Electron microscopy of Microsporum cookei after 'in vitro' treatment with protoanemonin: a combined SEM and TEM study

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D Mares1

  • 1Istituto di Botanica dell'Università di Ferrara, Italy.

Mycopathologia
|October 1, 1989
PubMed

Insights

Protoanemonin (PrA) exhibits antifungal properties against Microsporum cookei by causing significant ultrastructural damage. This ranunculaceous derivative disrupts fungal cell morphology, particularly affecting cytoplasmic microtubules.

Area of Science:

  • Mycology
  • Biochemistry
  • Antimicrobial Research

Background:

  • Dermatophytes like Microsporum cookei cause superficial fungal infections.
  • Protoanemonin (PrA), a ranunculaceous derivative, has potential as an antifungal agent.
  • Understanding the cellular mechanisms of PrA is crucial for developing new treatments.

Purpose of the Study:

  • To investigate the antifungal activity of protoanemonin (PrA) against the dermatophyte Microsporum cookei.
  • To elucidate the ultrastructural changes induced by PrA in M. cookei using electron microscopy.
  • To explore the potential molecular targets of PrA within fungal cells.

Main Methods:

  • Transmission and scanning electron microscopy were employed to observe fungal ultrastructure.
  • Microsporum cookei cultures were treated with protoanemonin (PrA).
  • Cellular morphology and internal structures were analyzed for anomalies.

Main Results:

  • PrA induced abnormal hyphal shapes and cytoplasmic multimembranous bodies in M. cookei.
  • Tubules of 25 and 60 nm diameters were observed within the cytoplasm.
  • Mitochondria, nuclei, and vacuoles showed various alterations, suggesting widespread cellular disruption.
  • Observed changes are consistent with PrA interacting with cytoplasmic microtubules.

Conclusions:

  • Protoanemonin (PrA) demonstrates significant antifungal effects on Microsporum cookei at the ultrastructural level.
  • The interaction of PrA with cytoplasmic microtubules is a likely mechanism of its antifungal action.
  • The hypothesis that sulphydryl groups are primary targets of PrA is supported by the observed cellular alterations.

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