Oxidative aging facilitates biological barrier penetration of polyethylene microplastics, amplifying systemic lipotoxicity in aquatic species.

Abstract

Background: Environmental aging processes, such as oxidation, can substantially modify the physicochemical properties and toxicity of microplastics (MPs). Nevertheless, most studies have focused on pristine MPs, overlooking aged forms that more accurately represent environmental exposure conditions. Understanding the toxicological consequences of oxidative aging is essential for realistic ecological risk assessment.

Results: We investigated the toxicological effects of pristine polyethylene (PE) and oxidized polyethylene (OPE) microplastics using a dual-species aquatic model comprising Daphnia magna and zebrafish (Danio rerio) embryos. Physicochemical characterization revealed that OPE particles exhibited increased surface roughness, a more negative surface charge, and a higher proportion of oxygen-containing functional groups on the particle surface compared with PE. Exposure to OPE induced pronounced lipid accumulation and significantly reduced heart rate in both models. Transcriptomic analysis indicated that OPE downregulated key genes related to lipid transport and metabolism, including mttp, apoea, and apobb. These findings were further validated by quantitative PCR and Oil Red O staining. Notably, zebrafish embryos exposed to OPE displayed developmental impairment even with intact chorions, implying enhanced bioavailability and barrier penetration of oxidized particles.

Conclusions: Our findings demonstrate that oxidative aging amplifies the biological toxicity of polyethylene microplastics by disrupting lipid metabolism and developmental processes. This study underscores the importance of considering environmentally aged MPs in ecological risk evaluations, as pristine particles may underestimate their actual hazard potential in aquatic ecosystems.