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Part. Fibre Toxicol., 07 June 2026 | https://doi.org/10.1186/s12989-026-00689-2 Oxidative aging facilitates biological barrier penetration of polyethylene microplastics, amplifying systemic lipotoxicity in aquatic species

Yejin Kim^1,2,#, Hyerin Lee^2,3,#, Eunji Lee^1,2, Yun Hak Kim⁴, Chang-Kyu Oh^2,5,*

¹Department of Convergence Medical Sciences, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea
²Department of Biochemistry, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea
³Interdisciplinary Program of Genomic Science, Pusan National University, Yangsan 50612, Republic of Korea
⁴Department of Biomedical Informatics, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea; Department of Anatomy, School of Medicine, Pusan National University
⁵Institute for Future Earth, Pusan National University, Busan 46241, Republic of Korea

^#These authors equally contributed to this paper.
^*Correspondence: Chang-Kyu Oh

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.

논문소개전체 설명

본 연구는 환경 중 산화(Oxidation) 과정을 거친 미세플라스틱이 pristine(순수) 미세플라스틱에 비해 생체 내에서 훨씬 강한 독성을 유발한다는 것을 물벼룩(Daphnia magna)과 제브라피시 배아(Zebrafish embryo)의 dual-species 모델을 통해 규명한 논문입니다.

물리화학적 변화 분석: 플라즈마 처리를 통해 환경 산화를 모사한 산화 폴리에틸렌(OPE)은 기존 PE에 비해 크기 변화는 미미했으나, 표면 거칠기가 증가하고 음전하가 강해졌으며 산소 함유 작용기가 증가하는 특징을 보였습니다.

생체 장벽 투과 및 독성 증폭: OPE는 물벼룩과 제브라피시 배아 모델 모두에서 pristine PE보다 높은 생체 내 축적률을 나타냈습니다. 특히 제브라피시 배아의 난막(Chorion) 장벽을 투과하여 심박수 감소 및 체장 감소 등의 발달 장애와 심혈관계 독성을 뚜렷하게 유발했습니다.

지질 대사 교란 메커니즘 규명: Transcriptomic(RNA-seq) 분석 결과, OPE 노출은 지질 수송 및 대사의 핵심 유전자인 mttp(Microsomal triglyceride transfer protein)와 apolipoprotein 패밀리(apoea, apobb 등)의 전사 수준을 강력하게 억제했습니다. 이로 인해 난황(Yolk)에서 발달 조직으로의 지질 이동이 차단되어 난황 sac 및 소화관 내에 이상 지질 축적(Lipotoxicity)이 일어나는 분자적 메커니즘을 최초로 확인했습니다.

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