Variability in soman toxicity in the rat: Correlation with biochemical and behavioral measures☆
References (27)
- et al.
Dealkylation as a mechanism for aging of cholinesterase after poisoning with pinacolyl methylphosphonofluoridate
Biochem. Pharmacol.
(1965) Correlation between signs of toxicity and some biochemical changes in rats poisoned with soman
Eur. J. Pharmacol.
(1974)Role of aliesterase in organophosphate poisoning
Fundam. Appl. Toxicol.
(1984)- et al.
The effect of carboxylesterase inhibition on interspecies differences in soman toxicity
Toxicol. Lett.
(1987) Anticholinesterases: Some problems in understanding their effects in whole animals
Anomalies in theories and therapy on intoxication by potent organophosphorus antichlonesterase compounds
Gen. Pharmacol.
(1982)Organophosphorus pesticides: Pharmacology
Prog. Med. Chem.
(1971)Toxic Phosphorus Esters
- et al.
Dealkylation studies on inhibited acetylcholinesterase
Biochem. J.
(1966) Pharmacology of organophosphorus compounds
Pharmacol. Rev.
(1959)
Cytological distribution and physiological function of cholinesterases
Anticholinesterase agents
History of the research with anticholinesterase agents
Cited by (45)
Organophosphate nerve agents
2020, Handbook of Toxicology of Chemical Warfare AgentsLY293558 prevents soman-induced pathophysiological alterations in the basolateral amygdala and the development of anxiety
2015, NeuropharmacologyCitation Excerpt :All animal experiments were conducted following the Guide for the Care and Use of Laboratory Animals (Institute of Laboratory Animal Resources, National Research Council), and were approved by the U.S. Army Medical Research Institute of Chemical Defense and the Uniformed Services University of the Health Sciences Institutional Animal Care and Use Committees, who are accredited by the Association for Assessment and Accreditation of Laboratory Animal Care International. Soman (pinacolyl methylphosphonofluoridate; obtained from the U.S. Army Edgewood Chemical Biological Center, Aberdeen Proving Ground, MD, USA) was diluted in cold saline and administered via a single subcutaneous injection (132 μg/kg, which is approximately 1.2 × LD50; Apland et al., 2013; Figueiredo et al., 2011a, 2011b; Jimmerson et al., 1989) to 111 rats. Following exposure to soman, rats were monitored for signs of seizure onset, and continuously rated for seizure severity according to the modified Racine scale (Apland et al., 2010; Racine et al., 1977; Racine, 1972): Stage 0, no behavioral response; Stage 1, behavioral arrest, orofacial movements, chewing; Stage 2, head nodding/myoclonus; Stage 3, unilateral/bilateral forelimb clonus without rearing, straub tail, extended body posture; Stage 4, bilateral forelimb clonus plus rearing; Stage 5, rearing and falling; Stage 6, full tonic seizures.
Organophosphate Nerve Agents
2015, Handbook of Toxicology of Chemical Warfare Agents: Second EditionPathophysiological mechanisms underlying increased anxiety after soman exposure: Reduced GABAergic inhibition in the basolateral amygdala
2014, NeuroToxicologyCitation Excerpt :All animal experiments were conducted following the Guide for the Care and Use of Laboratory Animals (Institute of Laboratory Animal Resources, National Research Council), and were approved by the U.S. Army Medical Research Institute of Chemical Defense and the Uniformed Services University of the Health Sciences Institutional Animal Care and Use Committees. Soman (pinacoyl methylphosphonofluoridate) obtained from Edgewood Chemical Biological Center (Aberdeen Proving Ground, MD, USA) was diluted in cold saline and administered, via a single subcutaneous injection (149 μg/kg, which is an approximate dose of 1.35 × LD50; Figueiredo et al., 2011; Jimmerson et al., 1989), to 78 rats. Rats were monitored for signs of seizure onset (on the average, SE was initiated 5.76 ± 1.37 min after exposure), and continuously rated for seizure severity according to the modified Racine Scale: Stage 0, no behavioral response; Stage 1, behavioral arrest, orofacial movements, chewing; Stage 2, head nodding/myoclonus; Stage 3, unilateral/bilateral forelimb clonus without rearing, straub tail, extended body posture; Stage 4, bilateral forelimb clonus plus rearing; Stage 5, rearing and falling; Stage 6, full tonic seizures (Apland et al., 2010; Racine et al., 1977; Racine, 1972).
The recovery of acetylcholinesterase activity and the progression of neuropathological and pathophysiological alterations in the rat basolateral amygdala after soman-induced status epilepticus: Relation to anxiety-like behavior
2014, NeuropharmacologyCitation Excerpt :All animal experiments were conducted following the Guide for the Care and Use of Laboratory Animals (Institute of Laboratory Animal Resources, National Research Council), and were approved by the U.S. Army Medical Research Institute of Chemical Defense and the Uniformed Services University of the Health Sciences Institutional Animal Care and Use Committees. Soman (pinacoyl methylphosphonofluoridate; obtained from Edgewood Chemical Biological Center, Aberdeen Proving Ground, MD, USA) was diluted in cold saline and administered via a single subcutaneous injection (154 μg/kg), which, based on previous studies, is an approximate dose of 1.4 × LD50 (Figueiredo et al., 2011a; Jimmerson et al., 1989). Following exposure to soman, rats were monitored for signs of seizure onset, and continuously rated for seizure severity according to the modified Racine Scale: Stage 0, no behavioral response; Stage 1, behavioral arrest, orofacial movements, chewing; Stage 2, head nodding/myoclonus; Stage 3, unilateral/bilateral forelimb clonus without rearing, straub tail, extended body posture; Stage 4, bilateral forelimb clonus plus rearing; Stage 5, rearing and falling; Stage 6, full tonic seizures (Racine et al., 1977; Racine, 1972).
Prediction of soman-induced cerebral damage by distortion product otoacoustic emissions
2010, ToxicologyCitation Excerpt :This also explains why, in our present and previous studies (Job et al., 2007) no difference in whole blood inhibition was ever detected between C+ and C− rats. Indeed, whole blood and plasma ChE activities are most often considered as an index of exposure to ChE inhibitors rather than as an index of central toxicity for which red blood cell AChE would have provided a better indicator (Lotti, 1995; Jimmerson et al., 1989; Young et al., 2001). Confirming other studies (Job et al., 2007 and refs therein), brain ChE inhibition induced by soman 4 h after intoxication was well correlated to the symptom severity and remains the best biomarker of soman neurotoxicity.
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The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the U.S. Army or the Department of Defense. In conducting the research described in this report, the investigators adhered to the ‘Guide for the Care and Use of Laboratory Animals’ (NIH 85-23) of the Institute of Laboratory Animal Resources, National Research Council, U.S.A.