[Ultrastructural study of moniliformin-induced lesions on the myocardium of rats and mice]
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Updated: Aug 14, 2026
Histological Quantification of Chronic Myocardial Infarct in Rats
Published on: December 11, 2016
Abstract:
Effects of moniliformin on the ultrastructure of the myocardium of mice and rats were studied. Mice were given moniliformin orally at the dosage of 29.46 mg/kg. One hour later lesions of the mitochondria of the myocardial cells were found which became more severe 2-3 hours later. Ultrastructural lesions were also observed in the myofibrils and sarcolemma. Rats were given moniliformin orally at the dosage of 6 mg/kg once daily for 56 days. Lesions of the mitochondria and myofibrils were relatively mild. Myocardiac specimens taken 21 days after toxin administration, lesions of the sarcolemma became more obvious. Various amounts of collagen were produced by the myocardiac cells. These moniliformin-induced lesions were similar to the ultrastructural changes in the myocardium of patients with Keshan disease. Our findings indicate that there may be a close and important relationship between moniliformin intoxication and Keshan disease.
Insights
Moniliformin causes myocardial cell damage in mice and rats, affecting mitochondria, myofibrils, and sarcolemma. These toxic effects resemble ultrastructural changes seen in Keshan disease, suggesting a link between moniliformin and the condition.
Area of Science:
- Toxicology
- Cell Biology
- Pathology
Context:
- Moniliformin is a mycotoxin produced by Fusarium species.
- Keshan disease is a severe cardiomyopathy linked to selenium deficiency, but other factors may be involved.
- Understanding the cellular mechanisms of moniliformin toxicity is crucial for disease research.
Purpose:
- To investigate the ultrastructural effects of moniliformin on myocardial cells in mice and rats.
- To compare moniliformin-induced cardiac lesions with the pathology of Keshan disease.
Summary:
- Mice treated with a single oral dose of moniliformin (29.46 mg/kg) exhibited rapid mitochondrial, myofibrillar, and sarcolemmal damage.
- Rats receiving daily oral doses (6 mg/kg for 56 days) showed milder mitochondrial and myofibrillar lesions, with progressive sarcolemmal damage and collagen deposition.
- The observed ultrastructural changes in moniliformin-intoxicated animals closely mimicked those found in human Keshan disease myocardium.
Impact:
- These findings suggest a significant role for moniliformin intoxication in the pathogenesis of Keshan disease.
- The study provides a potential etiological link between mycotoxin exposure and this human cardiomyopathy.
- Further research into moniliformin's mechanism of action could reveal new therapeutic targets for cardiac diseases.
