Oxidative Stress Induced by Micro(Nano)plastics

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 8589

Special Issue Editors


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Guest Editor
Department of Health Sciences, Università degli Studi di Milano, 20142 Milan, Italy
Interests: nanoplastics; oxidative stress; bone microenvironment; extracellular vesicles; cancers; multiple myeloma
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Guest Editor
Department of Health Sciences, University of Milan, 20146 Milan, Italy
Interests: cancer; extracellular vesicles; drug delivery; nanoparticles

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Guest Editor
Department of Environmental Science and Policy, University of Milan, 20122 Milan, Italy
Interests: ecotoxicology; biomarkers; environmental pollution; emerging contaminants
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thanks to their unique properties, plastics have revolutionized our daily lives. However, their widespread use and inefficient waste management have made them major environmental pollutants. Once released into the environment, plastics undergo transformation processes that generate micro(nano)plastics. Numerous studies have highlighted their ubiquitous presence and potential risks to ecosystems and human health. In this context, micro(nano)plastics represent a new environmental challenge closely linked to the "One Health" concept. Scientific evidence indicates that one of the primary mechanisms through which micro(nano)plastics affect living organisms involves the induction of oxidative stress. REDOX balance plays a crucial role in regulating physiological and pathological processes, and disturbances to this balance may underlie the harmful effects of micro(nano)plastics. This Special Issue focuses on the impact of micro(nano)plastics in inducing oxidative stress in aquatic and terrestrial organisms and their implications for human health. Particular attention will be given to novel mechanisms by which micro(nano)plastics disrupt cellular microenvironments and biological systems. We welcome original research articles, reviews, and short communications from observational (human biomonitoring) and experimental (in vivo and in vitro) studies addressing these critical issues.

Dr. Lavinia Casati
Dr. Alessandro Villa
Dr. Marco Parolini
Guest Editors

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Keywords

  • micro(nano)plastics
  • oxidative stress
  • One Health
  • in vitro and in vivo models
  • organisms
  • cellular microenvironment

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Published Papers (3 papers)

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Research

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15 pages, 1384 KB  
Article
Superoxide Dismutase 3 Deficiency Disrupts the Regulation of Oxidative Stress Caused by Polystyrene Nanoplastics
by Yugyeong Sim, Jin-Hyoung Kim, Jeong-Soo Lee, Jinyoung Jeong and Hyun-Ju Cho
Antioxidants 2025, 14(11), 1378; https://doi.org/10.3390/antiox14111378 - 19 Nov 2025
Cited by 1 | Viewed by 497
Abstract
Nanoplastics have been recognized as emerging pollutants posing potential risks to ecosystems and human health. They are now detected ubiquitously in the environment and even human tissues, where their small size allows for tissue accumulation and cellular penetration. Growing evidence links nanoplastics to [...] Read more.
Nanoplastics have been recognized as emerging pollutants posing potential risks to ecosystems and human health. They are now detected ubiquitously in the environment and even human tissues, where their small size allows for tissue accumulation and cellular penetration. Growing evidence links nanoplastics to oxidative stress, yet the specific contribution of extracellular accumulation to toxicity remains poorly understood. To address this, we used zebrafish, a transparent vertebrate model suitable for toxicological studies, to explore the role of extracellular antioxidant defenses in polystyrene nanoplastic (PSNP)-induced oxidative stress. In particular, we focused on superoxide dismutase 3 (SOD3), which is an enzyme that regulates extracellular reactive oxygen species by catalyzing the detoxification of superoxide radicals. Zebrafish Sod3a is a homolog of human SOD3, preserving conserved metal-binding sites critical for enzymatic function. We established sod3a mutant zebrafish and examined their responses following PSNP exposure. In sod3a mutant larvae, tissue accumulation of PSNPs was higher than in wild-type (WT), and this was associated with elevated oxidative stress, enhanced cell death, and abnormalities in intestinal function and immune responses. Collectively, these observations reveal the functional importance of SOD3 during PSNP-induced oxidative stress and provide new insight into extracellular antioxidant mechanisms that mitigate PSNP-induced toxicity. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Micro(Nano)plastics)
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26 pages, 12307 KB  
Article
Parthenolide Restores Testosterone Biosynthesis After Nanoplastic Exposure by Blocking ROS-Driven NF-κB Nuclear Translocation
by Peng Zhao, Hao Yan, Runchang Wang, Jie Zhao, Xiangqin Zheng, Dinggang Li, Xitong Guo, Fengming Ji, Chunlan Long, Lianju Shen, Guanghui Wei and Shengde Wu
Antioxidants 2025, 14(11), 1315; https://doi.org/10.3390/antiox14111315 - 31 Oct 2025
Viewed by 815
Abstract
Nanoplastics are pervasive contaminants that adversely affect male reproductive function, yet the molecular basis of polystyrene nanoplastic (PS-NP) toxicity in immature testes and effective preventive strategies remain unclear. Here, male mice (postnatal days 22–35, PND 22–35) and TM3 Leydig cells were exposed to [...] Read more.
Nanoplastics are pervasive contaminants that adversely affect male reproductive function, yet the molecular basis of polystyrene nanoplastic (PS-NP) toxicity in immature testes and effective preventive strategies remain unclear. Here, male mice (postnatal days 22–35, PND 22–35) and TM3 Leydig cells were exposed to graded PS-NPs, followed by transcriptomic profiling to identify differentially expressed genes (DEGs). Candidate therapeutics were prioritized using Connectivity Map (CMap) analysis and molecular docking, and protein interactions were examined by co-immunoprecipitation (Co-IP). PS-NPs accumulated in immature testes, eliciting excessive reactive oxygen species (ROS) and activation of NF-κB. These events coincided with the downregulation of steroidogenic enzymes (CYP11A1 and StAR) and disruption of testicular microarchitecture. In TM3 cells, PS-NPs suppressed testosterone synthesis in a concentration-dependent manner; this effect was fully reversed by pretreatment with N-acetylcysteine (NAC) or Bay 11-7082. Co-IP demonstrated p65–steroidogenic factor-1 (SF-1) binding consistent with formation of a transcriptional repressor complex targeting steroidogenic genes. CMap and docking analyses nominated parthenolide (PTL) as a candidate inhibitor of NF-κB nuclear translocation (predicted binding affinity, −6.585 kcal/mol), and PTL mitigated PS-NP-induced impairment of testosterone synthesis in vitro. Collectively, these data indicate that PS-NPs disrupt testosterone biosynthesis in immature testes through the ROS/NF-κB/p65–SF-1 axis, while PTL emerges as a candidate small molecule to counter nanoplastic-associated reproductive toxicity. These findings underscore translational relevance and support future evaluation under chronic low-dose exposure conditions, including in vivo validation of PTL efficacy, pharmacokinetics, and safety. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Micro(Nano)plastics)
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Review

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39 pages, 1558 KB  
Review
Antioxidant Intervention Against Microplastic Hazards
by Zhihua Wang, Yunting Wang, Jian Zhang, Guoquan Feng, Shuhan Miao, Rongzhu Lu, Xinyu Tian and Yang Ye
Antioxidants 2025, 14(7), 797; https://doi.org/10.3390/antiox14070797 - 27 Jun 2025
Cited by 6 | Viewed by 6872
Abstract
Microplastic pollution (<5 mm) poses a serious threat to the environment and human health, inducing cellular stress damage in organisms (especially through oxidative stress). The damage results from excessive reactive oxygen species and impaired defense mechanisms, affecting energy production, organelles, and triggering inflammation. [...] Read more.
Microplastic pollution (<5 mm) poses a serious threat to the environment and human health, inducing cellular stress damage in organisms (especially through oxidative stress). The damage results from excessive reactive oxygen species and impaired defense mechanisms, affecting energy production, organelles, and triggering inflammation. Antioxidants (such as vitamin C, curcumin, and quercetin) reduce stress markers and inflammation by neutralizing harmful molecules, activating protective pathways, and regulating autophagy, providing potential protection. However, practical applications face challenges such as low absorption rates, large individual variations, and unclear long-term safety. Research needs to delve into the molecular interaction mechanisms, develop effective delivery systems for antioxidant combinations, and formulate evidence-based strategies. Addressing the complexity of microplastics (size, shape, additives) and their cross-ecosystem impacts requires multidisciplinary collaboration. This review explores the oxidative stress mechanisms induced by microplastics, assesses the potential and limitations of antioxidant interventions, and provides a basis for environmental health risk management. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Micro(Nano)plastics)
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