Biochemical and histochemical alterations following acute soman intoxication in the rat

Rc, Gupta; Gt, Patterson; Dettbarn, Wolf D.

doi:10.1016/0041-008x(87)90244-4

Cited by 65 publications

(14 citation statements)

References 16 publications

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“…Calculated half-times of reactivation for plasma CarbE of the rats treated with 0.5 × LD 50 of dichlorvos, sarin, and soman were 1.2, 2.0, and 2.7 h, respectively. Similar results were reported by Gupta et al (1987a), who found 50% of spontaneous reactivation of plasma CarbE 24 h after poisoning of rats with 100 µg/kg soman. Gupta et al (1987b) also reported 94% of reactivation of plasma CarbE in rats treated with 200 µg/kg tabun, but 7 days after poisoning.…”

Section: The Relationship Between Carbe Activity and Toxicity Of Wnassupporting

confidence: 92%

Biotransformation of Warfare Nerve Agents

Jokanović¹

2015

Handbook of Toxicology of Chemical Warfare Agents

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Section: The Relationship Between Carbe Activity and Toxicity Of Wnassupporting

confidence: 92%

Biotransformation of Warfare Nerve Agents

Jokanović¹

2015

Handbook of Toxicology of Chemical Warfare Agents

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“…Brain regions with much lower AChE activity showed the highest percentage inhibition mainly because they contained lower numbers of binding sites. To our knowledge, this finding is in accordance only with VX, an OP nerve agent [Gupta et al, 19911, while in contrast to most carbamate and OP compounds [Gupta et al, , 1987Gupta andKadel, 1989a, 1990a, 19911. Whether there are regional differences in affinity for aldicarb in the AChE molecular forms remains to be seen.…”

Section: Discussionsupporting

confidence: 64%

Subacute toxicity of aldicarb: Prevention and treatment with memantine and atropine

Gupta

Kadel

1991

Drug Development Research

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Gupta, R.C., and W.L. Kadel: Subacute toxicity of aldicarb: Prevention and treatment with memantine and atropine. Drug Dev. Res. 24:343-353, 1991. Daily administration (i.p.) of aldicarb in male Sprague-Dawley rats at various dosage levels for 21 days revealed 1) 0.1 mg/kg, nontoxic dose: 2) 0.2 mg/kg, moderately toxic dose; and 3) 0.4 mg/kg, severely toxic dose. Inhibition of acetylcholinesterase (AChE) in discrete brain regions and diaphragm muscle was dose dependent. Toxic signs were predominantly peripheral even though AChE inhibition was significantly higher in the brain (except striatum). Besides AChE inhibition, marked inactivation of carboxylesterases (false targets) was observed, suggesting a protective mechanism especially against low dosage by reducing free concentration of aldicarb. After 30 min following the 7th, 14th, or 21st dose of aldicarb, the degree of inhibition of esterase(s) remained the same, and consequently no tolerance developed to aldicarb. On day 21, administration of memantine HCI (18 mg/kg, i.p.) and atropine sulfate (16 mg/kg, i.p.) 30 min and 15 min, respectively, prior to aldicarb (0.4 mg/kg) injection provided complete protection. Therapeutic administration of these antidotes completely reversed the clinical manifestations of intoxication. The present findings indicated that memantine provided protection and reversal of AChE from inhibition in addition to reversible blockage of hyperneuromuscular activity.

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“…Some of these structures were studied in our paper and their influencing either by soman or huperzine was different. The not-uniform AChE inhibition in the different brain structures following untreated intoxication with nerve agents in rats and guinea-pigs [27,28] was demonstrated. This non-uniform inhibition suggests that some brain structures more sensitive to huperzine or OP than others can be functionally important for toxic/prophylactic action.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Acetylcholinesterase in Different Structures of the Rat Brain Following Soman Intoxication Pretreated with Huperzine A

Bajgar

Hájek

Karasová

et al. 2007

IJMS

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Acetylcholinesterase (AChE) activities in different brain parts were determined quantitatively in rats treated with huperzine A, soman, and huperzine A followed by soman, using histochemical and biochemical methods. Following soman intoxication (1.2 x LD 50 , i.m.), AChE activity was decreased to 30-80% of control values depending on the brain structure. The most sensitive area was the frontal cortex and the most relatively resistant was ncl. ruber. Huperzine A treatment only caused a change in AChE activity varying from 70 to 100 % of control values. In rats pretreated with huperzine A and intoxicated with soman, AChE activity was significantly higher than that observed after soman. In these animals, survival of rats pretreated with huperzine was observed while the mortality of unpretreated animals was near to 80 %. The results suggest that huperzine A is good candidate for further study for clinical use as a prophylactic drug against nerve agent poisoning.Int. J. Mol. Sci. 2007, 8 1166

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Biochemical and histochemical alterations following acute soman intoxication in the rat

Cited by 65 publications

References 16 publications

Biotransformation of Warfare Nerve Agents

Biotransformation of Warfare Nerve Agents

Subacute toxicity of aldicarb: Prevention and treatment with memantine and atropine

Inhibition of Acetylcholinesterase in Different Structures of the Rat Brain Following Soman Intoxication Pretreated with Huperzine A

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