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Mechanisms of Cell Toxicity Caused by Degraded Microplastics

YAKUGAKU ZASSHI 2024 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Yuya Haga, Sota Manabe, Hirofumi Tsujino, Haruyasu Asahara, Kazuma Higashisaka, Yasuo Tsutsumi

Summary

This review examined the molecular and cellular mechanisms by which degraded microplastics cause toxicity, focusing on how physical and chemical changes during environmental weathering alter plastic particle biological activity. The paper discussed oxidative stress, membrane disruption, and inflammatory pathways as key toxicity mechanisms of degraded microplastic fragments.

Body Systems
Models
Study Type Environmental

Microplastics (MPs), defined as plastic particles less than 5 mm in size, are ubiquitous in the environment. The accumulation of MPs in various environmental compartments, such as the ocean, soil, and air, has raised considerable concerns regarding their impact on ecological systems, including marine life and human health. Notably, MPs have been detected in marine organisms such as shellfish and fish, and have even been found in the human body, including in the blood and placenta. Moreover, considering that MPs have been detected in drinking water, human exposure to these particles in daily life is inevitable. To assess the risk posed by MPs to human health, it is essential to consider their physiological and chemical properties, including size, shape, surface modification, and material composition. However, current risk analyses focus primarily on spherical MPs with smooth surfaces, which differ substantially from most of the MPs detected in the environment. Environmental factors, such as ocean waves and ultraviolet radiation, alter the properties of MPs, including size, shape, and surface characteristics. In this review, we summarize current research on MPs, with a particular emphasis on the effects of MP degradation on human health. Furthermore, we generated MPs with surface degradation and evaluated their impact on cell toxicity, along with the underlying biological mechanisms.

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