Subacute and sublethal ingestion of microcystin-LR impairs lung mitochondrial function by an oligomycin-like effect

Flávia Muniz de Mesquita1, Dahienne Ferreira de Oliveira2, Dayene de Assis Fernandes Caldeira1

  • 1Carlos Chagas Filho Institute of Biophysics, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.

Insights

Subacute exposure to microcystin-LR (MC-LR) cyanotoxin causes lung damage, including collagen deposition and collapsed alveoli. MC-LR also impairs lung mitochondrial function, suggesting a potential oligomycin-like effect.

Area of Science:

  • Toxicology
  • Environmental Health
  • Pulmonary Medicine

Background:

  • Microcystin-LR (MC-LR) is a prevalent cyanotoxin with known organ toxicity.
  • Subacute and sublethal exposure effects on the lungs remain understudied.

Purpose of the Study:

  • To investigate the histological and functional impacts of subacute, sublethal MC-LR exposure on mouse lungs.

Main Methods:

  • Male BALB/c mice were gavaged with MC-LR (30 µg/kg) for 20 days.
  • Respiratory mechanics, lung histology, and mitochondrial function were assessed.
  • In vitro assays evaluated direct effects on mitochondrial function.

Main Results:

  • No significant changes in respiratory mechanics were observed.
  • Histopathology revealed increased collagen deposition, immune cell infiltration, and alveolar collapse.
  • Mitochondrial function was significantly impaired both in vivo and in vitro.
  • MC-LR exhibited an oligomycin-like effect on lung mitochondria.

Conclusions:

  • Subacute, sublethal MC-LR exposure causes significant lung damage and mitochondrial dysfunction.
  • MC-LR's impact on lung mitochondria warrants further investigation into oral intoxication mechanisms.

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