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Introducción. El dengue es un problema de salud pública para el departamento de La Guajira. El control se ha enfocado en el vector con el uso de insecticidas, entre ellos los organofosforados. Objetivo. Evaluar el estado de la sensibilidad a insecticidas organofosforados de quince poblaciones de Aedes aegypti (L.) en el departamento de La Guajira, Colombia. Materiales y métodos. Se realizaron bioensayos para temefos, malatión y pirimifos- metil en larvas de tercer estadio y mosquitos adultos de Ae. aegypti en los municipios de Albania, Barrancas, Dibulla, Distracción, El Molino, Fonseca, Hatonuevo, La Jagua del Pilar, Maicao, Manaure, Riohacha, San Juan del Cesar, Uribia, Urumita y Villanueva, siguiendo la metodología de la Organización Mundial de la Salud (OMS) y la técnica de botellas usando la guía de los de los Centers for Disease Control and Prevention, respectivamente. Se determinó la sensibilidad por medio de la relación de resistencia a CL50 y CL95 (RRCL50, RRCL95) para temefos y a dosis y tiempo diagnóstico para temefos, malatión y pirimifos-metil en las poblaciones de campo evaluadas, usando como control la cepa sensible Rockefeller. Resultados. Las 15 poblaciones del departamento de La Guajira son sensibles a: temefos (relación de la resistencia a CL50<5,0; relación de resistencia a CL95<5,0; 98 a 100 % de mortalidad); pirimifos-metil (99 a 100 % de mortalidad) y malatión (100 % de mortalidad). Conclusión. Con base en los resultados obtenidos, es factible el uso de temefos, malatión y pirimifos-metil para el control de Ae. aegypti en las poblaciones evaluadas.
Introduction. Dengue is a public health problem in La Guajira region. Control has focused on the vector using insecticides, including organophosphates. Objective. To evaluate the state of susceptibility to organophosphates insecticides in fifteen Aedes aegypti (L.) populations in La Guajira, Colombia. Materials and methods. We collected samples of third-instar larvae and adult mosquitoes of Ae. aegypti in the municipalities of Albania, Barrancas, Dibulla, Distracción, El Molino, Fonseca, Hatonuevo, La Jagua del Pilar, Maicao, Manaure, Riohacha, San Juan del Cesar, Uribia, Urumita, Villanueva. Bioassays for temefos, malathion, and pirimiphos-methyl were carried out following the methodology of the World Health Organization, and the bottle technique using the guidance of the Centers for Disease Control and Prevention. Susceptibility to temefos was determined through the resistance ratio between lethal concentration 50 and lethal concentration 95; for the compounds temefos, malathion and pirimiphos-methyl, susceptibility was calculated using diagnostic dose and diagnostic time in the populations evaluated. Rockefeller susceptible strain was used as a control. Results. All evaluated populations of Ae. aegypti from La Guajira were found to be susceptible to temefos (ratio resistance to CL50<5.0; ratio resistance to CL95<5.0; 98 - 100 % mortality); pirimiphosmethyl (99 - 100 % mortality), and malathion (100 % mortality). Conclusion. Based on the results, the use of temefos, malathion, and pirimiphosmethyl is feasible for the control of Ae. aegypti in the evaluated populations.
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Aedes , Insecticides, Organophosphate , Temefos , Insecticide Resistance , Colombia , MalathionABSTRACT
Objective To investigate the susceptibility of Anopheles sinensis to malathion, deltamethrin and lambda-cyhalothrin in Puyang City, Henan Province, so as to provide the scientific basis for local malaria vector control. Methods An. sinensis was captured from Puyang County, Puyang City of Henan Province in September 2018 and July 2020, and the susceptibility of field captured An. sinensis to malathion, deltamethrin and lambda-cyhalothrin was tested using the filter-paper bioassay recommended by WHO. The insecticide resistance level was assessed based on the WHO criteria. Results In 2018 and 2010, the half knock-down times (KT50) of malathion were 91.08 min and 40.95 min for An. sinensis, with knock-down rates of 37.50% and 60.87% 60 min post-exposure to malathion and 24-hour mortality rates of 90.91% and 100%, respectively, and the insecticide resistance levels were moderately resistant (M) and susceptible (S). The KT50 of deltamethrin were 415.56 min and 341.19 min for An. sinensis in 2018 and 2020, with knock-down rates of 22.92% and 16.98% 60 min post-exposure to malathion and 24-hour mortality rates of 22.92% and 16.98%, and the insecticide resistance levels were all resistant (R). The KT50 of lambda-cyhalothrin were 164.22 min and 236.22 min for An. sinensis in 2018 and 2020, with knock-down rates of 30.39% and 38.30% 60 min postexposure to malathion and 24 h mortality rates of 19.60% and 21.28%, respectively, and the insecticide resistance levels were all R. Conclusion An. sinensis is relatively susceptible to malathion but has developed high-level resistance to deltamethrin and lambda-cyhalothrin in Puyang City, Henan Province..
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Resumo O agrotóxico malathion vem sendo amplamente utilizado no mundo em programas de controle de arboviroses e em 2015 foi classificado pela Agência Internacional para Pesquisas em Câncer (IARC) como provável agente carcinogênico para seres humanos. Este trabalho objetivou a sistematização das evidências dos efeitos carcinogênicos e mutagênicos associados à exposição do malathion e seus análogos, malaoxon e isomalathion. A busca foi realizada nas bases de dados TOXLINE, PUBMED e SCOPUS por artigos originais publicados de 1983 a 2015. Do total de 273 artigos elegíveis, foram selecionados 73. Os resultados dos estudos in vitro e in vivo evidenciaram danos genéticos e cromossômicos provocados pelo malathion; os estudos epidemiológicos evidenciaram associações significativamente positivas para cânceres de tireóide, de mama, e ovariano em mulheres na menopausa. Estas evidências do efeito carcinogênico do malathion devem ser considerados diante de sua utilização em programas de controle de arboviroses.
Abstract Malathion has been widely used worldwide in arbovirus control programs. In 2015, it was classified by the International Agency for Research on Cancer (IARC) as a probable carcinogen to humans. This work aimed to systematize the evidence of the carcinogenic and mutagenic effects associated with the exposure of malathion and its analogs, malaoxon and isomalathion. The search was carried out in Toxline, PubMed and Scopus databases for original papers published from 1983 to 2015. In all, 73 papers were selected from a total of 273 eligible papers. The results of in vitro and in vivo studies showed mainly genetic and chromosomal damages caused by malathion. The epidemiological studies evidenced significant positive associations for thyroid, breast, and ovarian cancers in menopausal women. This evidence of the carcinogenic effect of malathion should be considered before its use in arbovirus control programs.
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Humans , Female , Malathion/toxicity , Mutagens/toxicityABSTRACT
Objective:To investigate the effect of Cannabis sativa extract on the development of neuro- and hepato-toxicity caused by malathion injection in rats.Methods:The extract of Cannabis sativa was obtained from the plant resin by chloroform treatment. Δ-Tetrahydrocannabinol content of the extract (20%) was quantified using gas chromatography–mass spectrometry. The doses of cannabis extract were expressed as Δ -tetrahydrocannabinol content of 10 or 20 mg/kg. Malathion (150 mg/kg) was intraperitoneally administered followed after 30 min by the cannabis extract (10 or 20 mg/kg, subcutaneously). Rats were euthanized 4 h later. Malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide and paraoxonase-1 (PON-1) activity were determined in brain and liver. Brain 5-lipoxygenase and butyrylcholinesterase (BChE) activity were measured as well. Histopathological examination of brain and liver tissue was also performed.Results:Compared to controls, malathion resulted in increased oxidative stress in brain and liver. MDA and nitric oxide concentrations were significantly increased (P<0.05) and GSH significantly decreased with respect to control levels (P<0.05). Malathion also significantly inhibited PON-1 and BChE activities but had no effect on brain 5-lipoxygenase. Brain MDA concentrations were not altered by cannabis treatment. Cannabis at 20 mg/kg, however, caused significant increase in nitric oxide and restored the GSH and PON-1 activity. Brain BChE activity significantly decreased by 26.1% (P<0.05) after treatment with 10 mg/kg cannabis. Cannabis showed no effect on brain 5-lipoxygenase. On the other hand, rats treated with cannabis exhibited significantly higher levels of liver MDA, nitric oxide and PON-1 activity compared with the malathion control group. Rats treated with only malathion exhibited spongiform changes, neuronal damage in the cerebral cortex and degeneration of some Purkinje cells in the cerebellum. There were also hepatic vacuolar degeneration and dilated and congested portal vein. These histopthological changes induced by malathion in brain and liver were reduced to great extent by cannabis administration at 20 mg/kg.Conclusions:Our data suggest that acute treatment with cannabis alleviates the malathion-induced brain and hepatic injury in rats possibly by maintaining the levels of GSH and PON-1 activity.
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Objective: To investigate the effect of Cannabis sativa extract on the development of neuro- and hepato-toxicity caused by malathion injection in rats. Methods: The extract of Cannabis sativa was obtained from the plant resin by chloroform treatment. Δ-Tetrahydrocannabinol content of the extract (20%) was quantified using gas chromatography-mass spectrometry. The doses of cannabis extract were expressed as Δ -tetrahydrocannabinol content of 10 or 20 mg/kg. Malathion (150 mg/kg) was intraperitoneally administered followed after 30 min by the cannabis extract (10 or 20 mg/kg, subcutaneously). Rats were euthanized 4 h later. Malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide and paraoxonase-1 (PON-1) activity were determined in brain and liver. Brain 5-lipoxygenase and butyrylcholinesterase (BChE) activity were measured as well. Histopathological examination of brain and liver tissue was also performed. Results: Compared to controls, malathion resulted in increased oxidative stress in brain and liver. MDA and nitric oxide concentrations were significantly increased (P<0.05) and GSH significantly decreased with respect to control levels (P<0.05). Malathion also significantly inhibited PON-1 and BChE activities but had no effect on brain 5-lipoxygenase. Brain MDA concentrations were not altered by cannabis treatment. Cannabis at 20 mg/kg, however, caused significant increase in nitric oxide and restored the GSH and PON-1 activity. Brain BChE activity significantly decreased by 26.1% (P<0.05) after treatment with 10 mg/kg cannabis. Cannabis showed no effect on brain 5-lipoxygenase. On the other hand, rats treated with cannabis exhibited significantly higher levels of liver MDA, nitric oxide and PON-1 activity compared with the malathion control group. Rats treated with only malathion exhibited spongiform changes, neuronal damage in the cerebral cortex and degeneration of some Purkinje cells in the cerebellum. There were also hepatic vacuolar degeneration and dilated and congested portal vein. These histopthological changes induced by malathion in brain and liver were reduced to great extent by cannabis administration at 20 mg/kg. Conclusions: Our data suggest that acute treatment with cannabis alleviates the malathion-induced brain and hepatic injury in rats possibly by maintaining the levels of GSH and PON-1 activity.
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We reported the case of a 24-year-old male patient that arrived unconscious; with no identifable vital signs, a complete lack of response to pain stimuli and presented an extremely myotic pupils. Due to the report of his relatives we diagnosed an acute self-induced organophosphate (OP) intoxication through the ingestion of a full bottle of malathion. Endotracheal intubation, chest compressions, and manual ventilation were performed until the heart monitor showed slow myocardial activity. The patient was treated with atropine in the absence of specifc antidote (pralidoxime). A continuous peripheral IV infusion of atropine was started at a rate of 2 mg IV every 3 min. Given the constant decline in the patient's heart rate, the dose was constantly increased according to the vital sign chart until complete atropinization was achieved (heart rate over 120'). After administering a total of 760, 1 mg/ml ampules within 12 hours, a signifcant improvement was observed. The patient was discharged from the hospital 8 days later with no further complications
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Humans , Poisoning , Atropine , Pesticide Utilization , Poverty , TherapeuticsABSTRACT
OBJECTIVE We want to investigate the mechanism of organophosphate- induced delayed neuropathy (OPIDN) and find appropriate therapeutic medicine. OPIDN, often leads to pares?thesias, ataxia and paralysis, occurs in the late-stage of acute poisoning or after repeated exposures to organophosphate (OP) insecticides or nerve agents, and may contribute to the Gulf War Syndrome. METHODS FDSS Ca2 +-influx assays, single-cell calcium imaging and patch-clamp electrophysiology were the major testing techniques. Transfected HEK293 cells and dorsal root ganglion (DRG) neurons were used to evaluate the effects of compounds. Wild type and trpa1 knockout mice and adult hyline brown hens were used to evaluate the neuropathological damages caused by the OPs. Transmission electron microscopy imaging was used to observe the nerve injuries ultrastructurally. High-throughput screen for TRPA1 inhibitors was accomplished by Ion Works Barracuda (IWB) automated electrophysiology assay. RESULTS TRPA1 (Transient receptor potential cation channel, member A1) channel mediates OPIDN. A variety of OPs, exemplified by malathion, activates TRPA1 but not other neuronal TRP channels. Malathion increases the intracellular calcium levels and upregulates the excitability of mouse DRG neurons in vitro. Mice with repeated exposures to malathion also develop local tissue nerve injuries and pain-related behaviors, which resembles the early symptoms of OPIDN. Both the neuropathological changes and the nocifensive behaviors can be attenuated by treatment of TRPA1 antagonist HC030031 or abolished by knockout of Trpa1 gene. In the classic hens OPIDN model, malathion causes nerve injuries and ataxia to a similar level as the positive inducer tri-ortho-cresyl phosphate (TOCP), which also activates TRPA1 channel. Treatment with HC030031 reduces the damages caused by malathion or TOCP. Duloxetine and Ketotifen, two commercially available drugs exhibiting TRPA1 inhibitory activity, show neuroprotective effects against OPIDN and might be used in emergency situations. CONCLUSION TRPA1 is the major mediator of OPIDN and targeting TRPA1 is an effective way for the treatment of OPIDN.
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Objective To investigate the effect of N
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OBJECTIVE@#To investigate the effect of N-nitro-l-arginine methyl ester (l-NAME), a non-selective nitric oxide synthase (NOS) inhibitor, and 7-nitroindazole (7-NI), a selective neuronal NOS inhibitor, on oxidative stress and tissue damage in brain and liver and on DNA damage of peripheral blood lymphocytes in malathion intoxicated rats.@*METHODS@#Malathion (150 mg/kg) was given intraperitoneally (i.p.) along with l-NAME or 7-NI (10 or 20 mg/kg, i.p.) and rats were euthanized 4 h later. The lipid peroxidation product malondialdehyde (MDA), nitric oxide (nitrite), reduced glutathione (GSH) concentrations and paraoxonase-1 (PON-1) activity were measured in both brain and liver. Moreover, the activities of glutathione peroxidase (GPx) acetylcholinesterase (AChE), and butyrylcholinesterase (BChE), total antioxidant capacity (TAC), glucose concentrations were determined in brain. Liver enzyme determination, Comet assay, histopathological examination of brain and liver sections and inducible nitric oxide synthase (iNOS) immunohistochemistry were also performed.@*RESULTS@#(i) Rats treated with only malathion exhibited increased nitric oxide and lipid peroxidation (malondialdehyde) accompanied with a decrease in GSH content, and PON-1 activity in brain and liver. Glutathione peroxidase activity, TAC, glucose concentrations, AChE and BChE activities were decreased in brain. There were also raised liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and increased DNA damage of peripheral blood lymphocytes (Comet assay). Malathion caused marked histopathological changes and increased the expression of iNOS in brain and liver tissues. (ii) In brain of malathion-intoxicated rats, l-NAME or 7-NI resulted in decreased nitrite and MDA contents while increasing TAC and PON1 activity. Reduced GSH and GPx activity showed an increase by l-NAME. AChE activity increased by 20 mg/kg l-NAME and 10 mg/kg 7-NI. AChE activity decreased by the higher dose of 7-NI while either dose of 7-NI resulted in decreased BChE activity. (iii) In liver of malathion-intoxicated rats, decreased MDA content was observed after l-NAME or 7-NI. Nitrite level was unchanged by l-NAME but increased after 7-NI which also resulted in decreased GSH concentration and PON1 activity. Either inhibitor resulted in decreased liver ALT activity. (iv) DNA damage of peripheral blood lymphocytes was markedly inhibited by l-NAME or 7-NI treatment. (v) iNOS expression in brain and liver decreased by l-NAME or 7-NI. (vi) More marked improvement of the histopathological alterations induced by malathion in brain and liver was observed after 7-NI compared with l-NAME.@*CONCLUSIONS@#In malathion intoxicated rats, the neuronal NOS inhibitor 7-NI and to much less extent l-NAME were able to protect the brain and liver tissue integrity along with improvement in oxidative stress parameters. The decrease in DNA damage of peripheral blood lymphocytes by NOS inhibitors also suggests the involvement of nitric oxide in this process.
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Objective To study the effect of citric acid given alone or combined with atropine on brain oxidative stress, neuronal injury, liver damage, and DNA damage of peripheral blood lymphocytes induced in the rat by acute malathion exposure. Methods Rats were received intraperitoneal (i.p.) injection of malathion 150 mg/kg along with citric acid (200 or 400 mg/kg, orally), atropine (1 mg/kg, i.p.) or citric acid 200 mg/kg + atropine 1 mg/kg and euthanized 4 h later. Results Malathion resulted in increased lipid peroxidation (malondialdehyde) and nitric oxide concentrations accompanied with a decrease in brain reduced glutathione, glutathione peroxidase (GPx) activity, total antioxidant capacity (TAC) and glucose concentrations. Paraoxonase-1, acetylcholinesterase (AChE) and butyrylcholinesterase activities decreased in brain as well. Liver aspartate aminotransferase and alanine aminotransferase activities were raised. The comet assay showed increased DNA damage of peripheral blood lymphocytes. Histological damage and increased expression of inducible nitric oxide synthase (iNOS) were observed in brain and liver. Citric acid resulted in decreased brain lipid peroxidation and nitric oxide. Meanwhile, glutathione, GPx activity, TAC capacity and brain glucose level increased. Brain AChE increased but PON1 and butyrylcholinesterase activities decreased by citric acid. Liver enzymes, the percentage of damaged blood lymphocytes, histopathological alterations and iNOS expression in brain and liver was decreased by citric acid. Meanwhile, rats treated with atropine showed decreased brain MDA, nitrite but increased GPx activity, TAC, AChE and glucose. The drug also decreased DNA damage of peripheral blood lymphocytes, histopathological alterations and iNOS expression in brain and liver. Conclusions The study demonstrates a beneficial effect for citric acid upon brain oxidative stress, neuronal injury, liver and DNA damage due to acute malathion exposure.
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Objective To understand the status of resistance to multiple insecticides and the frequencies of kdr mutations in Culex pipiens pallens from north?central Anhui Province. Methods From July to September,2014,the C. pipiens pallens mosquito larvae were collected in Huaibei,Bengbu and Chuzhou cities of the north?central Anhui Province and reared to adults. The female adult mosquitoes at 3-5 days post emergence were tested for susceptibility to the four insecticides,namely 0.05%deltamethrin,5%malathion,0.1%bendiocarb and 4%DDT,by using the standard WHO resistance tube bioassay. The detec?tion of the point mutations of the kdr gene at codon 1014 was conducted by PCR and DNA sequencing in the deltamethrin?resis?tant and?susceptible mosquitoes. Results High levels of resistance to all the four insecticides were found in all the three tested populations,although mosquito mortality varied among populations and test insecticides. Among the test insecticides,DDT showed lowest mortality with no significant difference(F=1.027,P>0.05)in all test populations,whereas significantly differ?ent mortalities were observed among populations for the remained three insecticides tested(deltamethrin,malathion,and ben?diocarb)(F = 23.823,33.955,128.841;all P < 0.01). Two types of non?synonymous kdr mutation at codon position 1014 (L1014F and L1014S)were observed. A positive correlation between L1014F mutation frequencies and deltamethrin resistance levels were detected in the three mosquito populations(r2=0.718,P<0.01). Conclusions The observed high levels of resis?tance to multiple?insecticides coupled with the occurrence of medium to high kdr frequencies in populations of C. pipiens pallens could profoundly affect the mosquito vector control programme in China. The local health departments need to strengthen vector dynamic monitoring and implement rational resistance management strategies.
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OBJECTIVE@#To study the effect of citric acid given alone or combined with atropine on brain oxidative stress, neuronal injury, liver damage, and DNA damage of peripheral blood lymphocytes induced in the rat by acute malathion exposure.@*METHODS@#Rats were received intraperitoneal (i.p.) injection of malathion 150 mg/kg along with citric acid (200 or 400 mg/kg, orally), atropine (1 mg/kg, i.p.) or citric acid 200 mg/kg + atropine 1 mg/kg and euthanized 4 h later.@*RESULTS@#Malathion resulted in increased lipid peroxidation (malondialdehyde) and nitric oxide concentrations accompanied with a decrease in brain reduced glutathione, glutathione peroxidase (GPx) activity, total antioxidant capacity (TAC) and glucose concentrations. Paraoxonase-1, acetylcholinesterase (AChE) and butyrylcholinesterase activities decreased in brain as well. Liver aspartate aminotransferase and alanine aminotransferase activities were raised. The comet assay showed increased DNA damage of peripheral blood lymphocytes. Histological damage and increased expression of inducible nitric oxide synthase (iNOS) were observed in brain and liver. Citric acid resulted in decreased brain lipid peroxidation and nitric oxide. Meanwhile, glutathione, GPx activity, TAC capacity and brain glucose level increased. Brain AChE increased but PON1 and butyrylcholinesterase activities decreased by citric acid. Liver enzymes, the percentage of damaged blood lymphocytes, histopathological alterations and iNOS expression in brain and liver was decreased by citric acid. Meanwhile, rats treated with atropine showed decreased brain MDA, nitrite but increased GPx activity, TAC, AChE and glucose. The drug also decreased DNA damage of peripheral blood lymphocytes, histopathological alterations and iNOS expression in brain and liver.@*CONCLUSIONS@#The study demonstrates a beneficial effect for citric acid upon brain oxidative stress, neuronal injury, liver and DNA damage due to acute malathion exposure.
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BACKGROUND: Workers in pesticide manufacturing industries are constantly exposed to pesticides. Genetic biomonitoring provides an early identification of potential cancer and genetic diseases in exposed populations. The objectives of this biomonitoring study were to assess DNA damage through comet assay in blood samples collected from industry workers and compare these results with those of classical analytical techniques used for complete blood count analysis. METHODS: Samples from controls (n = 20) and exposed workers (n = 38) from an industrial area in Multan, Pakistan, were subjected to various tests. Malathion residues in blood samples were measured by gas chromatography. RESULTS: The exposed workers who were employed in the pesticide manufacturing industry for a longer period (i.e., 13-25 years) had significantly higher DNA tail length (7.04 μm) than the controls (0.94 μm). Workers in the exposed group also had higher white blood cell and red blood cell counts, and lower levels of mean corpuscular hemoglobin (MCH), MCH concentration, and mean corpuscular volume in comparison with normal levels for these parameters. Malathion was not detected in the control group. However, in the exposed group, 72% of whole blood samples had malathion with a mean value of 0.14 mg/L (range 0.01-0.31 mg/L). CONCLUSION: We found a strong correlation (R2 = 0.91) between DNA damage in terms of tail length and malathion concentration in blood. Intensive efforts and trainings are thus required to build awareness about safety practices and to change industrial workers' attitude to prevent harmful environmental and anthropogenic effects.
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Blood Cell Count , Chromatography, Gas , Comet Assay , DNA , DNA Damage , Environmental Monitoring , Erythrocyte Count , Erythrocyte Indices , Hematologic Tests , Leukocytes , Malathion , Occupations , Pakistan , Pesticides , TailABSTRACT
Malathion is an organophosphorous insecticide, used worldwide for pest and disease control; however, it could also affect the reproductive patterns of several species. The aim of this study was to determine the effects of malathion in the cellularity and sperm differentiation in testis and epididymis of rats. Twenty adult male Sprague Dawley rats were divided into a malathion-treated group (n=10, dose of 170 mg/kg via subcutaneous injection for a period of 13 days) and control group (n=10, injected only with normal saline). After treatments, the rats were sacrificed by regulated euthanasia and assessed for sperm count in testis and epididymis and epididymal teratospermia degree. The results showed a significant decrease in body, testicular and epididymal weight in animals treated with malathion. Testicular sperm counts in treated rats exhibited a significant decrease in the number of sperm compared to controls (42.56x106 vs. 95.99x106), as well as in epididymis (77.55x106 vs. 106.54x106). Concerning the degree of teratospermia, a significant increase of abnormal sperm in the epididymis of treated rats versus controls (42.1% vs. 21%, respectively) was observed. We conclude that malathion has a cytotoxic effect in rats, significantly reducing the number of sperm produced by the seminiferous tubules and affecting their quality and number during the process of maturation and capacitation in their transit through the epididymis, thus increasing the level of teratospermia.
El malatión es un insecticida organofosforado, ampliamente usado en el control de plagas y pestes, sin embargo también puede afectar a los patrones reproductivos de las especies. El objetivo de este trabajo fue determinar los efectos de malatión en la celularidad y diferenciación de espermatozoides en testículo y en epidídimo de ratas. Veinte ratas macho adultas de la cepa Sprague Dawley, fueron divididos en grupo tratado con malatión (n=10) en dosis de 170 mg/kg de peso, inyección sub cutánea (s.c.), por un período de 13 días (duración del ciclo del epitelio seminífero) y grupo control (n=10), los cuales solo fueron inyectados con suero fisiológico. Finalizado el tratamiento las ratas fueron sacrificadas por eutanasia normada y se procedió a medir el recuento espermático en testículo y epidídimo y el grado de teratospermia en epidídimo. Los resultados obtenidos muestran una disminución significativa en el peso corporal, testicular y del epidídimo de ratas machos tratados con malatión. El recuento espermático en testículo de ratas tratadas, al compararlos con ratas controles, muestra una disminución significativa en el número de espermatozoides (42,56x106 / 95,99x106), igual comportamiento se observó en epidídimo (77,55 x106 / 106,54 x106). Al determinar el grado de teratospermia se observó un aumento significativo de espermatozoides anormales, en el epidídimo de las ratas tratadas versus los controles (42,1% y 21%, respectivamente). Se concluye que malatión tiene un efecto citotóxico en ratas, disminuyendo significativamente el número de espermatozoides producidos por los túbulos seminíferos y afectando la calidad y el número de ellos durante el proceso de maduración y capacitación, en su tránsito por el epidídimo, aumentando el nivel de teratospermia.
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Male , Reproduction/drug effects , Spermatozoa/drug effects , Testis/drug effects , Malathion/toxicity , Cell Differentiation/drug effects , Rats, Sprague-Dawley , Epididymis/drug effects , Insecticides, Organophosphate/adverse effectsABSTRACT
OBJECTIVE To investigate the effects of aerobic exercise on enteric nervous injury in rats exposed to malathion.METHODS Adult male Wistar rats were treated with non-load swi mming every other day,three ti mes a week,each one hour,for six weeks.Before exercise,the rats were trea-ted with malathion 100 mg·kg -1·d -1 by oral gavage,six days a week,for six weeks.The activities of seru m acetylcholinesterase(AChE)and butyrocholinesterase(BuChE)were determined.In addition,the s mall intestinal propulsion indexes were measured.Also,the distribution of nerve plexus in ileu m was observed.The i mmunohistoche mical method was used to measure the levels of protein gene-related petide 9.5 (PGP9.5),substance P (SP),and vasoactive intestinal peptide (VIP).RESULTS Co m-pared with normal control,malathion exposure decreased the activities of seru m AChE and BuChE (P<0.01 ),increased the s mall intestinal propulsion indexes (P <0.05).In addition,the levels of PGP9.5 decreased (P<0.05).At the sa me ti me,the levels of SP increased,and the levels of VIP decreased (P<0.05).Aerobic exercise did not change the activites of cholinesterases,but decreased s mall intes-tinal propulsion indexes,increased the levels of PGP9.5,decreased the levels of SP,and increased the levels of VIP.Co mpared with the malathion exposure only,the rats in malathion ad ministration co mbined with aerobic exercise group de monstrated much lower activites of cholinesterase (P <0.01 ),and the s mall intestinal propulsion indexes decreased fro m (89 ±4)% to (79 ±5)%(P <0.01 ).Moreover,the levels of PGP9.5 increased fro m 0.012 ±0.003 to 0.029 ±0.015 (P <0.01 ).At the sa me ti me,the levels of SP decreased fro m0.174 ±0.067 to 0.1 10 ±0.057(P<0.05),and the levels of VIP increased fro m 0.0076 ±0.0029 to 0.01 1 1 ±0.0047 (P <0.05).The levels of above para meters were sa me or close to those of the normal control.CONCLUSION Malathion exposure induced disorders of enteric nervous syste m in rats,and the aerobic exercise abated the toxic response in enteric nervous syste m of malathion exposure rats.However,these effects were not mediated through recovery of cholinesterases inhibition.
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Dada la presencia colinérgica en el sistema nociceptivo y la frecuente exposición al malatión, plaguicida organofosforado inhibidor de la Acetilcolinesterasa, se evaluó el impacto del aumento en el tono colinérgico inducido por la exposición a dosis bajas de malatión sobre la conducta nociceptiva y motora en ratas. Se estudiaron 20 ratas Sprague Dawley, machos (350-400g); en un grupo control (n=10) se inyectó 1mL NaCl 0,9% diario (i.p.) y a un grupo experimental (n=10) se inyectó 1mL de malatión (40mg.Kg-1.dia-1, en NaCl 0,9%, i.p) diario por 7 días. Se evaluó el primero, cuarto y séptimo día de tratamiento, el umbral nociceptivo (tiempo de reacción en la plancha caliente a 50ºC), la motricidad (distancia recorrida en 5 minutos) como evaluador de respuesta motora, y la actividad de la Butirilcolinesterasa plasmática (BuChE) como un marcador de actividad colinérgica. La actividad BuChE disminuyó progresivamente en 23,6%; 48,9% y 53,2%, el primero, cuarto y séptimo día, respectivamente, mostrando una cinética inhibitoria del tipo logarítmica: % Inhibición BuChE = 53,73 x (1+1,22-0,81xdía); r=0,93; P<0,05. Las dosis utilizadas corresponden a un nivel de exposición no letal con el fin de lograr cronicidad. La motricidad fue similar en ambos grupos (controles: 108,5 ± 30,1; malatión: 102,1 ± 43,9 cm; P>0,05; X ± DE) al igual que el umbral nociceptivo (controles:13,5 ± 5,4; malatión 15,2 ± 6,5s; P>0,05). Los datos obtenidos muestran que a pesar de la intensa inhibición de la BuChE inducida por bajas dosis de malatión, la participación funcional colinérgica en el proceso de la nocicepción es muy reducida o marginal, lo cual sugiere el predominio de otros neurotransmisores en el procesamiento nociceptivo espinal y supraespinal.
Due to cholinergic presence in the nociceptive system and the frequent exposition to Malathion, an organophosphorated pesticide with an Achetylcholinesterase inhibitory effect, the impact of the increased cholinergic tone induced by a low dose of malathion on the nociceptive and motor behavior of rats was tested. Male Sprague Dawley rats (350-400g) were divided into two groups: Control (n=10) injected with 1mL NaCl 0.9% daily (i.p.) and Malathion (n=10) injected with 1mL of malathion (40 mg.Kg-1.day-1, in NaCl 0.9%, i.p) daily for 7 days. At days 1, 4 and 7 of treatment the nociceptive threshold was evaluated by the hot-plate method at 50ºC, motor activity by total rat displacement in 5 min, and the plasmatic Butyrylcholinesterase (BuChE) activity as a cholinergic biomarker. BuChE activity progressively decreased by 23.6%; 48.9% and 53.2% at days 1, 4 and 7 of treatment, respectively, showing a logarithmic inhibitory kinetics: % of BuChE inhibition= 53.73 x (1+1,22-0,81xday); r=0,93; P<0,05. The tested exposition dose was non-lethal in order to simulate chronic toxicity. Despite the BuChE inhibition, no statistical differences between both groups were found, neither for the nociceptive threshold (Controls:13.5±5,4; Malathion 15.2±6.5s; P>0.05; Mean±SD) nor for motor activity (Controls:108.5±30,1; malathion:102.1±43.9cm; P>0.05). These results strongly suggest that despite the intense BuChE inhibition induced by exposition to a low dose of malathion, the contribution of the cholinergic system in nociception is reduced or even marginal, which reveals the action of other neurotransmitters in this process.
ABSTRACT
En Venezuela, el malation ha sido ampliamente usado en forma continua en programas de control de aedes aegypti. Por tal motivo se realizó un estudio en mosquitos provenientes de zonas urbanas con alta casuística de dengue de los estados: Amazonas, Aragua, Bolívar, Lara, Mérida y Zulia, para determinar el status de susceptibilidad en este vector al malatión, en comparación con la cepa susceptible referencial, Rockefeller (Rock). Se hicieron bioensayos en botellas tratadas con el insecticida malatión evaluando la dosis diagnóstica 100ug/mL en 30 minutos y ensayos bioquímicos en microplacas para determinar mecanismos metabólicos asociados al status frente al insecticida. Los resultados de los bioensayos mostraron que existe susceptibilidad a malatión, lo cual fue confirmado por pruebas bioquímicas. Sin embargo, se encontraron diferencias significativas entre todas las cepas evaluadas con valores de P<0,005 para esterasas alfa (α), esterasas beta (β) y acetilcolinesterasa normal (Ache) y acetilcolinesterasa inhibida (Achei). La prueba de comparación de medias de Bonferroni encontró similitud entre la cepa Rock, mazonas y Lara para esterasas α y β. Se encontró similitud de la cepa Rock con las cepas de Bolívar y Zulia para las pruebas con Ache y Achei. Este estudio concluye que el malatión mostró su potencial de uso en el control del vector del dengue de las localidades evaluadas.
In Venezuela, malathion has been widely used continuously in control programs for Aedes aegypti. Therefore, a study in mosquitoes from urban areas with high dengue casuistry in the states of Amazonas, Aragua, Bolivar, Lara, Merida and Zulia was conducted to determine the status of this vector susceptibility to malathion, compared with the reference susceptible strain, Rockefeller. Bioassays were done on bottles treated with the insecticide malathion, 100ug/mL evaluating the diagnostic doses in 30 minutes and biochemical assays in microplates were performed to determine metabolic mechanisms associated with status against insecticide. The bioassay results showed that there is malathion susceptibility, which was confirmed by biochemical tests. However, significant differences were found among all strains assessed values of P<0.005 for esterases alpha (α), beta esterases (β) and standard acetylcholinesterase (AChe) and inhibited acetylcholinesterase (Achei). The mean comparison test of Bonferroni showed similarity between the strains Rock, Amazon and Lara for esterases α and β. Similarity was found between the strains Rock, Bolivar and Zulia for the Ache and Achei tests. This study concludes that malathion showed its potential use in controlling the dengue vector in the locations evaluated.
Subject(s)
Humans , Male , Female , Aedes/growth & development , Esterases/administration & dosage , Malathion/analysis , Dengue , Yellow FeverABSTRACT
The restriction of the mechanisms of cell proliferation in murine seminiferous epithelium, in terms of induction of programmed cell death until recently has not been fully analyzed. The aim of this work was to assess the effect of Malathion (MP) on testicular morphology and function in mouse spermatogenesis. For the experiments, male albino mice of strain NMRI-IVIC, weighing between 30-40 g were used, and divided into control and experimental groups of 5 each. The animals of the experimental groups were injected with a single dose of MP: 241mg/kg weight (1/12 LD 50 ) resuspended in 0.9% saline, intraperitoneally. Animals were sacrificed at 8.3, 16.6 and 33.2 days post-injection (first, second and third spermatogenic cycles). Testicular samples were obtained for light microscopy (LM), transmission electron microscopy procedures, and to detect apoptosis and p53 antigen by immunohistochemical methods. Blood was collected to quantify testosterone and plasmatic cholinesterase activity. From 8.3 days, Sertoli cell vacuolization, karyolisis of pachytene spermatocytes and Leydig cells and a decreased in average of the diameter of seminiferous tubules was observed. No damage to inter-Sertoli cells junctions was detected. Percentage of seminiferous tubules showing germ cells apoptosis was increased from 8.3 days, plasmatic acetylcholinesterase activity was reduced in the group treated only 24 hours after administration of MP. Serum testosterone levels were low in treated animals at 16. 6 and 33.2 days. p53 was mostly expressed in pachytene spermatocytes from 8d. The findings of this study indicate that MP alters the testicular function affecting the DNA and interfering with spermatogenesis as well as steroidogenesis.
La restricción de los mecanismos de proliferación celular en epitelio seminífero murino, en términos de inducción de muerte celular programada hasta hace poco no había sido completamente analizada.El objetivo de este trabajo fue evaluar el efecto de malathion (MP) sobre la morfología y la función testicular del ratón.Ratones macho albinos de la cepa NMRI-IVIC, con pesos entre 30-40 g fueron utilizados, se dividieron en grupos control y experimental. Los grupos experimentales fueron inyectados por vía intraperitoneal con una dosis única deMP:241mg/kg de peso (1/12 DL50) resuspendido en 0,9% de solución salina.Los animales fueron sacrificados en el día 8,3, 16,6 y 33,2 después de la inyección (primer, segundo y tercer ciclos de la espermatogénesis).Se obtuvieron muestras de testículo para estudio en microscopía de luz (ML), microscopía electrónica de transmisión, para la detección de apoptosis y el antígeno p53 (proliferación celular), por métodos inmunohistoquímicos.Se recogió sangre para cuantificar la testosterona y la actividad plasmática de colinesterasa.Desde el día 8,3 día se observó vacuolización de células de Sertoli, cariolisis de espermatocitos en paquiteno y células de Leydig, y una disminución en el promedio del diámetro de los túbulos seminíferos. No se detectó daño en las uniones entre células de Sertoli. El porcentaje de túbulos seminíferos que mostraban células germinales en apoptosis se incrementó a los 8,3 días, laactividad de la acetilcolinesterasa plasmática se redujo en el grupo tratado sólo 24 horas después de la administración de MP.Los niveles séricos de testosterona disminuyeron en los animales tratados a los 16,6 y 33,2 días.P53 se expresó sobre todo en los espermatocitos en paquiteno desde los 8,3 días.Los resultados de este estudio indican que MP altera la función testicular, afecta al ADN e interfiere con la espermatogénesis, así como con la esteroidogénesis.
Subject(s)
Animals , Male , Mice , Spermatogenesis/drug effects , Spermatozoa/cytology , Cell Proliferation/drug effects , Malathion/toxicity , Spermatozoa/drug effects , ApoptosisABSTRACT
Background & objectives: Under the national antimalaria programme DDT was introduced in early 1950s for vector control and later hexachloro cyclohexane (HCH) followed by malathion and recently synthetic pyrethroids in 1990s to manage the insecticide resistance in Anopheles culicifacies. Subsequent replacement led to development of multiple resistances in An. culicifacies in Surat district in Gujarat State. Indoor residual spray (IRS) was completely withdrawn in southern villages in Surat in 2002. This study was undertaken in these areas to study the persistence of resistance to DDT, malathion and deltamethrin after sequential withdrawal of IRS with these insecticides at different times. Methods: Susceptibility tests on An. culicifacies were conducted using standard WHO methods and kits. Mortality, knockdown time and lethal times were calculated for An. culicifacies exposed to WHO prescribed diagnostic concentrations of different insecticide impregnated papers. Results: Persistence of DDT-resistance was observed even after 30 yr of its withdrawal from IRS. Similarly, persistence of malathion resistance was also observed after 9 yr of its withdrawal from IRS, while reversal of deltamethrin-resistance was observed very fast within 2-3 yr after its withdrawal from IRS in 2002. Interpretation & conclusion: Present data indicate that the quantum of reversion of insecticide resistance in a population is relative and depends on the genetic stability of the respective resistance genes in the mosquitoes. In the present study withdrawal of pyrethroid-IRS resulted in increased susceptibility against pyrethroids alone and was independent of existence of resistance to insecticides of other groups. This study emphasizes that appropriate rotation of different insecticides; including carbamates may prevent or delay the onset of resistance.
Subject(s)
Animals , Anopheles/drug effects , Anopheles/genetics , Anopheles/physiology , DDT/toxicity , Genetics, Population , India , Insecticide Resistance/genetics , Insecticides/toxicity , Malathion/toxicity , Mortality , Mosquito Control/methods , Nitriles/toxicity , Pyrethrins/toxicity , Regression Analysis , Time FactorsABSTRACT
El uso de drogas de abuso es un grave problema de salud y problema social en todo el mundo. Se conocen muy bien los efectos en salud de la exposición aguda o crónica a drogas de abuso. También que causan efectos directos en la placenta o en órganos en desarrollo de los embriones, causando malformaciones congénitas. Existe sin embargo muy poca información sobre efectos diferidos de la exposición a estos agentes durante las últimas etapas del desarrollo fetal o las primeras etapas de desarrollo postnatal.Estos agentes causan alteraciones irreversibles en la diferenciación y programación celular, que pueden ser consideradas como malformaciones bioquímicas y funcionales, responsables de alteraciones funcionales orgánicas o neuroconductuales que favorecenel desarrollo de enfermedades más tarde en la vida. En el presente trabajo se describen los efectos persistentes de la exposición a drogas de abuso ilícitas (opiáceos, cocaína, ketamina, tolueno, cannabinoides y anfetamina y sus derivados) y a drogas de abusolegalmente permitidas (alcohol etílico - nicotina y consumo de tabaco no se describen por formar parte de publicación previa en Cuadernos). Exposición a estos agentes favorece el desarrollo de una serie de enfermedades y alteraciones de la conducta más tarde en la vida. Además, se presenta evidencia que la exposición prenatal a varios químicos (plomo, el plaguicida malatión, bisfenol) y a varias drogas de abuso (opioides, etanol, cannabinoides) determinan cambios persistentes que favorecen el desarrollo de adicciones a drogas de abuso más tarde en la vida. Se concluye que, además de los problemas sociales y de salud derivadas del uso por adultos de drogas de abuso, la exposición fetal causa cambios que determina el desarrollo de varias enfermedades más tarde en la vida, incluyendo adicción a drogas de abuso. En consecuencia, la legislación gubernamental que restrinja el acceso y uso de estas drogas...
The use of drugs of abuse is a serious health and social problem through all the world. The eff ects of acute and chronic exposure of drugs of abuse on health are well known. They also cause direct eff ects on placenta o the developing embryo organs, causing congenital malformations. There is however very scarce information on the delayed eff ects of exposure to these agents during the last stages of fetal development or the early stages of postnatal development. These agents cause irreversible alterations in cell diff erentiation and programming, that could be considered as biochemical and functional malformations, responsible of functional organic or neurobehavioral alterations that favors the development of diseases later in life. The present report describes persistent effects of prenatal exposure to illicit drugs of abuse (opiates, cocaine, ketamine, toluene, cannabinoids, and amphetamine derivates) and to legal drugs of abuse (ethyl alcohol; nicotine and tobacco smoking are not reviewed since they were analyzed in a previouspublication in Cuadernos). Exposure to these agents favors the development of a myriad of diseases and behavioral alterations later in life. In addition, evidence is presented that prenatal exposure to various chemicals (lead, the pesticide malathion, bisphenol) andseveral drugs of abuse (opioids, ethanol, cannabinoids) determine persistent changes that favor the development of addictions to drugs of abuse later in life. It is concluded that, besides the known health and social problems derived by adults use of drugs of abuse, fetal exposure causes changes that determine the development of various diseases later in life, including drug addiction.Therefore, the dictation of Governmental regulations to decrease access to and use of these drugs, including the softest drugs such as cannabinoids, is fundamental to protect future generations health...