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Effects of myotoxins on skeletal muscle fibers
1Department of Anatomy and Cell Biology, State University of New York, Brooklyn 11203, USA.
Abstract:
This review highlights various aspects of a number of experimental myological alterations, induced by different chemical toxicants, including anticholinesterase, colchicine, vincristine, chloroquine, tetanus toxin, botulinum toxin, reserpine and emetine. Despite their chemical diversity and mechanism(s) of action, it is evident from the data discussed here that remarkably different toxic agents exert quite similar effects and induce toxic myopathies. The latter include preferential involvement of slow-twitch red muscle, mitochondrial derangement, denervation-like alterations, formation of membranous whorls, tubular aggregates, autophagic vacuoles and axonal sprouts. The non-invasive experimental models discussed here are valuable in studying various aspects of myopathology in the absence of any mechanical damage to the innervating elements from neurons to axonal terminals.
Insights
Diverse chemical toxicants induce similar toxic myopathies, affecting slow-twitch red muscle and causing mitochondrial damage. These experimental models offer insights into muscle pathology without nerve damage.
Area of Science:
- Toxicology
- Muscle Biology
- Neurology
Background:
- Chemical toxicants can induce myological alterations.
- Understanding these alterations is crucial for diagnosing and treating muscle diseases.
Purpose of the Study:
- To review experimental myological alterations induced by various chemical toxicants.
- To identify common pathological features despite diverse toxic agents and mechanisms.
- To highlight the utility of non-invasive experimental models in studying toxic myopathies.
Main Methods:
- Review of experimental studies involving chemical toxicants like anticholinesterase, colchicine, vincristine, and others.
- Analysis of induced myological alterations, including mitochondrial changes, denervation-like effects, and specific structural formations.
- Focus on non-invasive experimental models.
Main Results:
- Diverse chemical agents (anticholinesterase, colchicine, vincristine, etc.) induce similar toxic myopathies.
- Common alterations include preferential slow-twitch red muscle involvement, mitochondrial derangement, denervation-like changes, membranous whorls, tubular aggregates, autophagic vacuoles, and axonal sprouts.
- Experimental models demonstrate myopathology without mechanical nerve damage.
Conclusions:
- Despite chemical diversity, various toxicants cause similar myopathic effects.
- Non-invasive experimental models are valuable for studying toxic myopathies and their underlying mechanisms.