Fatal, suicidal Malathion poisonings

Farago, Anna F.

doi:10.1007/bf00577694

Cited by 18 publications

(3 citation statements)

References 9 publications

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“…The highest concentration of malathion was found in gastric content (Farago, 1967;Morgade & Barquet, 1982;Jadhav et al, 1992;Mahat, N.A. et al, 2012).…”

Section: Discussionmentioning

confidence: 95%

Ultrastructure of the Midgut of theThird Larval Instar of Chrysomya megacephala (Diptera:Calliphoridae) fed on malathion treated diet

Bakr

Ramadan

Elsawy

et al. 2012

Egyptian Academic Journal of Biological Sciences, D. Histology

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Our study established the histopathlogical effect of different dosages malathion on the third larval instar of Chrysomya megacephala. The concentration of malathion increased gradually during the larval stages reaching the maximum concentration in the third instar larvae.The midgut of third larval instar was studied using transmission electron microscope. The most significant alterations were increasing damage to the larvae midgut including columnar prominent ,fat vacuoles, atrophied microvilli. These results indicate that malathion retard larval development.

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“…The highest concentration of malathion was found in gastric content (Farago, 1967;Morgade & Barquet, 1982;Jadhav et al, 1992;Mahat, N.A. et al, 2012).…”

Section: Discussionmentioning

confidence: 95%

Ultrastructure of the Midgut of theThird Larval Instar of Chrysomya megacephala (Diptera:Calliphoridae) fed on malathion treated diet

Bakr

Ramadan

Elsawy

et al. 2012

Egyptian Academic Journal of Biological Sciences, D. Histology

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“…Malathion is a dimethyl-organophosphate with a low toxicity in humans. However, many fatal human ingestions of malathion have been documented in the literature, with the lethal doses estimated to range from 350 mg kg -1 to 1000 mg kg -1 (12). In addition to atropine, oximes, and supportive measures, FFP was administered during two days.…”

Section: Discussionmentioning

confidence: 99%

Fresh Frozen Plasma as a Successful Antidotal Supplement in Acute Organophosphate Poisoning

Vučinić

Zlatković

Antonijević

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Despite improvements to intensive care management and specifi c pharmacological treatments (atropine, oxime, diazepam), the mortality associated with organophosphate (OP) poisoning has not substantially decreased. The objective of this examination was to describe the role of fresh frozen plasma (FFP) in acute OP poisoning. After a deliberate ingestion of malathion, a 55-year-old male suffering from miosis, somnolence, bradycardia, muscular fasciculations, rales on auscultation, respiratory insuffi ciency, as well as from an inhibition of red blood cell acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BuChE), was admitted to hospital. Malathion was confi rmed in a concentration of 18.01 mg L -1 . Apart from supportive measures (including mechanical ventilation for four days), antidotal treatment with atropine, oxime -pralidoxime methylsulphate (Contrathion ® ), and diazepam was administered, along with FFP. The potentially benefi cial effects of FFP therapy included a prompt increase of BuChE activity (from 926 IU L -1 to 3277 IU L -1 ; reference range from 7000 IU L -1 to 19000 IU L -1 ) and a reduction in the malathion concentration, followed by clinical recovery. Due to BuChE replacement, albumin content, and volume restitution, FFP treatment may be used as an alternative approach in patients with acute OP poisoning, especially when oximes are not available.

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“…[2][3][4] The toxic doses of malathion in human poisoning cases were between 350 and 1300 mg/kg. [5][6][7] It is well established that OPs inhibit acetylcholinesterase (AChE) at the nerve synapses and neuromuscular junction (NMJ), where degradation of acetylcholine (ACh) into choline and acetic acid is a natural step. Rapid toxicity of OPs is because of their good absorption and high affinity to AChE.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of muscular electrophysiological and mitochondrial dysfunction following exposure to malathion, an organophosphorus pesticide

et al. 2013

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Muscle dysfunction in acute organophosphorus (OP) poisoning is a cause of death in human. The present study was conducted to identify the mechanism of action of OP in terms of muscle mitochondrial dysfunction. Electromyography (EMG) was conducted on rats exposed to the acute oral dose of malathion (400 mg/kg) that could inhibit acetylcholinesterase activity up to 70%. The function of mitochondrial respiratory chain and the rate of production of reactive oxygen species (ROS) from intact mitochondria were measured. The bioenergetic pathways were studied by measurement of adenosine triphosphate (ATP), lactate, and glycogen. To identify mitochondrial-dependent apoptotic pathways, the messenger RNA (mRNA) expression of bax and bcl-2, protein expression of caspase-9, mitochondrial cytochrome c release, and DNA damage were measured. The EMG confirmed muscle weakness. The reduction in activity of mitochondrial complexes and muscular glycogen with an elevation of lactate was in association with impairment of cellular respiration. The reduction in mitochondrial proapoptotic stimuli is indicative of autophagic process inducing cytoprotective effects in the early stage of stress. Downregulation of apoptotic signaling may be due to reduction in ATP and ROS, and genotoxic potential of malathion. The maintenance of mitochondrial integrity by means of artificial electron donors and increasing exogenous ATP might prevent toxicity of OPs.

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Fatal, suicidal Malathion poisonings

Cited by 18 publications

References 9 publications

Ultrastructure of the Midgut of theThird Larval Instar of Chrysomya megacephala (Diptera:Calliphoridae) fed on malathion treated diet

Ultrastructure of the Midgut of theThird Larval Instar of Chrysomya megacephala (Diptera:Calliphoridae) fed on malathion treated diet

Fresh Frozen Plasma as a Successful Antidotal Supplement in Acute Organophosphate Poisoning

Mechanisms of muscular electrophysiological and mitochondrial dysfunction following exposure to malathion, an organophosphorus pesticide

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