Olive Oil Phenolics Shield Brain Cells from Cyclopiazonic Acid, a Common Foodborne Toxin Many People Overlook
Nikhil Prasad Fact checked by:Thailand Medical News Team Jun 08, 2026 1 hour, 25 minutes ago
Medical News: A new study by Spanish researchers has revealed that compounds found in extra virgin olive oil can help protect brain cells from damage caused by cyclopiazonic acid (CPA), a little-known but potentially dangerous foodborne toxin produced by certain species of Aspergillus and Penicillium fungi. The findings add to growing evidence that natural compounds found in the Mediterranean diet may play an important role in defending the brain against toxic substances commonly found in contaminated foods.
Scientists discover that extra virgin olive oil phenolics protect brain cells from mitochondrial damage caused by
the fungal food toxin cyclopiazonic acid
The study was conducted by researchers from the Research Group in Alternative Methods for Determining Toxic Effects and Risk Assessment of Contaminants and Mixtures (RiskTox), Laboratory of Food Chemistry and Toxicology, Faculty of Pharmacy and Food Science, University of Valencia, Spain.
A Foodborne Toxin with Serious Health Concerns
Cyclopiazonic acid is a fungal toxin that can contaminate a variety of food products including maize, rice, peanuts, millet, cheese, figs, poultry meat and animal feed. Previous studies have linked exposure to the toxin with weight loss, diarrhea, muscle degeneration, organ damage, convulsions and even death in severe cases. Scientists have also suspected that the toxin may contribute to neurological damage, but the exact mechanisms involved have remained poorly understood.
To investigate this issue, researchers exposed SH-SY5Y human neuronal cells, a widely used laboratory model for studying brain disorders, to different concentrations of CPA and carefully examined the resulting cellular changes.
Mitochondria Identified as a Major Target
One of the most important discoveries was that CPA specifically damages mitochondria, the structures inside cells responsible for producing energy.
Interestingly, the toxin did not cause a significant increase in general cellular reactive oxygen species during the early stages of exposure. However, a more detailed analysis revealed that mitochondria themselves were experiencing severe oxidative stress.
The researchers found that CPA exposure increased mitochondrial superoxide production in a concentration-dependent manner. At higher toxin concentrations, mitochondrial superoxide levels increased by as much as 165 percent compared to untreated cells. Such increases indicate intense oxidative damage occurring within the cell's energy-producing machinery.
At the same time, mitochondrial membrane potential, an important indicator of mitochondrial health and function, fell by up to 19 percent. A reduction in mitochondrial membrane potential is often regarded as an early warning sign of mitochondrial dysfunction and impaired cellular energy production.
Oxidative Damage Extends Beyond Mitochondria
The study also showed that CPA triggered significant lipid peroxidation, a destructive process in which free radicals attack cell membranes.
Levels of malondialdeh
yde, a major marker of lipid damage, increased steadily with increasing toxin exposure. Compared to normal cells, lipid peroxidation increased by 7 percent, 18 percent and 25 percent at the three tested toxin concentrations.
These findings suggest that CPA-induced mitochondrial damage can trigger broader oxidative injury throughout the cell, potentially compromising neuronal survival and function.
Critical Antioxidant Defense Systems Shut Down
Perhaps even more concerning was the discovery that CPA suppressed several genes responsible for protecting cells against oxidative stress.
The toxin reduced the activity of key antioxidant defense genes including NRF2, NOS2, HO1, CAT, KEAP1, NQO1, GPX1 and GSR. Some of the strongest reductions were observed in NOS2, which fell by 93 percent, NQO1 by 83 percent and HO1 by 79 percent at the highest toxin concentration tested.
The NRF2 pathway is widely recognized as one of the body's most important defense systems against oxidative damage. When this pathway becomes suppressed, cells become increasingly vulnerable to inflammation, oxidative injury and long-term degeneration.
The findings suggest that CPA not only causes oxidative stress but also weakens the cell's ability to defend itself against that damage.
This
Medical News report highlights growing concerns that chronic exposure to fungal toxins in contaminated foods may contribute to cellular changes associated with neurodegenerative diseases and age-related neurological decline.
Olive Oil Extract Demonstrates Strong Neuroprotective Effects
The researchers then investigated whether phenolic compounds found in extra virgin olive oil could counteract the harmful effects of CPA.
They tested tyrosol, oleuropein and a complete extra virgin olive oil extract rich in naturally occurring phenolic compounds.
The results were striking. The extra virgin olive oil extract consistently improved neuronal cell survival and protected against toxin-induced damage across all tested CPA concentrations. In some experiments, cell viability increased by as much as 78 percent compared to cells exposed only to the toxin.
Tyrosol also demonstrated significant protective effects. When combined with CPA, tyrosol increased cell viability by up to 45 percent. Oleuropein provided protection as well, although its effects were less consistent and appeared to be dependent on toxin concentration.
Why Whole Olive Oil Works Better
According to the researchers, the superior performance of the olive oil extract likely results from the combined action of numerous bioactive compounds working together.
Extra virgin olive oil contains a complex mixture of phenolic alcohols, secoiridoids, flavonoids, lignans and other antioxidant molecules. Rather than acting individually, these compounds may produce synergistic effects that provide stronger cellular protection than any single compound alone.
This observation supports previous research suggesting that whole-food components often provide greater biological benefits than isolated ingredients.
Conclusions
The study provides compelling new evidence that cyclopiazonic acid damages brain cells primarily by targeting mitochondria and triggering mitochondrial oxidative stress. The toxin increased mitochondrial superoxide production, disrupted mitochondrial function, promoted lipid peroxidation and severely weakened critical antioxidant defense pathways. Together, these changes create conditions that make neuronal cells far more vulnerable to injury and degeneration.
Importantly, the researchers demonstrated that phenolic compounds from extra virgin olive oil can substantially reduce this damage. The complete olive oil extract was particularly effective, outperforming individual compounds such as tyrosol and oleuropein, suggesting that the combined activity of multiple olive oil polyphenols delivers enhanced neuroprotection. These findings not only improve scientific understanding of how CPA harms brain cells but also identify extra virgin olive oil phenolics as potential dietary agents capable of helping protect against foodborne toxin-induced neurological damage. Further animal and human studies will be needed to determine whether these protective effects can be replicated in real-world settings.
The study findings were published in the peer reviewed journal: Toxins.
https://www.mdpi.com/2072-6651/18/6/252
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