Professor Seung-Ah Yoo’s Team (Catholic University College of Medicine) First to Identify the Cause
- Writer :External Affairs Team
- Date :2026.02.10
- Views :47

△ Prof. Seung-Ah Yoo, Prof. Hyang-Sook Lim, Dr. Min-Kyung Nam, and Graduate Student Chae-Rin Kim
As concerns grow over the impact of ubiquitous microplastics on human health, a joint research team—led by Professors Seung-Ah Yoo and Hyang-Sook Lim (Co-corresponding authors) and Dr. Min-Kyung Nam and Chae-Rin Kim (Co-first authors) from the Department of Biomedicine at the Catholic University of Korea College of Medicine—has become the first in the world to identify that the "surface chemical properties" of microplastics are the key factors determining brain inflammation and neuronal damage.
This study is highly significant as it moves beyond simply looking at the size or exposure amount of microplastics. Instead, it precisely analyzes how the chemical structures formed on the surface of microplastics affect the brain.
In the environment, microplastics interact with various substances, causing their surface properties to change over time. During this process, electrical chemical structures such as amine groups ($-NH_2$, a bond of nitrogen and hydrogen) or carboxyl groups ($-COOH$, a bond of carbon, oxygen, and hydrogen) are exposed on the surface. Until now, the specific impact of these changes on brain health remained largely unknown.
The research team conducted an analysis focusing on microglia—the immune cells in the brain that remove harmful substances—using polystyrene microplastics with different surface chemical structures. The experimental results revealed that microplastics with exposed amine groups (PS-$NH_2$) penetrated microglia much faster than ordinary microplastics or those with carboxyl groups, inducing a powerful inflammatory response.
Specifically, in microglia treated with amine-exposed microplastics, inflammatory signaling substances such as TNF-$\alpha$ and IL-6 increased significantly. This indicates that the microglia shifted toward a pro-inflammatory state (M1 type).
The researchers identified that the core cause of this change is the excessive generation of Reactive Oxygen Species (ROS) within the mitochondria (the cell's energy powerhouse). PS-$NH_2$ caused a continuous generation of superoxide in the mitochondria, which led to a chain reaction increasing the production of hydrogen peroxide ($H_2O_2$) and nitrogen oxides ($NO$), ultimately destroying the cellular energy production system. Consequently, these activated brain immune cells were confirmed to cause secondary damage to surrounding neurons.
In short, the team experimentally proved that the surface properties of microplastics stimulate brain immune cells, and this reaction can lead to neuronal death. Furthermore, the team identified a potential way to control this toxic reaction.
By applying Trolox, an antioxidant and Vitamin E analog, the researchers found that inflammatory signals and neuronal damage induced by ROS were significantly reduced at the molecular level. This provides a crucial clue for developing strategies to prevent and protect against neurotoxicity caused by microplastics in the future.
Professor Seung-Ah Yoo stated, "This study is the first in the world to identify how the 'invisible surface' of microplastics affects brain immune responses and nerve damage. It will serve as an important scientific basis for understanding the link between environmental pollutants and neurodegenerative diseases and for redefining the risks of microplastics."
The results of this study, titled "Amine-modified polystyrene particles induce surface chemistry-driven immunotoxicity in microglia: Protective effects of trolox," were published in January 2026 in the international journal Ecotoxicology and Environmental Safety. The research team has also filed two domestic patent applications related to the evaluation and inhibition of neuro-immunotoxicity based on microplastic surface characteristics.
△ Conceptual diagram showing how amine-modified polystyrene microplastics (PS-$NH_2$) induce cytotoxicity and inflammatory responses in microglia, increase oxidative stress through mitochondrial superoxide generation, and the mitigating effects of Trolox on neurotoxicity.

