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Updated: Apr 25, 2026
Microarray Analysis for Saccharomyces cerevisiae
Published on: April 7, 2011
Effects of microcystin-LR on Saccharomyces cerevisiae growth, oxidative stress and apoptosis
Elisabete Valério1, Arminda Vilares2, Alexandre Campos3
1Unidade de Água e Solo, Departamento de Saúde Ambiental, Instituto Nacional de Saúde Dr. Ricardo Jorge, Avenida Padre Cruz, 1649-016 Lisboa, Portugal; Centro Interdisciplinar de Investigação Marinha e Ambiental (CIIMAR/CIMAR), Universidade do Porto, Rua dos Bragas 289, 4050-123 Porto, Portugal.
Abstract:
Microcystins (MC) are cyanotoxins occurring globally, known for causing acute hepatotoxicity in humans/animals, tumor promotion in animals and potential carcinogenicity. The mechanism of MC toxicity is considered a multi-pathway process involving the inhibition of protein phosphatases PP1/PP2A and the production of reactive oxygen species (ROS). However, their mechanism of action is not fully characterized, thus hampering the complete hazard identification. In this study, we evaluated the effect of several microcystin-LR concentrations on the growth, ROS levels, antioxidant system response and apoptosis induction on Saccharomyces cerevisiae. Our results showed that the growth of S. cerevisiae was not inhibited when compared to control cells. However, the staining of cells with DHR123 and DHE revealed an intracellular increase of the ROS levels. This ROS increase resulted in an augment of catalase activity and inhibition of SOD. All these facts suggest that hydrogen peroxide was the main ROS induced by MCLR. Signs of apoptosis were also detected in the cells exposed to toxin. Our results show that S. cerevisiae VL3 displays MCLR toxicity effects known to occur in higher eukaryotes and confirmed that it can be a simple and good model to help further in the elucidation of MCLR molecular mechanisms of toxicity.
Insights
Microcystin-LR (MCLR) exposure increased reactive oxygen species (ROS) and induced apoptosis in yeast cells. This study confirms Saccharomyces cerevisiae as a valuable model for understanding microcystin toxicity mechanisms.
Area of Science:
- Environmental Science
- Toxicology
- Biochemistry
Background:
- Microcystins (MCs) are potent cyanotoxins with global distribution.
- MC toxicity involves protein phosphatase inhibition and reactive oxygen species (ROS) production.
- The precise molecular mechanisms of MC toxicity remain incompletely understood.
Purpose of the Study:
- To investigate the effects of microcystin-LR (MCLR) on Saccharomyces cerevisiae.
- To evaluate MCLR-induced changes in cell growth, ROS levels, antioxidant responses, and apoptosis.
- To assess the utility of S. cerevisiae as a model organism for MC toxicity studies.
Main Methods:
- Exposure of S. cerevisiae VL3 to varying concentrations of MCLR.
- Measurement of intracellular ROS levels using DHR123 and DHE staining.
- Assay of antioxidant enzyme activity (catalase, SOD).
- Detection of apoptosis induction.
Main Results:
- MCLR did not inhibit S. cerevisiae growth.
- Intracellular ROS levels significantly increased upon MCLR exposure.
- Catalase activity was augmented, while superoxide dismutase (SOD) activity was inhibited.
- Apoptosis was induced in MCLR-exposed yeast cells.
- Hydrogen peroxide was identified as the primary ROS species.
Conclusions:
- S. cerevisiae exhibits MCLR-induced toxicity responses similar to higher eukaryotes.
- S. cerevisiae VL3 serves as a robust and simple model for elucidating MC molecular toxicity mechanisms.
- This yeast model aids in understanding the broader toxicological impacts of microcystins.
