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Toxicity of microcystin from cyanobacteria growing in a source of drinking water

Ireneusz Majsterek1, Paulina Sicinska, Małgorzata Tarczynska

  • 1Department of Molecular Genetics, University of Lodz, 12/16 Banacha, 90-237 Lodz, Poland. imajst@bio.lodz.pl

Comparative Biochemistry and Physiology. Toxicology & Pharmacology : CBP
|November 24, 2004
PubMed

Insights

Cyanobacterial microcystin-LR extract (CEM) is highly toxic to mammalian mitochondria. Even low doses may activate mitochondrial defense, while higher doses significantly inhibit respiration, indicating mitochondria as toxicity indicators.

Area of Science:

  • Environmental Toxicology
  • Mitochondrial Biochemistry
  • Cyanobacterial Toxinology

Background:

  • Microcystin-LR (MC-LR), a cyanobacterial heptapeptide, poses significant health risks.
  • Mitochondrial morphological changes are a primary cellular response to MC-LR toxicity.
  • Sulejow Reservoir, a drinking water source in Poland, experiences Microcystis aeruginosa blooms.

Purpose of the Study:

  • To investigate the toxicity of cyanobacterial microcystin-containing extract (CEM) on mammalian mitochondrial respiratory complexes.
  • To compare the effects of CEM extract with standard MC-LR on mitochondrial function.
  • To evaluate the potential of mitochondria as in vivo indicators of microcystin toxicity.

Main Methods:

  • Harvesting Microcystis aeruginosa blooms from Sulejow Reservoir.
  • Quantifying MC-LR concentration in CEM extract using High-Performance Liquid Chromatography (HPLC).
  • Incubating isolated Bos taurus mitochondria with varying concentrations and exposure times of both CEM extract and standard MC-LR.

Main Results:

  • A low concentration (1 nM) of MC-LR in CEM extract activated the cytochrome c oxidase complex, potentially a defense mechanism.
  • Higher concentration (1 µM) of MC-LR in CEM extract significantly inhibited mitochondrial oxidase complex activity (87% inhibition) compared to standard MC-LR (58% inhibition).
  • The potent inhibition by CEM extract suggests a toxicity comparable to long-term water consumption.

Conclusions:

  • Cyanobacterial microcystin-containing extract (CEM) exhibits high toxicity towards mammalian mitochondria.
  • Mitochondrial function, particularly the respiratory complex, serves as a sensitive indicator of microcystin toxicity.
  • Mitochondria can be valuable in vivo biomarkers for assessing risks associated with long-term exposure to contaminated water sources.

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