Long-Term Study of Brain Lesions Following Soman, in Comparison to DFP and Metrazol Poisoning

The long-term histopathological effects of acute lethal (95 μg kg-1) and sublethal (56 μg kg-1) doses of soman were studied in rats and were compared to lesions caused by equipotent doses of either another cholinesterase (ChE) inhibitor, DFP (1.8 mg kg-1), or a non-organophosphorus convulsant, metra...

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Bibliographic Details
Published in:Human & experimental toxicology 1992-11, Vol.11 (6), p.517-523
Main Authors: Kadar, T., Cohen, G., Sahar, R., Alkalai, D., Shapira, S.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Brain - drug effects
Brain - pathology
Chemical and industrial products toxicology. Toxic occupational diseases
Isoflurophate - toxicity
Lethal Dose 50
Male
Medical sciences
Pentylenetetrazole - toxicity
Rats
Rats, Sprague-Dawley
Soman - toxicity
Toxicology
Various organic compounds
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Summary:The long-term histopathological effects of acute lethal (95 μg kg-1) and sublethal (56 μg kg-1) doses of soman were studied in rats and were compared to lesions caused by equipotent doses of either another cholinesterase (ChE) inhibitor, DFP (1.8 mg kg-1), or a non-organophosphorus convulsant, metrazol (100 mg kg-1). Severe toxic signs were noted following one LD50 dose administration of all the compounds, yet only soman induced brain lesions. Moreover, even when administered at a sublethal dose (0.5 LD50), soman induced some histological changes without any clinical signs of intoxication. Soman-induced brain lesions were assessed quantitatively using a computerized image analyser. The analysis was carried out for up to 3 months following administration, and a dynamic pattern of pathology was shown. The cortical thickness and area of CA1 and CA3 cells declined significantly as early as 1 week post-exposure. No pathological findings were detected following DFP and metrazol administration. It is therefore suggested that brain lesions are not common for all ChE inhibitors and that convulsions per se are not the only factor leading to brain damage following the administration of soman. The degenerative process (found also with the sublethal dose of soman) might be due to a secondary effect, unrelated to soman's clinical toxicity, but leading to long-term brain injuries.
ISSN:0960-3271
1477-0903
DOI:10.1177/096032719201100613