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ROS-mediated cytotoxicity and cell death pathways in SH-SY5Y cells exposed to beauvericin, patulin, and their
Claudia Moyano-López1, Paula Llorens1, Ana Juan-García1
1Laboratory of Food Chemistry and Toxicology, Faculty of Pharmacy and Food Science, University of Valencia, Av. Vicent Andrés Estellés s/n, Burjassot, València 46100, Spain.
Abstract:
Beauvericin (BEA) and patulin (PAT) are foodborne mycotoxins with known cytotoxic effects, but their combined impact on neuronal cells is unclear. This study evaluates the individual and interactive neurotoxic effects of BEA and PAT in undifferentiated SH-SY5Y human neuroblastoma cells for 24 h and 48 h, focusing on oxidative stress, lipid peroxidation (LPO), cell cycle progression, and cell death. Both toxins increased reactive oxygen species (ROS), with greater levels under co-exposure, while LPO was mainly elevated by individual treatments. Combined exposure led to cell cycle arrest, characterized by SubG1 accumulation and reduction in S and M phases. Apoptosis and necrosis varied with time and dose, with co-exposure favoring late apoptosis and necrosis. These results demonstrate that BEA and PAT act an enhanced manner through oxidative and cell cycle-related mechanisms, underscoring the importance of considering co-exposures in neurotoxicity risk assessment.
Insights
Beauvericin (BEA) and patulin (PAT) mycotoxins enhance neurotoxicity when combined, increasing oxidative stress and causing cell cycle arrest. Co-exposure effects are crucial for assessing neuronal cell risks.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Beauvericin (BEA) and patulin (PAT) are mycotoxins with known cytotoxic effects.
- Their combined impact on neuronal cells remains largely uncharacterized.
Purpose of the Study:
- To evaluate the individual and interactive neurotoxic effects of BEA and PAT.
- To investigate mechanisms including oxidative stress, lipid peroxidation, cell cycle, and cell death in neuronal cells.
Main Methods:
- Utilized undifferentiated SH-SY5Y human neuroblastoma cells.
- Exposed cells to BEA and PAT individually and in combination for 24 and 48 hours.
- Assessed reactive oxygen species (ROS), lipid peroxidation (LPO), cell cycle progression, and cell death.
Main Results:
- Both BEA and PAT increased ROS, with synergistic effects upon co-exposure.
- Lipid peroxidation was primarily elevated by individual toxin treatments.
- Combined exposure induced cell cycle arrest (SubG1 accumulation) and altered apoptosis/necrosis pathways.
Conclusions:
- BEA and PAT exhibit enhanced neurotoxicity through combined oxidative and cell cycle-related mechanisms.
- Co-exposure to these mycotoxins poses a significant risk to neuronal cells.
- Findings highlight the importance of considering mycotoxin mixtures in neurotoxicity risk assessments.
