Sarcoplasmic lipase and non-specific esterase inhibition in myofibers of rats intoxicated with the organophosphate isofenphos

Citation
Ee. Calore et al., Sarcoplasmic lipase and non-specific esterase inhibition in myofibers of rats intoxicated with the organophosphate isofenphos, EXP TOX PAT, 51(1), 1999, pp. 27-33
Citations number
21
Categorie Soggetti
Pharmacology & Toxicology
Journal title
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
ISSN journal
09402993 → ACNP
Volume
51
Issue
1
Year of publication
1999
Pages
27 - 33
Database
ISI
SICI code
0940-2993(199901)51:1<27:SLANEI>2.0.ZU;2-H
Abstract
The expression of sarcoplasmic esterases, lipases as well as the lipid cont ent in the myofibers of the diaphragm of rats intoxicated with the organoph osphate isofenphos was studied. Lipid accumulation was documented at light, electron microsopic and by morphometric studies. The distribution of these lipid droplets was irregular and abundant in myofibers with numerous mitoc hondria (predominantly oxidative fibers). Histochemical inhibition of sarco plasmic esterases and lipases was observed in the intoxicated animals. This sarcoplasmic inhibition of esterases occurs roughly in parallel to the inh ibition of plasma cholinesterase activity. The inhibition of sarcoplasmic l ipases may explain, at least partially, the accumulation of lipids. This in hibition probably makes difficult the use of lipids as fuel, especially in the oxidative fibers. In contrast to the small amount of muscle necrosis, ( 1.30 +/- 0.745), metabolic muscle impairment was intense and extensive, i.e ., decreased activities of esterases and lipases in the sarcoplasm, that sh ould contribute to muscle weakness. Therefore, because segmental necrosis w as most prominent in oxidative fibers (and these fibers use lipids as the p rincipal fuel and contain the greater amount of lipases in the sarcoplasm), it is possible that inhibition of activity of lipases is responsible for t he segmental necrosis. Although the exact role of these metabolic changes i s not known, it is possible that they contribute not only to the induction and evolution of muscle cell necrosis but also to the muscle weakness and c linical impairment of animals and humans in the acute intoxication by these compounds.