Developments in alternative treatments for organophosphate poisoning

Iyer, Rupa; Iken, Brian; Leon, Alex

doi:10.1016/j.toxlet.2015.01.007

Cited by 54 publications

(35 citation statements)

References 43 publications

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“…Experimentally induced convulsive SE in rodents by neurotoxins such as kainate or pilocarpine or diisopropylfluorophosphate (DFP), an organophosphate, causes irreversible brain damage if not adequately treated immediately (Lemercier et al, 1983; Furtado et al, 2012; Iyer et al, 2015; Brandt et al, 2016; Puttachary et al, 2016a and b). The duration and severity of SE determines the outcome of epileptogenesis.…”

Section: Severity Of Status Epilepticus Determines Epileptogenesismentioning

confidence: 99%

Glial source of nitric oxide in epileptogenesis: A target for disease modification in epilepsy

Sharma

Puttachary

Thippeswamy

2017

J of Neuroscience Research

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Epileptogenesis is the process of developing an epileptic condition and/or its progression once it is established. The molecules that initiate, promote, and propagate remarkable changes in the brain during epileptogenesis are emerging as targets for prevention/treatment of epilepsy. Epileptogenesis is a continuous process that follows immediately after status epilepticus (SE) in animal models of acquired temporal lobe epilepsy (TLE). Both SE and epileptogenesis are potential therapeutic targets for the discovery of anticonvulsants and antiepileptogenic or disease-modifying agents. For translational studies, SE targets are appropriate for screening anticonvulsive drugs prior to their advancement as therapeutic agents, while targets of epileptogenesis are relevant for identification and development of therapeutic agents that can either prevent or modify the disease or its onset. The acute seizure models do not reveal antiepileptogenic properties of anticonvulsive drugs. This review highlights the important components of epileptogenesis and the long-term impact of intervening one of these components, nitric oxide (NO), in rat and mouse kainate models of TLE. NO is a putative pleotropic gaseous neurotransmitter and an important contributor of nitro-oxidative stress that coexists with neuroinflammation and epileptogenesis. The long-term impact of inhibiting the glial source of NO during early epileptogenesis in the rat model of TLE is reviewed. The importance of sex as a biological variable in disease modification strategies in epilepsy is also briefly discussed.

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Section: Severity Of Status Epilepticus Determines Epileptogenesismentioning

confidence: 99%

Glial source of nitric oxide in epileptogenesis: A target for disease modification in epilepsy

Sharma

Puttachary

Thippeswamy

2017

J of Neuroscience Research

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“…Iken; Leon, 2015). In China, a drop in relative OPs usage is balanced by a growing demand for pesticides that now exceeds that of all other countries around the world, increasing risks of chronic exposure for farmland workers.…”

Section: Organophosphorus Compounds Agrochemicals: Organophosphorus Pmentioning

confidence: 99%

“…After the binding, the hydrolysis of ACh is catalyzed Mainly because of the Food Quality Protection Act, OP compounds have been restricted to agricultural sectors in the US. Despite the fact that chlorpyrifos remained an extensive OP insecticide, its overall employment was reduced by around 50% since 2000 (Iyer;Iken;Leon, 2015).…”

Section: Toxicology and Interaction Of Ops With Acetylcholinesterasementioning

confidence: 99%

Enzimas degradantes de organofosforados: Base molecular e perspectivas para biorremediação enzimática de agroquímicos

et al. 2017

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RESUMO Muitos compostos organofosforados (OP) são utilizados até hoje na agricultura como pesticidas e, infelizmente, como agentes de guerra química (ou agentes dos nervos) também. Os pesticidas organofosforados e os agentes dos nervos são moléculas extremamente tóxicas, uma vez que atuam como inibidores da enzima Acetilcolinesterase (AChE). O efeito mais preocupante da exposição a estes compostos é a toxicidade colinérgica aguda, ou seja, a perda de coordenação muscular. Uma vez que o indivíduo se contamina, o processo de intoxicação começa através da ligação do OP no sítio ativo da enzima AChE inativando-a. Os tratamentos atuais para pessoas expostas a baixas doses de OP podem ser realizados com atropina, oximas e benzodiazepínicos. Processos de remediação importantes envolvem o emprego de técnicas de biorremediação utilizando diferentes enzimas degradantes, como a Fosfotriesterase da Agrobacterium radiobacter e SMP-30. Devido ao elevado número de intoxicações anualmente, é crucial buscar métodos de tratamento mais potentes e eficazes, e nesta linha, as técnicas envolvendo biorremediação parecem ser bastante promissoras para este propósito.

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“…Cholinesterase inhibitors are known to exert unregulated and excessive stimulation of both muscarinic and nicotinic receptors in the central and autonomic nervous systems due to an accumulation of acetylcholine, and the symptoms are commonly referred to as 'acute cholinergic crisis' . (11,22) Although the physiological basis for VLF power is far more complex than HF and LF power, with some authors recommending that VLF be used in the interpretation of short-term HRV data, (4) it has been suggested that VLF power is associated with parasympathetic activity.…”

Section: Figure 1 Flowchart Of Patient Inclusionmentioning

confidence: 99%

“…(9) Symptoms of OP and carbamate poisoning include cholinergic crisis, CNS dysfunction, and neuromuscular paralysis. (9,11) Because diagnosis and treatment of OP and carbamate poisoning greatly depend on the severity of cholinergic symptoms and because HRV reflects autonomic status, the authors hy-pothesized that some HRV parameters may be of value in diagnosing OP and carbamate poisoning among patients visiting the emergency department (ED); thus, we conducted this study to evaluate the utility of HRV.…”

Section: Introductionmentioning

confidence: 99%

Heart rate variability analysis in acute poisoning by cholinesterase inhibitors

2017

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Heart rate variability (HRV) has been associated with a variety of clinical situations. However, few studies have examined the association between HRV and acute poisoning. Organophosphate (OP) and carbamate inhibit esterase enzymes, particularly acetylcholinesterase, resulting in an accumulation of acetylcholine and thereby promoting excessive activation of corresponding receptors. Because diagnosis and treatment of OP and carbamate poisoning greatly depend on the severity of cholinergic symptoms, and because HRV reflects autonomic status, some HRV parameters may be of value in diagnosing OP and carbamate poisoning among patients visiting the emergency department. Patients who visited the emergency department of the study hospital between September 2008 and May 2010 with the chief complaint of acute poisoning or overdose were included. Cases that involved ingestion of OP or carbamate insecticides were classified as poisoning by cholinesterase inhibitors and compared with other cases of poisoning or overdose. The timedomain analysis included descriptive statistics of R-R intervals and instantaneous heart rates. The frequency-domain analysis used fast Fourier transformation. A Poincaré plot, which is a scatterplot of R-R intervals against the preceding R-R interval, was used for the nonlinear analysis. Very-low-frequency (VLF) power and the ratio of low-frequency-to-high-frequency power (LF/HF) were the most effective parameters for distinguishing cholinesterase inhibitor poisoning among cases of acute poisoning, with areas under the receiveroperating characteristic curve of 0.76 and 0.87, respectively. Cholinesterase inhibitor poisoning was a significant factor determining VLF power and the LF/HF ratio after adjusting for possible confounding variables, including age over 40, gender, and tracheal intubation. Frequency-domain parameters of HRV, such as VLF power and the LF/HF ratio, might be considered as potential diagnostic methods to distinguish cholinesterase inhibitor poisoning from other cases of intoxication in the early stages of emergency care.

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Developments in alternative treatments for organophosphate poisoning

Cited by 54 publications

References 43 publications

Glial source of nitric oxide in epileptogenesis: A target for disease modification in epilepsy

Glial source of nitric oxide in epileptogenesis: A target for disease modification in epilepsy

Enzimas degradantes de organofosforados: Base molecular e perspectivas para biorremediação enzimática de agroquímicos

Heart rate variability analysis in acute poisoning by cholinesterase inhibitors

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