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

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

Animals ; Chromatography, Thin Layer ; Dichlorvos ; blood ; Dimethoate ; blood ; Insecticides ; blood ; Methyl Parathion ; blood ; Mice ; Organothiophosphorus Compounds ; blood

OBJECTIVETo investigate the protective effects of vigabatrin and atropine against the acute toxicity of dimethoate in male Kun-min mice.

METHODSThe therapeutic schedules of vigabatrin (50 or 100 mg/kg) and (or) atropine (2.5 or 5.0 mg/kg) were performed according to the L(9) (3(4)) orthogonal test table. The survival time, the righting reflex and the onset of muscle fasciculations were observed after the administration of dimethoate.

RESULTSFirst, the main effects of vigabatrin, atropine and the interaction between them were statistically significant in the Univariate analysis of the survival time at the alpha level of 0.05 (F(V)= 4.73, P(V)= 0.015, F(A)= 50.88, P(A)= 0.000, F(VxA)= 4.17, P(VxA)= 0.007). The range of atropine was more than double of that of vigabatrin or their interaction (R(A)> 2RV or 2R(VxA)). So not only atropine and vigabatrin but also their combination interaction protected mice against dimethoate lethality. The atropine played the major role in diminishing the lethality induced by dimethoate. Second, only vigabatrin, while not atropine, delayed the mice from dimethoate-induced muscle fasciculation according its statistical results (F(V)= 6.87, P(V)= 0.003, F(A)= 0.03, P(A)= 0.968, F(VxA)= 1.134, P(VxA)= 0.356). It should be noted that vigabatrin could not completely prevent dimethoate induced-muscle fasciculation in the test. At last, both atropine and vigabatrin could maintain the righting reflex in the intoxication, however there was no interaction between them (F(V)= 5.81, P(V)= 0.006, F(A)= 9.05, P(A)= 0.001, F(VxA)= 1.34, P(VxA)= 0.257).

CONCLUSIONCombined treatment with atropine and vigabatrin in the organophosphates intoxication seems reasonable and acceptable.

Acute Disease ; Animals ; Atropine ; therapeutic use ; Dimethoate ; poisoning ; Disease Models, Animal ; Insecticides ; poisoning ; Male ; Mice ; Vigabatrin ; therapeutic use

Seventy-three fungal species belonging to forty-three genera were isolated from 40 samples of Saccharrum officinarum (collected from Naage-Hamadi canal in Qena Governorate, Egypt). Aspergillus, Trichoderma, Mucor and Pythium were the most common genera on the two isolation media. The dominant species of Aspergillus were A. niger, A. flavus, A. ustus, A. terreus and A. wentii. Some species were dominant on 40 g/l sucrose such as Aspergillus niger, A. flavus, Emericella nidulans, Trichoderma viride, Torula herbarum and Mamaria echinoeotryoides, while the dominant species on 10 g/l glucose were Mucor circinelloides, Aspergillus niger, Torula herbarum and Trichoderma viride. Mycotoxins including aflatoxins B1, B2, G1 and G2, zearalenone and diacetoxyscirpenol were detected in the examined samples of Saccharrum officinarum. The mycelial growth of A. flavus, A. niger, Fusarium moniliforme and Torula herbarum decreased with the increase in Dimethoate concentrations, although 25 ppm was less effective than the higher levels of the insecticide (75~200 ppm). Dimethoate stimulated the activity of Go-T in A. niger, F. moniliforme and T. harbarum, while the Go-T activity was inhibited in A. flavus with the Dimethoate treatments.
Aflatoxins ; Aspergillus ; Aspergillus niger ; Cryptococcus ; Dimethoate ; Egypt* ; Emericella ; Fusarium ; Glucose ; Mucor ; Mycotoxins* ; Niger ; Pythium ; Saccharum* ; Sucrose ; Trichoderma ; Zearalenone

Acute Disease ; Animals ; Dimethoate ; analogs & derivatives ; poisoning ; Disease Models, Animal ; Male ; Mice ; Muscle Weakness ; chemically induced ; pathology ; Muscles ; pathology

OBJECTIVETo study the effect of dimethoate on the monoamine Neurotransmitters, including norepinephrine (NE), epinephrine (E), serotonin (5-HT), dopamine (DA) and its metabolite (3, 4-hydroxyphenylacetic acid, DOPAC) in the serum of rats and furthermore to explore the non-cholinergic mechanism of organophosphate induced toxicity.

METHODSGroups of rats were treated with saline and 38.9, 83.7 and 180 mg/kg dimethoate respectively and were decapitated at the different time course from 0.5 to 24 hours after the administration. The monoamines neurotransmitters were determined by the reverse-phase high-performance liquid chromatography with the electrochemical detection.

RESULTSThe serum concentrations of DA (8.42% - 248.42% of the control), DOPAC (17.22% - 68.21% of the control) increased, according with the DM dosage and the exposure time, while the levels of NE (9.65% - 38.26% of the control) and E (11.00% - 32.62% of the control) contents decreased at the same time.

CONCLUSIONThese findings indicate that dimethoate induced toxic effects can alter the monoamine levels at the different dosage and the time exposure in the serum of rats. It suggests that some non-cholinergic mechanisms may be involved in the dimethoate intoxication.

3,4-Dihydroxyphenylacetic Acid ; blood ; Animals ; Biogenic Monoamines ; blood ; Dimethoate ; toxicity ; Dopamine ; blood ; Dose-Response Relationship, Drug ; Epinephrine ; blood ; Male ; Norepinephrine ; blood ; Rats ; Rats, Sprague-Dawley ; Serotonin ; blood

Acute Disease ; Animals ; Astrocytes ; metabolism ; pathology ; Cats ; Dimethoate ; analogs & derivatives ; poisoning ; Female ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Poisoning ; metabolism ; pathology

OBJECTIVETo examine the therapeutic effect of combined use of obidoxime and atropine with artificial ventilation on respiratory muscle paralysis caused by omethoate poisoning in rats.

METHODSRats were exposed to 2 times the dose of LD50 omethoate and treated with atropine (10 mg/kg) to counteract cholinergic symptoms. When the rats' respiratory frequency became slower and breathed with difficulty, the trachea intubation and artificial ventilation was carried out. The rats in group A were continuously treated with atropine. The dose of obidoxime for Group B, C and D were 8, 15, 20 mg/kg respectively, given at the same time as artificial ventilation and 1, 2, 3 hours later. The doses of atropine was reduced to 1/3 - 2/3 of the first dose so as to maintain the rats atropinized. If the rat survival was beyond 60 minutes after withdrawal of artificial ventilation, the combined treatment was considered successful. The function of isolated phrenic diaphragm of the rats was observed with MS-302 physiological and pharmacological analysis instrument.

RESULTSNone of the rats in Group A was successful after withdrawal from artificial ventilation and the function of phrenic diaphragm appeared poor; whereas > 80% of the rats in B, C, D Group were successful after withdrawal from artificial ventilation in 3 h and the function of phrenic diaphragm remained well. The survival rate in B, C and D groups were higher after withdrawal from artificial ventilation than that in Group A(P < 0.01). The function of phrenic diaphragm in Group B, C and D were gradually decreased after ACh was added into the container.

CONCLUSIONSCombined use of suitable dose of obidoxime and atropine with artificial ventilation for respiratory muscle paralysis caused by omethoate poisoning could promote the recovery of diaphragm function and reduce the death rate in poisoned rats.

Animals ; Atropine ; administration & dosage ; Dimethoate ; analogs & derivatives ; poisoning ; Drug Therapy, Combination ; Obidoxime Chloride ; administration & dosage ; Rats ; Respiration, Artificial ; Respiratory Paralysis ; drug therapy