Elevated choline levels in brain: A non-cholinergic component of organophosphate toxicity
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Molecular interactions of chemical warfare agents with biological systems
2022, Sensing of Deadly Toxic Chemical Warfare Agents, Nerve Agent Simulants, and their Toxicological AspectsCrossroads in the evaluation of paraoxonase 1 for protection against nerve agent and organophosphate toxicity
2012, Toxicology LettersCitation Excerpt :An efficient therapeutic strategy to combat against accidental or intentional exposure to organophosphate (OP) or chemical warfare nerve agent (CWNA) is of high demand both in civilian and military sectors. The rapid dangerous toxic effects of OP or CWNA exposure is primarily due to the irreversible inhibition of the abundant cholinergic enzyme, acetylcholinesterase (AChE) which is present in both central and peripheral nervous systems (Aldridge and Davison, 1953; Bajgar, 2004; Flynn and Wecker, 1986). The irreversible inhibition of AChE, which catabolizes the major neurotransmitter acetylcholine (ACh), can lead to the accumulation of ACh in the nervous system resulting in cholinergic crisis (Aldridge and Davison, 1953; Flynn and Wecker, 1986).
In vitro efficacy of paraoxonase 1 from multiple sources against various organophosphates
2011, Toxicology in VitroCitation Excerpt :The primary mode of action of various organophosphates (OPs) and chemical warfare nerve agents (CWNAs) is irreversible inhibition of the enzyme acetylcholinesterase (AChE) both in central and peripheral nervous systems (Aldridge and Davison, 1953; Shih et al., 2005). Accumulation of acetylcholine (ACh) leads to hypercholinergy, seizure, neuropathology and neurobehavioral deficits (Bajgar, 2004; Flynn and Wecker, 1986). The current treatment for OPs and CWNAs consist of a regimen of atropine, a muscarinic ACh receptor antagonist to counteract accumulation of ACh, 2-pralidoxime to reactivate OP-inhibited AChE, and benzodiazepines to treat seizures (Kadriu et al., 2009; Koplovitz and Stewart, 1994; Shih et al., 2007; Worek et al., 1996).
Recombinant paraoxonase 1 protects against sarin and soman toxicity following microinstillation inhalation exposure in guinea pigs
2011, Toxicology LettersCitation Excerpt :It can hydrolyze large amounts of OPs and CWNAs compared to the stoichiometric bioscavenger human butyrylcholinesterase (BChE), which acts in a 1:1 ratio, and would thus require smaller doses and would reduce the cost of treatment (Doctor et al., 1991; Doctor and Saxena, 2005; Lenz et al., 2005; Lenz et al., 2007; Rochu et al., 2007). The mechanism of action of OPs and CWNAs has been well described as the irreversible inhibition of acetylcholinesterase (AChE) in the central and peripheral nervous system leading to abnormal accumulation of acetylcholine resulting in overstimulation of cholinergic transmission (Aldridge and Davison, 1953; Bajgar, 2004; Flynn and Wecker, 1986). An effective countermeasure strategy for OP and CWNA toxicity has been centered on the development of catalytic bioscavenger enzymes as pretreatments which can rapidly hydrolyze large amounts of OPs and CWNAs in the blood before they reach their targets.
Protective efficacy of catalytic bioscavenger, paraoxonase 1 against sarin and soman exposure in guinea pigs
2011, Biochemical PharmacologyCitation Excerpt :Chemical warfare nerve agents (CWNAs) and organophosphate (OP) pesticides exert their biological effects mainly by the irreversible inhibition of acetylcholinesterase (AChE), an enzyme involved in the catabolism of neurotransmitter acetylcholine (ACh) [1–3].