL (1.7–2.5-fold) and SC-HL (1.8–2.3-fold) was detected. No resistance to lindane was found. Thus, multiple resistance mechanisms against commonly available and widely used pediculicides and insecticides are apparently occurring. [Copyright &y& Elsevier]

Vulpia bromoides is a grass species naturally tolerant to acetolactate synthase (ALS) and acetyl-coenzyme A carboxylase (ACCase) inhibiting herbicides. The mechanism of tolerance to ALS herbicides was determined as cytochrome P450-monooxygenase mediated metabolic detoxification. The ALS enzyme extract partially purified from V. bromoides shoot tissue was found to be as sensitive as that of herbicide susceptible Lolium rigidum to ALS-inhibiting sulfonylurea (SU), triazolopyrimidine (TP), and imidazolinone (IM) herbicides. Furthermore, phytotoxicity of the wheat-selective SU herbicide chlorsulfuron was significantly enhanced in vivo in the presence of the known P450 inhibitor malathion. In contract, the biochemical basis of tolerance to ACCase inhibiting herbicides was established as an insensitive ACCase. In vitro ACCase inhibition assays showed that, compared to a herbicide susceptible L. rigidum, the V. bromoides ACCase was moderately (4.5- to 9.5-fold) insensitive to the aryloxyphenoxypropionate (APP) herbicides diclofop, fluazifop, and haloxyfop and highly insensitive (20- to >71-fold) to the cyclohexanedione (CHD) herbicides sethoxydim and tralkoxydim. No differential absorption or de-esterification of fluazifop-P-butyl was observed between the two species at 48 h after herbicide application, and furthermore V. bromoides did not detoxify fluazifop acid as rapidly as susceptible L. rigidum. It is concluded that two co-existing resistance mechanisms, i.e., an enhanced metabolism of ALS herbicides and an insensitive target ACCase, endow natural tolerance to ALS and ACCase inhibiting herbicides in V. bromoides. [Copyright &y& Elsevier]

Resistance to organophosphorus (OP) insecticides in Lucilia cuprina arises from two mutations in carboxylesterase E3 that enable it to hydrolyse the phosphate ester of various organophosphates, plus the carboxlyester in the leaving group in the case of malathion. These mutations are not found naturally in the orthologous EST23 enzyme in Drosophila melanogaster. We have introduced the two mutations (G137D and W251L) into cloned genes encoding E3 and EST23 from susceptible L. cuprina and D. melanogaster and expressed them in vitro with the baculovirus system. The ability of the resultant enzymes to hydrolyse the phosphate ester of diethyl and dimethyl organophosphates was studied by a novel fluorometric assay, which also provided a sensitive titration technique for the molar amount of esterase regardless of its ability to hydrolyse the fluorogenic substrate used. Malathion carboxylesterase activity was also measured. The G137D mutation markedly enhanced (>30-fold) hydrolysis of both classes of phosphate ester by E3 but only had a similar effect on the hydrolysis of dimethyl organophosphate in EST23. Introduction of the W251L mutation into either gene enhanced dimethyl (23–30-fold) more than diethyl (6–10-fold) organophosphate hydrolysis and slightly improved (2–4-fold) malathion carboxylesterase activity, but only at high substrate concentration. [Copyright &y& Elsevier]

The neuropeptide adipokinetic hormone (AKH) binds to the AKH receptor (AKHR) to regulate carbohydrate and lipid metabolism. It also participates in the insect anti-stress response. We used RT-qPCR to detect the expression levels of 39 neuropeptides in malathion-susceptible (MS) and malathion-resistant (MR) strains of Bactrocera dorsalis. AKH and AKHR were highly expressed in the MR strain. Using a malathion bioassay and RNA interference (RNAi), we demonstrated that AKHR is involved in the susceptibility of B. dorsalis to malathion. We found significantly reduced expression of two detoxification enzyme genes (glutathione-S-transferase , GST and α-esterase , CarE) after AKHR RNAi. Based on our previous data, GSTd10 and CarE6 participate the direct metabolism of malathion in this fly, which is also verified by a malathion metabolism assay by HPLC using the crude enzymes in the current study. These results suggest that AKHR plays an important role in affecting malathion susceptibility via detoxification enzyme genes. [Display omitted] • AKH and its receptor AKHR were highly expressed in the malathion-resistant strain of B. dorsalis. • RNAi of AKHR reduced the expression of GST and CarE that are responsible for malathion metabolism. • RNAi of AKHR reduced the sensitivity of B. dorsalis to malathion. [ABSTRACT FROM AUTHOR]

Most of approximately 1.8 billion people involved in agriculture protect their food products using pesticides especially insecticides which may remain in foods as pesticide residues. Among insecticides organophosphates such as malathion have been widely used around the world and others such as parathion has been restricted because of their toxicity. Carvacrol (CAR) is the main component of Satureja khuzestanica. Since chemical composition of foods can alter toxicity of pesticides, in this work, the effect of coadministration of CAR and organophosphates on renal function has been studied and compared with the effect of coadministration of carvacrol loaded beta cyclodextrin-alginate-chitosan (BAC) based nanoflowers. Serum levels of urea and creatinine and histological examination were analyzed after 10 days of administration of chemicals. Malathion and parathion significantly increased urea and creatinine and induced renal inflammation. However, coadministration of CAR or BAC-CAR modified urea and creatinine and improved renal inflammation. BAC-CAR modified serum levels of urea more efficient than CAR (P < 0.05). It is concluded that BAC could be considered as a carrier for drugs used to treat renal disorders. Carvacrol can be used in the formulation of organophosphate pesticides, which may control pests more efficiently than conventional organophosphate pesticides. Unlabelled Image • Most of approximately 1.8 billion people are involved in agriculture. • Carvacrol can be loaded on beta cyclodextrin-alginate-chitosan (BAC) nanoflowers. • Malathion and parathion significantly increased renal injury. • Coadministration of CAR or BAC-CAR modified improve renal injury • CAR or BAC-CAR can be used in the formulation of organophosphate pesticides [ABSTRACT FROM AUTHOR]