Assessing the combined toxicity of conventional and newer insecticides on the cotton mealybug <Emphasis Type="Italic">Phenacoccus solenopsis</Emphasis>

Reduced susceptibility to insecticides often results in failure of insect pest control and repetitive use of broad-spectrum insecticides, which could have detrimental effects on beneficial arthropods and surrounding agro-ecosystems. The cotton mealybug, Phenacoccus solenopsis Tinsley is a pest of worldwide importance that can be effectively controlled using a number of insecticides. This insect has developed resistance due to injudicious use and repeated exposure to insecticides throughout the year. The aim of the present study was to investigate the toxicity of the insecticides chlorpyrifos, deltamethrin, spinosad, emamectin benzoate and indoxacarb tested either singly or in combination on laboratory susceptible (Lab-PK) and field population (Field Pop) of P. solenopsis. In the Field Pop, combination of chlorpyrifos with either spinosad or emamectin benzoate or indoxacarb showed a synergistic effect at 1:1, 1:10 and 1:20. The combination of deltamethrin with either emamectin benzoate or indoxacarb at all ratios showed synergistic effect, while the combination of deltamethrin with spinosad at 1:1 and 1:20 ratios showed antagonistic effects and that at 1:10 ratio showed synergistic effect against Field Pop. The results of synergism experiments using piperonyl butoxide (PBO) and S,S,S-tributylphosphorotrithioate (DEF) enzyme inhibitors, when combined with insecticides against the Field Pop, toxicities of all tested insecticides were significantly increased. The present study suggests that insecticide combinations and synergism could help achieve effective control of less susceptible populations of P. solenopsis. This would contribute to suitably managing resistance of this pest to insecticides with reduced negative impacts on the surrounding environment.     

Pyrethroids and piperonyl-butoxide affect human T-lymphocytes in vitro.

Synthetic pyrethroids are increasingly used as insecticides and are claimed to have a relatively low human toxicity. The aim of this study was to examine the in vitro effects of the synthetic pyrethroid S-bioallethrin alone and in combination with the common synergist piperonyl-butoxide (PBO) on human blood lymphocytes and basophils in atopic individuals and non-atopic control subjects. S-bioallethrin and PBO also caused inhibition of lymphocyte proliferation (MTT-test) after a 72-h culture period in a concentration dependent manner. In contrast to the MTT-measurements the combined agents are more effective in inhibiting interleukin-4 (IL-4)- and interferon-gamma (IFN-gamma)-production. The regulatory IL-4/IFN-gamma balance showed a significant difference between atopic and non-atopic subjects after a culture period of 24-48 h in the presence of micromolar S-bioallethrin (P < 0.001). Furthermore S-bioallethrin, PBO and the combined agents induced histamine release from human basophils. Although this effect was little compared to histamine liberators like FMLP and anti-IgE, the response to S-bioallethrin and PBO was significantly different in atopic donors compared with non-atopics (P < 0.01). In scratch test experiments 4 of 18 tested atopic volunteers showed positive reaction (wheals and flares) to S-bioallethrin and permethrin, whereas no reaction could be measured in the control group (age-matched). These findings demonstrate the immuno- and allergo-toxicological properties of the synthetic pyrethroid S-bioallethrin combined with the synergistic PBO using this in vitro approach with human lymphocytes and basophils.     

Oxidation of pesticides by purified cytochrome P-450 isozymes from mouse liver

5 cytochrome P-450 isozymes were purified from the livers of uninduced mice and reconstituted with purified NADPH cytochrome P-450 reductase and phospholipid. The pesticides parathion, fonofos, DEF, Mocap and profenofos were oxidized by the reconstituted monooxygenase system to form acetylcholinesterase (AChE) inhibitors. The bioactivation varied with the pesticide substrate and the cytochrome P-450 isozyme. Aldrin epoxidation occurred with all 5 isozymes, with cytochrome P-450 A1 being the most active. All fraction metabolized the pesticide synergist piperonyl butoxide (PBO) to form an inhibitory cytochrome P-450-PBO-metabolite complex. The reduced complex produced a spectrum in the Soret region which was characteristic for each of the cytochrome P-450 isozymes. Inhibition of aldrin epoxidation by PBO was found to be unrelated to the nature of the Soret spectrum.     

Malaria vector control strategies. What is appropriate towards sustainable global eradication?

Malaria a mosquito-borne disease caused by Plasmodium remains to be a main global burden despite concerted efforts to eliminate it. While diverse control strategies have been put in place for mosquito-borne diseases, vector control continues to be a critical component in infection prevention. Vector control majorly focuses on the eradication of mosquitoes using a variety of chemical insecticides that includes organochlorides, carbamates, organophosphates, and pyrethroids. The use of conventional insecticide-based as mosquito control strategies poses several challenges such as the widespread development of insecticide resistance, environmental damage concerns, and effects on non-target organisms. These challenges create a demand for the development and use of alternative pest control strategies that are sustainable, safer, and environmentally friendly to mosquito vector management. This review provides insight into alternative sustainable interventions for mosquito vector control in the form of biorational pesticides. Biorational pesticides are pesticides that have little or no effect on humans and environments and include entomopathogenic microorganisms, insect growth regulators, and endosymbiotic bacteria. It also puts into perspective their environmental impacts, benefits, and challenges. Further, countries like Sri Lanka, that are certified as malaria free by World Health Organization (WHO) incorporated the use of entomopathogenic bacteria, insect growth regulators and larvivorous fish in their national vector control programs leading to the successful elimination of malaria in 2016. We therefore highlight success stories of the countries that have implemented these interventions bringing out the lessons for countries that are battling malaria epidemics.     

Elevation of cell proliferation via generation of reactive oxygen species by piperonyl butoxide contributes to its liver tumor-promoting effects in mice

Piperonyl butoxide (PBO) is a pesticide synergist used with pyrethroids as a domestic insecticide, and it acts as a non-genotoxic hepatocarcinogen in rats and mice. To clarify whether oxidative stress is involved in the liver tumor-promoting effect of PBO in mice, male mice were subjected to two-thirds partial hepatectomy, followed by N-diethylnitrosamine (DEN) treatment, and given a diet containing 0.6% PBO for 25 weeks. The incidences of cytokeratin (CK) 8/18-positive foci, adenomas, and carcinomas significantly increased in the DEN + PBO group compared with the DEN-alone group. The PCNA-positive ratio significantly increased in non-tumor hepatocytes, CK8/18-positive foci and adenomas in the DEN + PBO group compared with the DEN-alone group. PBO increased reactive oxygen species (ROS) production in microsomes but did not change oxidative DNA damage as assessed by 8-hydroxydeoxyguanosine (8-OHdG). In real-time RT–PCR, PBO upregulated the expression of genes related to metabolism, such as Cytochrome P450 1a1, 2a5, and 2b10, and metabolic stress, such as Por and Nqo1, but downregulated Egfr and Ogg1. PBO also increased early response genes downstream of mitogen-activated protein kinase (MAPK), such as c-Myc that is induced by excessive ROS production, and G1/S transition-related genes, such as E2f1 and Ccnd1. Thus, PBO can generate ROS via the metabolic pathway without any induction of oxidative DNA damage, activate cell growth, increase c-Myc- and E2F1-related pathways, and act as a liver tumor promoter of DEN-induced hepatocarcinogenesis in mice.     

Influence of pyrethroids and piperonyl butoxide on the Ca(2+)-ATPase activity of rat brain synaptosomes and leukocyte membranes

Pyrethroids are widely used insecticides of low acute toxicity in mammals but the consequences of long-term exposure are of concern. Their insecticidal action is related to neurotoxicity and, in addition, there are indications of mammalian immunotoxicity. In order to clarify structure-activity relationships of the membrane interactions of pyrethroids, the present study compared the influence of selected pyrethroids, i.e. permethrin and the more water soluble esbiol (S-bioallethrin), both type I, and cyfluthrin, type II, on the Ca(2+)-ATPase activity of rat brain synaptosomes and peritoneal leukocyte membranes. The pyrethroids were tested alone as well as mixed with the enhancing substance piperonyl butoxide (PBO) at concentration ratios of 1:5 and 1:10. At the highest concentration tested, permethrin (10 microM) alone inhibited the ATPase activity of leukocyte membranes by 20%, whereas the synaptosomes were affected less. Esbiol and cyfluthrin alone did not affect either membrane preparation significantly, whereas PBO (50 microM) alone caused 10-15% inhibition. Mixtures of either pyrethroid with PBO inhibited the ATPase activity of both types of membranes (up to 40% inhibition) in a synergistic manner, which always tended to be supra-additive. With esbiol a true potentiation took place. The synergistic interaction between pyrethroid and PBO was most apparent with mixtures of a concentration ratio of 1:5. The ATPase activity of leukocyte membranes tended to be more susceptible to inhibition than that of synaptosomes. The results are in accordance with the assumption that the mammalian toxicity of pyrethroids can be ascribed to a general disturbance of cell membrane function in neuronal tissue. The results indicate that it may also be the case in the immune apparatus.     

Acute effects of binary mixtures of Type II pyrethroids and organophosphate insecticides on <Emphasis Type="Italic">Oreochromis niloticus</Emphasis>

Pyrethroid and organophosphate insecticides have been used for more than 20 years worldwide to control a variety of insect pest in different settings. These pesticides have been detected in a variety of environmental samples, including surface waters and sediments and therefore there is significant concern about their potential toxic effects on non-target organisms. Mixtures of compounds from these groups of pesticides have been found to frequently show enhanced toxicity but it has been a challenge to predict whether or not enhanced toxicity will occur for a given combination of compounds. This study therefore studied the effects of binary pyrethroid-organophosphate mixtures using cypermethrin, deltamethrin and dimethoate in an acute toxicity test system with Oreochromis niloticus. The 96?h LC50s for individual insecticides were 9.13?µg/l, 9.42?µg/l and 45.52?mg/l for cypermethrin, deltamethrin and dimethoate respectively. These showed that the pyrethroid insecticides were highly toxic to Oreochromis niloticus and were far more toxic than dimethoate. All mixtures were also more toxic than single insecticides throughout the concentration-response curve with mixtures resulting in mortality at concentrations which the individual pesticides in the mixture were below their respective NOECs. In addition, observed mixture toxicities deviated from the predicted mixture effects based either on the Concentration Addition (CA) or Independent Action (IA) models independent of mixture ratio. However, the extent of observed mixture mortality deviation was dependent on the effect level. Significant deviations (MDR?>?2.0) were observed at lower concentrations indicating synergistic effects at lower and possibly environmentally relevant concentrations. This is not unexpected since organophosphate insecticides are known to inhibit acetylcholinesterase as well as inactivate esterase, resulting in reduced detoxification of pyrethroid insecticides and consequently greater toxicity than would be expected. This has important implications for risk assessment of mixtures since the risk of pyrethroid-organophosphate mixtures may be underestimated if either the CA or IA model is employed.     

Piperonyl butoxide enhances the bioconcentration and photoinduced toxicity of fluoranthene and benzo[a]pyrene to larvae of the grass shrimp (Palaemonetes pugio)

Piperonyl butoxide (PBO) is a commonly used synergist in many pyrethroid formulations due to its ability to interfere with cytochrome P450 (CYP) monooxygenases. Because PBO can co-occur in the estuarine environment with polycyclic aromatic hydrocarbons (PAHs), a class of compounds metabolized by CYP isozymes, the overall objective of this study was to investigate the influence of PBO on the bioconcentration and photoinduced toxicity of two common PAH contaminants, fluoranthene (FLU) and benzo[a]pyrene (BaP), on the larvae of the grass shrimp (Palaemonetes pugio). PBO alone was not particularly toxic to grass shrimp larvae. In dark exposures and under simulated sunlight (UV-A=211.0+/-7.0 microW/cm(2), UV-B=9.8+/-2.4microW/cm(2)), 96-h LC(50) values were similar (814.4 and 888.6 microg/L, respectively), suggesting that PBO toxicity is not enhanced in the presence of sunlight. The presence of sublethal concentrations of PBO in single PAH toxicity tests increased the bioconcentration of the two tested PAHs, and these increases were greatest at the lowest tested PAH concentrations. Mean bioconcentration factors (BCF) at the three lowest FLU and BaP treatments increased 14.3- and 7.1-fold, respectively, in the low PBO (127 microg/L) exposure compared to that of the no PBO exposure. Under simulated sunlight, PBO exposure also increased the photoinduced toxicity of the two tested PAHs, and this increase occurred in a PBO concentration-dependent fashion. For FLU, 96-h LC(50) values decreased from 2.35 microg/L in the absence of PBO to 0.76 microg/L in the high PBO (256 microg/L) exposure. For BaP, 96-h LC(50) values similarly decreased from 1.02 microg/L in the absence of PBO to 0.30microg/L in the high PBO exposure. The presence of PBO also influenced the PAH tissue residue-response relationship, but in different ways for FLU and BaP. For FLU, slopes of the tissue residue-response relationship decreased in the presence of PBO, and for BaP, there was a trend towards increased slopes in the presence of PBO. These results demonstrate that sublethal levels of PBO increase the bioconcentration and photoinduced toxicity of certain PAH in grass shrimp larvae, and underscore the need to consider the potential for PBO to synergize the toxicity of co-occurring environmental contaminants in future risk assessments.     

Pesticide genotoxicity in cotton picking women in Pakistan evaluated using comet assay

To control agricultural pests and meet the increasing food demands, pesticides use has been increased substantially over time. Although pesticides are relatively specific to their targets, they can affect non-target organisms and are hazardous for the population around the application areas particularly to the individuals engaged in different types of agricultural activities. This situation is worse in developing and under-developed countries where personal protective equipment is merely used and regulatory guidelines are hardly practiced. In the present study, DNA damage in women exposed to pesticides while picking cotton with bare hands was assessed using single cell gel electrophoresis assay or comet assay. The presence of pesticides in blood serum of exposed individuals was also analyzed using high-performance liquid chromatography. Blood samples were collected from 138 (69 exposed and 69 control) randomly selected females from a major cotton growing area (Bahawalpur District) of the Punjab province of Pakistan. DNA damage, as determined by the mean comet tail length, was significantly higher (p?p?相似文献   

Evaluation of in vivo liver genotoxic potential of Wy-14,643 and piperonyl butoxide in rats subjected to two-week repeated oral administration

Wy-14,643 (WY), a peroxisome proliferator-activated receptor-alpha agonist, and piperonyl butoxide (PBO), a pesticide synergist, induce oxidative stress and promote hepatocarcinogenesis in the liver of rodents. These chemicals belong to a class of non-genotoxic carcinogens, but DNA damage secondary to the oxidative stress resulting from reactive oxygen species generation is suspected in rodents given these chemicals. To examine whether WY or PBO have DNA-damaging potential in livers of rats subjected to repeated oral administration for 14 days, the in vivo liver comet assay was performed in partially hepatectomized rats, and the expression of some DNA-repair genes was examined. Then, to examine whether they have genotoxic potential, the in vivo liver initiation assay was performed in rats. In the comet assay, positive results were obtained at 3 h after the last treatment of WY, and some DNA-repair genes such as Apex1, Mlh1, Xrcc5, and Gadd45 were up-regulated in the liver. In the liver initiation assay, negative results were obtained for both WY and PBO. The results of the present study suggest that WY, but not PBO, causes some DNA damage in livers of rats, but such DNA damage was repaired by the increased activity of some DNA repair genes and may not lead to a DNA mutation.     

Comparative study on pesticide mixture of organophosphorus and pyrethroid in commercial formulation

The marketing of mixtures of organophosphate and pyrethroid insecticides has become very common in developing countries and has resulted in an increase in the prevalence of toxicity. The present study aimed to evaluate the toxic effects of a commercial preparation of the pesticide mixture durasin, which contains 60% diazinon and 0.5% deltamethrin, compared with the individual commercial pesticides of diazinon 30% and deltamethrin 5%. Forty male albino rats weighing 160 ± 20 g were divided into; DA (diazinon 20 mg/Kg b.w.), DA (deltamethrin 2 mg/Kg b.w.), M (durasin 20 mg/Kg b.w.) and control (C); cholinesterase (ChE), malonaldehyde (MDA), glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD), total cholesterol (TC), triglyceride (TG) and non-specific esterase's isoenzymes in rat's blood were determined following 7 and 14 days of treatment. The weekly- recorded biochemical results were used as criteria for estimating the joint effects of the tested pesticide mixture. Antioxidant defense mechanisms and lipid peroxidation in rat plasma displayed the same responses with intensities which were related to the different treatments. Biochemical analysis showed that (DA) or (DM) individually cause alteration in lipid metabolism and non-specific esterase, while mixture treatment (M) induced antagonistic effects toward all the tested parameters except total reduced glutathione level, which was synergistic at the 2nd week. In conclusion the commercial mixture (M) under study has potentially greater toxic impact than the components alone in the rat.     

The protective role of vitamin E on gill and liver tissue histopathology and micronucleus frequencies in peripheral erythrocytes of Oreochromis niloticus exposed to deltamethrin

Deltamethrin, is a commonly used pyrethroid pesticide. Vitamin E is a antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. Therefore, it was evaluated whether deltamethrin induced histopathological changes and nuclear abnormalities using micronucleus test in Oreochromis niloticus, and the possible protective effect of vitamin E against deltamethrin inducing adverse effects in O. niloticus were investigated. Fish was fed with no pesticide+control diet, no pesticide+vitamin E-supplemented diet, 1.45μg/l deltamethrin+control diet, 1.45μg/l deltamethrin+vitamin E-supplemented diet for 30 days. Pesticide and diet quality made an impact on histopathological lesions. In treatments of deltamethrin, group fed with control diet showed much greater damage in comparison with group fed with vitamin E supplemented diet. Vitamin E decreased some histopathological changes induced by deltamethrin, but did not confer complete protection. Deltamethrin treatment has been shown to results in a significant increase in the frequency of micronucleus. However, coadministration of deltamethrin and vitamin E showed decrease in the frequency of micronucleus as compared to deltamethrin treated fish. Our results indicate that, the MN assay and histopathology can be used as bioassays for monitoring pollution in aquatic medium. On the other hand, it was observed that vitamin E decreased the genotoxicity and histopathological changes induced by deltamethrin.     

Tumourigenic studies on deltamethrin in Swiss albino mice

Deltamethrin, an alpha-cyano type II synthetic pyrethroid insecticide is used to control a wide range of insects on a variety of crops. Deltamethrin is reported to cause many adverse effects on non-target species. Deltamethrin is reported to cause DNA damage and micronuclei induction in human lymphocytes. It is highly toxic for other organisms such as aquatic invertebrates, fish and Daphnia. About the tumorigenic risk (both tumour initiating and promoting) associated with deltamethrin exposure, very few reports are available in literature. In the present set of investigations, deltamethrin has been evaluated for its tumorigenic and co-carcinogenic (tumour initiating and tumour promoting) potential following long term dermal exposure in Swiss albino mice. The results revealed that deltamethrin has only tumour initiating potential in both the sexes of Swiss albino mice, initiated with deltamethrin and promoted by standard tumour promoter, 12-O-tetra decanoyl phorbol-13-acetate (TPA). In the single dose initiated mice (deltamethrin 4 mg/kg body weight, once only), 44% males and 43% females developed benign skin tumours. A much higher incidence of tumorigenesis was recorded in multiple dose initiated animals (deltamethrin 4 mg/kg body weight, three times per week for 3 weeks), where 71% male and 75% female mice developed tumours at the site of application of deltamethrin. Deltamethrin exposure failed to show any tumour promoting and complete tumorigenic potential at all the three tested dose levels.     

Toxicity and risk of permethrin and naled to non-target insects after adult mosquito management

We derived laboratory LC50 values, assessed non-target insect risks, and conducted a field bioassay for ultra-low-volume (ULV) aerosol applications of insecticides used to manage adult mosquitoes. The house cricket, Acheta domesticus (L.), was used as an indicator species for medium- to large-bodied ground dwelling insects. The 24-h LC₅₀ values for Permanone^® (formulated product of permethrin), Permanone + piperonyl butoxide (PBO), technical grade permethrin, and technical grade permethrin + PBO ranged from 0.052 to 0.9 μg/cm². The 24 h LC₅₀ for technical grade naled and Trumpet^® (formulated product of naled) were 0.038 and 0.44 μg/cm², respectively. The synergist ratio was 2.65 for Permanone + PBO and 1.57 for technical grade permethrin + PBO. The toxicity of technical grade permethrin was about 10-fold greater than Permanone. A risk assessment using modeled estimated environmental concentrations resulted in risk quotients (RQ) that exceeded regulatory levels of concern, but when compared to field-derived actual environmental concentrations RQs did not exceed a regulatory level of concern, except in the case of technical grade naled. These results were expected because higher tiered risk assessments using field-verified data generally lead to lower risk estimates. Field bioassays using caged crickets showed no significant mortality for permethrin or naled after a single truck-mounted ULV application. The results of the risk assessment using actual environmental concentrations are supported by the field bioassays and suggest that a single ULV application of synergized or unsynergized permethrin and naled most likely will not result in population impacts on medium- to large-bodied insects.     

DNA damage,immunotoxicity, and neurotoxicity induced by deltamethrin on the freshwater crayfish,Procambarus clarkii

Pyrethroid pesticides are applied to both agricultural and aquacultural industries for pest control. However, information of their impact on the commercial important freshwater crayfish, Procambarus clarkii is scarce. Therefore, the present study aimed to characterize to effects of a commonly used pyrethroid pesticide, deltamethrin on DNA damage, immune response, and neurotoxicity in P. clarkii. Animals were exposed to 7, 14, and 28 ng/L of deltamethrin, which correspond to 1/8, 1/4, and 1/2 of the LC₅₀ (96 hours) of this pyrethroid to P. clarkii. Significant increase of olive tail moment (OTM) and 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG) was found after deltamethrin exposure in a dose‐dependent way. Total hemocyte counts (THC) and activities of immune‐related enzymes including acid phosphatase (ACP), lysozyme (LZM), and phenoloxidase (PO) were all decreased and significantly lower than control at concentration of 28 ng/L after 96 hours exposure. Acetylcholinesterase (AChE) activity, an indicator of neurotoxic effect was investigated and it was decreased significantly in muscles at 14 and 28 ng/L after 24 hours exposure. The level of intracellular reactive oxygen species (ROS) in hemocytes was also measured and the significant increase of ROS was found at 14 and 28 ng/L concentrations. The results revealed that deltamethrin induced DNA damage, immunotoxicity, and neurotoxicity in P. clarkii by excessive generation of ROS. Because of the dose‐dependent responses of all parameters under exposure of deltamethrin at environmentally realistic concentrations, these parameters could be used as sensitive biomarkers for risk assessment of deltamethrin in aquaculture area.     

Protein carbonyls: novel biomarkers of exposure to oxidative stress-inducing pesticides in freshwater fish Channa punctata (Bloch)

It has been established in mammalian system including humans that direct damage to proteins or chemical modification of amino acids in proteins during oxidative stress can give rise to protein carbonyls. Protein carbonyl induction, as a biomarker of oxidative stress was used in laboratory studies to assess the toxic effects of pesticides in freshwater fish, Channa punctata (Bloch), exposed to deltamethrin, endosulfan and paraquat. Protein carbonyls were measured in gills, kidney and liver. Significant (P<0.05-0.001) increase in protein carbonyls was observed in response to single 48h exposure to various pesticides in all the tissues. The time kinetics study involving deltamethrin (0.75μg/L) also showed a significant (P<0.05-0.001) induction of protein carbonyls in all the organs. The induction was significant (P<0.05-0.001) in all the durations of exposure (12h, 96h, 7 days, 14 days, 28 days). However, relatively pronounced induction was observed during shorter duration of exposure. The findings of the present investigation showed that deltamethrin had the maximum oxidative stress-inducing potential among the three pesticides used and gills are the most sensitive organs prone to oxidative damage. It is suggested that measurement of carbonyl groups may provide a convenient technique for detecting and quantifying oxidative modification of proteins during oxidative stress. The induction of protein carbonyl in fish was identified as a potentially useful biomarker of oxidative stress that warrants its application in the field investigations.     

Estrogenicity of Organophosphorus and Pyrethroid Pesticides

Although organophosphorus and pyrethroid pesticides are considered environmental contaminants, their estrogenic potentials are still ubiquitous and unclear. The present study was undertaken to evaluate the estrogenic activities of nine pesticides (phoxim, malathion, monocrotophos, dimethoate, opunal, fenvalerate, cypermethrin, permethrin, and deltamethrin) using three in vitro methods [E-Screen assay, estrogen receptor (ER) competitive binding assay, and pS2 expression assay]. All the pyrethroid pesticides tested induced MCF-7 cell proliferation significantly, while organophosphorus pesticides did not. The estrogenic potency were ranked as permethrin > fenvalerate > cypermethrin > deltamethrin. The proliferation induced by cypermethrin, permethrin, and deltamethrin was blocked by ICI 182.780, while fenvalerate only partly inhibited it. In addition, pyrethroid pesticides inhibited the binding of [ 3 H]estradiol to ER, while the organophosphorus failed to do so. Fenvalerate, permethrin, and cypermethrin induced pS2 mRNA expression with varying potency, while there were no significant effects in deltamethrin-treated groups. Our findings provide evidence to support the idea that pyrethroid pesticides tested produce an ER-specific, agonist response. Fenvalerate induced MCF-7 cell proliferation by a mechanism not involving ER-mediated pathway. Organophosphorus pesticides tested showed no estrogenic potential. Compared with the pS2 expression assay, E-Screen was a more sensitive and useful assay for screening of the xenoestrogenic chemicals.     

Estrogenicity of organophosphorus and pyrethroid pesticides

Although organophosphorus and pyrethroid pesticides are considered environmental contaminants, their estrogenic potentials are still ubiquitous and unclear. The present study was undertaken to evaluate the estrogenic activities of nine pesticides (phoxim, malathion, monocrotophos, dimethoate, opunal, fenvalerate, cypermethrin, permethrin, and deltamethrin) using three in vitro methods [E-Screen assay, estrogen receptor (ER) competitive binding assay, and pS2 expression assay]. All the pyrethroid pesticides tested induced MCF-7 cell proliferation significantly, while organophosphorus pesticides did not. The estrogenic potency were ranked as permethrin > fenvalerate > cypermethrin > deltamethrin. The proliferation induced by cypermethrin, permethrin, and deltamethrin was blocked by ICI 182.780, while fenvalerate only partly inhibited it. In addition, pyrethroid pesticides inhibited the binding of [3H]estradiol to ER, while the organophosphorus failed to do so. Fenvalerate, permethrin, and cypermethrin induced pS2 mRNA expression with varying potency, while there were no significant effects in deltamethrin-treated groups. Our findings provide evidence to support the idea that pyrethroid pesticides tested produce an ER-specific, agonist response. Fenvalerate induced MCF-7 cell proliferation by a mechanism not involving ER-mediated pathway. Organophosphorus pesticides tested showed no estrogenic potential. Compared with the pS2 expression assay, E-Screen was a more sensitive and useful assay for screening of the xenoestrogenic chemicals.