Medical treatment of acute poisoning with organophosphorus and carbamate pesticides

Academy of Sciences and Arts of Republic Srpska, Banja Luka, Republic Srpska, Bosnia and Herzegovina.
Toxicology Letters (Impact Factor: 3.36). 08/2009; 190(2):107-15. DOI: 10.1016/j.toxlet.2009.07.025
Source: PubMed

ABSTRACT Organophosphorus compounds (OPs) are used as pesticides and developed as warfare nerve agents such as tabun, soman, sarin, VX and others. Exposure to even small amounts of an OP can be fatal and death is usually caused by respiratory failure. The mechanism of OP poisoning involves inhibition of acetylcholinesterase (AChE) leading to inactivation of the enzyme which has an important role in neurotransmission. AChE inhibition results in the accumulation of acetylcholine at cholinergic receptor sites, producing continuous stimulation of cholinergic fibers throughout the nervous systems. During more than five decades, pyridinium oximes have been developed as therapeutic agents used in the medical treatment of poisoning with OP. They act by reactivation of AChE inhibited by OP. However, they differ in their activity in poisoning with pesticides and warfare nerve agents and there is still no universal broad-spectrum oxime capable of protecting against all known OP. In spite of enormous efforts devoted to development of new pyridinium oximes as potential antidotes against poisoning with OP only four compounds so far have found its application in human medicine. Presently, a combination of an antimuscarinic agent, e.g. atropine, AChE reactivator such as one of the recommended pyridinium oximes (pralidoxime, trimedoxime, obidoxime and HI-6) and diazepam are used for the treatment of OP poisoning in humans. In this article the available data related to medical treatment of poisoning with OP pesticides are reviewed and the current recommendations are presented.

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Available from: Milan Jokanovic, Aug 11, 2015
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    • "In nonfatal cases, the illness generally lasts less than 24 h [10]. After long-term exposure acetyl cholinesterase inhibition results in the accumulation of acetylcholine at cholinergic receptor sites, producing continuous stimulation of cholinergic fibbers throughout the nervous systems [13]. Bendiocarbamate exposure is dangerous to pregnant animals as well as women because transfer to the developing foetus was found [10]. "
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    ABSTRACT: The aim of this work was to determinate the effect of carbamate insecticide bendiocarb (2,2-dimethyl-1,3-benzodioxol-4-yl N-methylcarbamate) on selected parameters of rabbit homeostasis. Animals were divided into four groups (control C, and experimental groups E1, E2 and E3 according to days of administration 10, 15 and 25 days). Animals from experimental groups received bendiocarb per os in a dose 5 mg/kg of body weight per day. Significant increase of creatinine content in E3 group (the longest administration of bendiocarb), increase of aspartate aminotransferase (E1 and E3 against control group) and gamma glutamyl transferase (E3 against control group) and decrease of glutamate dehydrogenase (E1 against control group) inform about possible failure of liver and/or kidney caused by bendiocarb. Decrease of haemoglobin (significantly in E3 group against control group), mean corpuscular haemoglobin (MCH) concentration (in all experimental groups), platelet count (in all experimental groups) can signify defection in haemoplastic system.
    Pesticide Biochemistry and Physiology 10/2010; DOI:10.1016/j.pestbp.2010.06.009 · 2.01 Impact Factor
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    • "Death usually occurs due to respiratory failure resulting from a combination of central and peripheral effects, paralysis of the respiratory muscles, and depression of the brain respiratory center [1] [2] [3]. Medical treatment of OP poisoning has been recently discussed by Jokanoví c [4]. The second effect is described as intermediate syndrome, occurring 24–96 h after exposure, characterized by acute ventilatory insufficiency due to paralysis of respiratory muscles. "
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    ABSTRACT: About 80 years have passed since the first cases of organophosphate induced delayed polyneuropathy (OPIDP), as the consequence of human poisoning with certain organophosphorus compounds, were described in the literature. OPIDP is a relatively rare neurodegenerative disorder in humans characterized by loss of function, ataxia and paralysis of distal parts of sensory and motor axons in peripheral nerves and ascending and descending tracts of spinal cord appearing 2-3 weeks after exposure or later. The molecular target for OPIDP is considered to be an enzyme in the nervous system known as neuropathy target esterase (NTE). This review discusses OPIDP in man with emphasis on clinical presentation, pathogenesis, molecular mechanisms, and possibilities for prevention/therapy.
    Clinical neurology and neurosurgery 09/2010; 113(1):7-10. DOI:10.1016/j.clineuro.2010.08.015 · 1.25 Impact Factor
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    • "In patients poisoned with OPs, diazepam shows beneficial effects in reducing anxiety and restlessness, reducing muscle fasciculation , arresting seizures, convulsions, controlling apprehension and agitation and possibly reducing morbidity and mortality when used in conjunction with atropine and an oxime. Diazepam should be given to patients poisoned with OP whenever convulsions or pronounced muscle fasciculation are present (World Health Organization, 1986; Jokanoví c, 2009a). The rate of spontaneous reactivation can be accelerated by pyridinium oximes that have a chemical structure which 'fits' the structure of the inhibited AChE. "
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    ABSTRACT: In this paper we review neurotoxic disorders appearing in patients poisoned with organophosphorus pesticides. These compounds cause four important neurotoxic effects in humans: the cholinergic syndrome, the intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP) and chronic organophosphate-induced neuropsychiatric disorder (COPIND). Compared to the cholinergic syndrome, that causes millions of cases of poisoning each year, other disorders involve much smaller numbers of patients. The review is focused on the neurotoxic effects appearing after acute and chronic exposure to organophosphates with emphasis on clinical presentation, pathogenesis, molecular mechanisms, and possibilities for prevention/therapy.
    05/2010; 29(3):195-201. DOI:10.1016/j.etap.2010.01.006
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