Acute toxicity and anti-enterotoxigenic activity of pigment extracted from Micrococcus roseus

Mahmoud Yolmeh1, Morteza Khomeiri2, Ezzatollah Ghaemi3

  • 1Department of Food Science and Nutrition, Faculty of Food Engineering, University of Campinas, Rua Monteiro Lobato, 80, Cidade Universitária Zeferino Vaz, Campinas, SP, CEP: 13083-862, Brazil. yolmeh@unicamp.br.

Insights

Pigments from Micrococcus roseus (PEM) significantly reduce the expression of staphylococcal enterotoxins (sea and seb) at sub-inhibitory levels. PEM also demonstrated low acute toxicity in mice, indicating its safety for potential applications.

Area of Science:

  • Microbiology
  • Biotechnology
  • Toxicology

Background:

  • Microbial pigments are gaining importance in food and pharmaceutical industries.
  • Natural pigments offer alternatives to synthetic compounds.
  • Staphylococcal enterotoxins pose significant health risks.

Purpose of the Study:

  • To evaluate the impact of Micrococcus roseus pigments (PEM) on the gene expression of staphylococcal enterotoxins (sea and seb).
  • To assess the acute toxicity of PEM in a mammalian model.

Main Methods:

  • Real-time PCR was employed to quantify the expression levels of sea and seb genes.
  • Sub-inhibitory concentrations of PEM were used against Staphylococcus aureus.
  • Acute toxicity was assessed in albino mice by monitoring liver enzymes (ALP, AST, ALT) and histopathological changes.

Main Results:

  • PEM significantly decreased the gene expression of both sea and seb in Staphylococcus aureus.
  • The expression of seb was found to be more sensitive to PEM than sea.
  • Mice treated with PEM showed no significant adverse effects on liver enzymes or tissue structure compared to controls.

Conclusions:

  • Micrococcus roseus pigments exhibit anti-enterotoxigenic properties by downregulating sea and seb gene expression.
  • PEM demonstrates a favorable safety profile, with low acute toxicity.
  • These findings suggest PEM as a promising natural agent for controlling staphylococcal enterotoxin production.

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