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Biochemical changes associated with muscle fibre necrosis after experimental organophosphate poisoning
1TDLM/CT Laboratoire de Toxicologie Médicale, Vilvoorde, Belgium.
Abstract:
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.
Insights
Biochemical markers can monitor rhabdomyonecrosis in organophosphate poisoning. This study tracked creatine and creatine phosphokinase levels in rats exposed to soman, identifying key indicators of muscle damage.
Area of Science:
- Biochemistry
- Toxicology
- Neuroscience
Background:
- Organophosphate (OP) poisoning can lead to neuromuscular complications, including rhabdomyonecrosis.
- Biochemical monitoring of these complications is crucial for understanding disease progression and evaluating treatments.
Purpose of the Study:
- To investigate the potential for biochemical monitoring of rhabdomyonecrosis following organophosphate poisoning.
- To assess the temporal evolution of specific biochemical parameters in rats exposed to soman.
Main Methods:
- Rats were administered 0.67 x LD50 of soman.
- Acetylcholinesterase (AChE) and serum ChE levels were measured at various time points (6, 16, 24, 48 h).
- Urinary creatine excretion, serum creatine phosphokinase (CPK) activity, and muscle protease/phosphorylase activity were analyzed.
Main Results:
- Significant inhibition of AChE in blood, brain, and diaphragm was observed.
- Rhabdomyonecrosis lesions in the diaphragm correlated with increased urinary creatine and serum CPK levels.
- Elevated calcium-activated neutral protease and phosphorylase a activities were detected in muscle tissue.
Conclusions:
- Biochemical markers such as urinary creatine and serum CPK are valuable for monitoring rhabdomyonecrosis in OP poisoning.
- These markers can aid in studying neuromuscular syndromes and assessing therapeutic interventions for OP toxicity.