Cholinesterases/genetics* ; Dimethoate/analogs & derivatives* ; Humans ; Occupational Exposure/adverse effects* ; Polymorphism, Genetic ; Telomere

Adult ; China ; Dimethoate/analogs & derivatives* ; Farmers/statistics & numerical data* ; Female ; Humans ; Male ; Middle Aged ; Occupational Exposure ; Pesticides/adverse effects* ; Polymorphism, Single Nucleotide ; Telomerase/genetics* ; Telomere/physiology*

OBJECTIVETo investigate the characteristics of pesticide poisoning in Jiangsu Province, China, and to provide a scientific basis for developing effective intervention measures and prevention strategies.

METHODSThe data from report cards of pesticide poisoning in Jiangsu Province from 2006 to 2013 were arranged using EXCEL tables, and assessed. Statistical analysis was applied to the epidemiological data using SPSS.

RESULTSFrom 2006 to 2013, a total of 32672 cases of pesticide poisoning were reported in Jiangsu Province. Most of the cases were caused by non-occupational poisoning (life poisoning) (72.78%). A majority of patients with pesticide poisoning were 35-54 years old (40.85%) or older than 65 years (15.69%). There were more female patients (58.22%) than male patients (41.78%). Among patients with occupational poisoning, male patients (50.90%) were more than female patients. Among patients with non-occupational poisoning, female patients were more than male patients (38.37%). Pesticide poisoning mainly occurred from July to September. The case-fatality rate of occupational poisoning (0.47%) was lower than that of non-occupational poisoning (7.10%). All 13 cities in Jiangsu Province reported cases of pesticide poisoning. There were more cases in the northern regions than in the southern regions. Pesticide poisoning was mainly caused by organophosphorus insecticides including methamidophos, dichlorvos, dimethoate, omethoate, and parathion, which accounted for 65.58%of all cases. Paraquat had the highest case-fatality rate (10.06%) among all pesticides, followed by tetramine (10.00%), dimethoate or omethoate (7.85%), methamidophos (7.79%), and dimehypo (7.68%).

CONCLUSIONPesticide poisoning cannot be ignored. The management and control should be improved in production and usage of highly toxic pesticides including organophosphorus insecticides, rodenticides, and herbicides. More attention should be paid to the protection of vulnerable groups including women, children, and the elderly.

Adult ; Age Distribution ; Aged ; China ; epidemiology ; Cities ; Dichlorvos ; Dimethoate ; analogs & derivatives ; Environmental Exposure ; prevention & control ; statistics & numerical data ; Female ; Herbicides ; poisoning ; Humans ; Insecticides ; poisoning ; Male ; Middle Aged ; Organothiophosphorus Compounds ; Paraquat ; Pesticides ; poisoning ; Poisoning ; epidemiology ; prevention & control ; Rodenticides

OBJECTIVETo determine the efficiency of selenium and/or vitamin E to alleviate lung oxidative damage induced by dimethoate, an organophosphorus compound.

METHODSAdult Wistar rats were exposed during 30 days either to dimethoate (0.2 g/L of drinking water), dimethoate+selenium (0.5 mg/kg of diet), dimethoate+vitamin E (100 mg/kg of diet), or dimethoate+selenium+vitamin E.

RESULTSExposure to dimethoate caused oxidative stress in lung evidenced by an increase of malondialdehyde, protein carbonyl groups and advanced oxidation protein products. An increase in glutathione peroxidase, superoxide dismutase, catalase and a decrease in acetylcholinesterase and butyrylcholinesterase activities, glutathione, non-protein thiols and vitamins C levels were observed. Histopathological changes in lung tissue were noted as emphysema, hemorrhages and hemosiderin deposits. Co-administration of selenium or vitamin E to the diet of dimethoate treated rats ameliorated the biochemical parameters as well as histological impairments. The joint effect of these elements was more powerful in antagonizing dimethoate-induced lung oxidative damage.

CONCLUSIONWe concluded that selenium and vitamin E ameliorated the toxic effects of this pesticide in lung tissue suggesting their role as potential antioxidants.

Acetylcholinesterase ; metabolism ; Animals ; Antioxidants ; administration & dosage ; pharmacology ; Ascorbic Acid ; metabolism ; Biomarkers ; Butyrylcholinesterase ; metabolism ; Dimethoate ; adverse effects ; Glutathione ; metabolism ; Lipid Peroxidation ; drug effects ; Lung Diseases ; diagnosis ; prevention & control ; Oxidative Stress ; Rats ; Rats, Wistar ; Selenium ; administration & dosage ; pharmacology ; Vitamin E ; administration & dosage ; pharmacology

OBJECTIVETo investigate the effect of fasudil on in vitro cultured cardiomyocytes (CMs) exposed to omethoate and its possible mechanism.

METHODSCardiomyocytes were isolated from male SD rats and were then cultured in DMEM conventionally. The CMs were divided into different groups based on the doses of omethoate and fasudil in culture media. After 3, 6, 12, and 24 h of culture, the survival rate of CMs in each group was measured, the CMs in the medium-dose omethoate and medium-dose fasudil groups were subject to shortening amplitude measurement , and the content of lactate dehydrogenase (LDH) in culture media and expression of Bcl-2 and Bax in CMs were measured.

RESULTSCompared with the normal control group, each omethoate group showed significantly lower survival rate of CMs, which was negatively correlated with the dose of omethoate (P < 0.01). Compared with the normal control group, the medium-dose omethoate and medium-dose fasudil groups showed significantly decreased shortening amplitudes of CMs at all time points (P < 0.01), and the shortening amplitudes of CMs were significantly higher in the medium-dose fasudil group than in the medium-dose omethoate group after 12 h and 24 h of culture (P < 0.01). The LDH level was significantly higher in the medium-dose omethoate and medium-dose fasudil groups than in the normal control group, and the medium-dose fasudil group showed significantly lower LDH level than the medium-dose omethoate group (P < 0.01). Compared with those in the normal control group, the Bcl-2 expression in the medium-dose omethoate and medium-dose fasudil groups was decreased significantly, and the Bax expression in the medium-dose omethoate group was increased significantly (P < 0.01). Compared with the medium-dose omethoate group, the medium-dose fasudil group had significantly increased Bcl-2 expression and significantly decreased Bax expression (P < 0.01).

CONCLUSIONFasudil can inhibit the abnormal expression of apoptosis regulatory proteins (Bcl-2 and Bax) induced by omethoate, which might be one of the factors that reduce the toxic effect of omethoate on CMs.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine ; analogs & derivatives ; pharmacology ; Animals ; Cells, Cultured ; Dimethoate ; analogs & derivatives ; toxicity ; Male ; Myocytes, Cardiac ; drug effects ; metabolism ; Pesticides ; poisoning ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo study the involvement of excitatory amino acid system in astrocytes activation caused by dimethoate.

METHODSPure-cultured astrocytes were gained by three passages from primary cultured rat nerve cells, then treated with 10(-6),10(-5),10(-4) mol/L dimethoate for 48 h, 50 micromol/L and 100 micromol/L MK801, a NMDA receptor blocker, was used to intervene the effects induced by 10(-4) mol/L dimethoate. HPLC-FLD was utilized to measure the concentrations of excitatory amino acid (EAA), RT-PCR was used to detect the expression levels of NR2B, GLT-1, GLAST, GFAP and S100beta mRNA, and immunofluorescence staining method was applied to measure the expression levels of GFAP and S100beta proteins.

RESULTSThe expression levels of GLAST mRNA in all exposure groups were 67.8%, 68.6% and 76.2% of control level, respectively, which were significantly lower than that of control group (P < 0.05); The concentrations of EAA significantly decreased in 10(-4) mol/L dimethoate group, as compared with control group (P < 0.01); the expression levels of GFAP mRNA in 10(-4) mol/L dimethoate group, of S100beta mRNA in 10(-5) mol/L dimethoate group, of GFAP protein in 10(-4) mol/L and 10(-5) mol/L dimethoate groups and S100beta protein in 10(-4) mol/L dimethoate group were significantly higher than those in control group (P < 0.01). The expression levels of GLT-1 and GLAST mRNA in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups increased significantly, as compared with 10(-4) mol/L dimethoate group (P < 0.01), the expression levels of NR2B mRNA in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups increased significantly, as compared with control group (P < 0.05 or P < 0.01); the concentration of Glu in 10(-4) mol/L dimethoate plus 100 micromol/L MK801 group increased significantly, as compared with 10(-4) mol/L dimethoate group (P < 0.01); the expression levels of GFAP mRNA and protein in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups decreased significantly (P < 0.01); S100beta protein expression level in 50 micromol/L MK801 intervention group was significantly higher than thatl in control group (P < 0.01).

CONCLUSIONExcitatory amino acid system involved in astrocytes activation caused by dimethoate. MK801 was useful to control astrocytes gliosis.

Animals ; Astrocytes ; drug effects ; metabolism ; Cells, Cultured ; Dimethoate ; toxicity ; Dizocilpine Maleate ; pharmacology ; Excitatory Amino Acids ; metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate ; antagonists & inhibitors

OBJECTIVETo evaluate the reproduction toxicity of the mixture composed of dichlorvos, dimethoate and malathion synergistic effect on male mice, and further explore its possible mechanisms.

METHODSThe 105 male mice were divided into 7 groups, including control (0 mg/kg), mix low (10.8 mg/kg), mix medium (21.5 mg/kg), mix high dose (43.0 mg/kg), dichlorvos (5.1 mg/kg), dimethoate (12.6 mg/kg) and malathion (25.3 mg/kg) group. The oral gavage for successive 35 days, and the mice were sacrificed on the 36(th) day. The body weight, and the quantity, activity and morphology of sperms were examined. The levels of sexual hormone were measured, including testosterone (T), follicle stimulating hormone (FSH), luteinizing hormone (LH) and estradiol (E(2)). Pathological changes of testicle and epididymis were observed by morphology, pathology and electron microscope.

RESULTSAfter 14 days exposure, the body weights of the mice were lower in the mix-high dose group ((22.40 ± 3.07) g) than those in control group ((26.73 ± 2.82) g) (P < 0.05). After 28 days exposure, the body weights of the mice were also lower in the mix-medium dose group ((30.00 ± 4.93) g) than those in control group ((33.13 ± 3.29) g) (P < 0.05). The sperm counts and sperm motility decreased significantly as the toxic concentration arised. Comparing to control group ((373.33 ± 14.65)×10(6)/g weight of epididymis and (75.17 ± 7.68)%), the spermatozoa count and sperm motility had decreased in mix-medium and mix-high dose groups ((321.17 ± 18.19)×10(6)/g weight of epididymis, (225.00 ± 19.67)×10(6)/g weight of epididymis, and (64.67 ± 9.91)%, (57.83 ± 9.66)%), and the sperm abnormality rates were higher in mix-medium and mix-high groups ((43.33 ± 8.66)‰ and (55.00 ± 13.80)‰) comparing to those in control group ((32.67 ± 8.17)‰). Compared to those in control group (FSH (1.41 ± 0.20), E(2)(17.32 ± 2.72), LH (8.75 ± 1.32) and T (3.45 ± 0.80) nmol/L), the serum level of FSH (3.14 ± 0.62) and (3.85 ± 0.37) nmol/L, E(2) (36.81 ± 6.68) and (43.76 ± 9.82) nmol/L in mix-medium and mix-high dose group increased (P < 0.01), while the level of LH (5.21 ± 1.23) and (4.27 ± 1.09) nmol/L and T (1.37 ± 0.38) and (0.73 ± 0.18) nmol/L decreased (P < 0.01). The morphological and ultramicrostructure results of testicle and epididymis indicated that the mature sperm numbers were decreased, and the cacoplastic sperm head and the tail of spermatozoon were observed in mix-high dose groups.

CONCLUSIONThe dichlorvos, dimethoate and malathion mixture had synergistic reproductive toxicity to the testicle and epididymis structure and function, and thus leading to the process of generation cell cytopoiesis abnormalities, simultaneously the hypothalamus-pituitary-gonad axis were also affected and thus resulted in parasecretion.

Animals ; Body Weight ; Dichlorvos ; toxicity ; Dimethoate ; toxicity ; Malathion ; toxicity ; Male ; Mice ; Mice, Inbred ICR ; Organ Size ; Sperm Count ; Sperm Motility ; Spermatozoa ; drug effects ; Toxicity Tests

OBJECTIVETo investigate the effect and mechanisms of dimethoate on the primary cultured cortical neuronal cell injury.

METHODSCortical neuronal cells were isolated and cultured in serum free medium for 6 days in vitro, and 1, 5, 10, 50 and 100 micromol/L dimethoate were added to the medium and intracellular SOD, MDA and GSH. The content of excitatory amino acid was measured after 48 hours. Flow cytometry was used to detect the neuronal cell apoptosis.

RESULTSAfter 48 h, the activity of SOD and the content of GSH decreased [(1.04 +/- 0.02), (0.99 +/- 0.02), (0.96 +/- 0.02), (0.91 +/- 0.02) U/mg pro] [(219.35 +/- 6.79), (205.6 +/- 6.29), (194.06 +/- 2.63), (93.68 +/- 7.56) mg/g pro], and the content of MDA increased obviously with 5, 10, 50 and 100 micromol/L dimethoate [(21.22 +/- 0.29), (24.01 +/- 0.34), (27.15 +/- 1.02), (32.91 +/- 1.39) nmol/mg pro]; The content of Asp from 10 to 100 micromol/L dose group was higher than the control group and the content of Glu from 1 to 100 micromol/L dose group was higher than the control group. The apoptosis rate had great significance between 1 to 100 micromol/L dose groups and control group. When treated with dimethoate, MDA content in neuron was positively correlated with the content of EAAs with the increase of dimethoate. The correlative coefficient was 0.937 and 0.759 respectively (P < 0.01), while it was negatively correlated with the content of GSH. The correlative coefficient was -0.868 and -0.801 respectively (P < 0.01).

CONCLUSIONThe oxidative damage and changes of excitatory amino acid content induced by Dimethoate contribute to the primary cultured rat cortical neuron apoptosis.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Cells, Cultured ; Cerebral Cortex ; cytology ; Dimethoate ; toxicity ; Excitatory Amino Acids ; metabolism ; Glutathione ; metabolism ; Malondialdehyde ; metabolism ; Neurons ; drug effects ; metabolism ; pathology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism

Chromatography, Gas ; methods ; Dimethoate ; blood ; Humans ; Insecticides ; blood ; Methyl Parathion ; blood

A 40-years-old man had taken organophosphate (dimethoate) before one day and he was treated with gastric irrigation only in the private hospital for one day. But he was found dead after several hours from discharge. Bereaved families suspected medical mistakes and claimed autopsy. After autopsy, we concluded that he was died by respiratory failure on account of dimethoate intoxication. Generally symptoms of organophosphate poisoning appear immediately, but this case shows unusual course of intoxication. Here in, we reported a delayed death due to organophosphate intoxication with literature review.
Autopsy ; Dimethoate ; Gastric Lavage ; Hospitals, Private ; Humans ; Medical Errors ; Organophosphate Poisoning ; Respiratory Insufficiency