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Ultrastructural study of moniliformin induced lesions of myocardium in rats and mice

D Zhao1, Q Feng, X Yan

  • 1Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing.

Insights

Moniliformin causes severe myocardial cell damage in mice, affecting mitochondria, myofibrils, and sarcolemma. These toxic effects resemble ultrastructural changes seen in Keshan disease, suggesting a link between moniliformin intoxication and the human condition.

Area of Science:

  • Toxicology
  • Cardiovascular Pathology
  • Myocardial Ultrastructure

Background:

  • Moniliformin is a mycotoxin known for its toxicity.
  • Keshan disease is a severe cardiomyopathy linked to selenium deficiency and potentially other factors.
  • Understanding the cellular effects of mycotoxins is crucial for public health.

Purpose of the Study:

  • To investigate the ultrastructural effects of moniliformin on the myocardium of mice and rats.
  • To compare moniliformin-induced cardiac lesions with those observed in Keshan disease.

Main Methods:

  • Acute oral administration of moniliformin to mice at the LD50 dose.
  • Subchronic oral administration of moniliformin to rats over 56 days.
  • Transmission electron microscopy to examine myocardial ultrastructure.

Main Results:

  • Mice exhibited rapid and severe mitochondrial, myofibrillar, and sarcolemmal lesions within hours of moniliformin exposure.
  • Rats showed milder mitochondrial and myofibrillar damage, with more pronounced sarcolemmal lesions developing by day 21.
  • The observed ultrastructural changes in moniliformin-treated animals closely mimicked those found in human Keshan disease.

Conclusions:

  • Moniliformin induces significant and characteristic ultrastructural damage to the cardiac muscle.
  • The similarity between moniliformin-induced lesions and Keshan disease pathology suggests a potential etiological role for moniliformin in this cardiomyopathy.
  • Further research is warranted to elucidate the precise relationship between moniliformin exposure and Keshan disease development.

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