Human & Experimental Toxicology · 1993 · 39 citations · 22 references
Life SciencesPharmacologyToxicologyCellular MetabolismEnzymologyNeurotoxicologyEnzyme InhibitionMuscle PathologyMuscle PhysiologyOrganophosphate ToxicologyAcute Organophosphate ExposureBiomarkers Of Organophosphate ExposureMuscle Fiber NecrosisMuscle NecrosisOrganophosphate Exposure EffectsOrganophosphate-induced NeurotoxicityPoisoningUrinary Excretion Rate
1. This study was initiated to ascertain the possibility of biochemically monitoring the rhabdomyonecrosis that occurs after organophosphate poisoning. The evolution of different parameters has been assessed in the rat 6, 16, 24 and 48 h following 0.67 x LD50 of soman. 2. Acetylcholinesterase (AChE) was inhibited to 60% of the control value in the diaphragm at 6 and 16 h and serum ChE levels inhibited to an average of 30% of the control value. At 24 h, total blood, brain and diaphragm AChE were inhibited by 40, 69 and 38%, respectively. 3. Rhabdomyonecrosis lesions occurred in the diaphragm after 24 h and were accompanied by a concurrent increase in urinary creatine excretion rate (300% of the control) and serum total creatine phosphokinase activity (280% of the control). Calcium-activated neutral protease and phosphorylase a activities were elevated in the muscle at the same time. 4. These biochemical markers will prove useful for investigating the possible relationships between the different neuromuscular syndromes occurring in the course of an OP poisoning and potential therapeutic or protective pharmacological measures.
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