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Antioxidants
Special Issues
Oxidative Stress Induced by Micro(Nano)plastics
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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: 10 February 2027 | Viewed by 14265

Editors

Dr. Lavinia Casati

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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
Special Issues, Collections and Topics in MDPI journals
Dr. Alessandro Villa

E-Mail Website
Guest Editor
Department of Health Sciences, University of Milan, 20146 Milan, Italy
Interests: cancer; extracellular vesicles; drug delivery; nanoparticles
Dr. Marco Parolini

E-Mail Website
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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (5 papers)

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Research

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19 pages, 2480 KB  
Article
Polystyrene Microplastics Induce Sustained Cardiovascular Redox Imbalance and Alter Mitochondrial Quality Control
by Ting-Yu Tsai, Pei-Hsuan Lu, Eddy Owaga, Yi-Sheng Tsai, Chia-Wen Chen and Rong-Hong Hsieh
Antioxidants 2026, 15(7), 816; https://doi.org/10.3390/antiox15070816 - 29 Jun 2026
Viewed by 306
Abstract
Microplastic exposure is an emerging environmental risk factor for cardiovascular health; however, whether cardiovascular alterations can be detected after exposure cessation remains unclear. This study investigated subclinical cardiovascular alterations following repeated oral exposure to polystyrene microplastics (PSMPs), with particular emphasis on redox imbalance [...] Read more.
Microplastic exposure is an emerging environmental risk factor for cardiovascular health; however, whether cardiovascular alterations can be detected after exposure cessation remains unclear. This study investigated subclinical cardiovascular alterations following repeated oral exposure to polystyrene microplastics (PSMPs), with particular emphasis on redox imbalance and mitochondrial function in delayed cardiovascular alterations. Male Sprague-Dawley rats were administered 0.5 μm PSMPs via oral gavage at varying dosages of 5 or 20 mg/kg every 5 days for 70 days, followed by a 35-day exposure-free period. Repeated exposure to PSMPs did not affect body or organ weights but altered cardiac serum biochemical markers. Cardiac tissue exhibited elevated NADPH oxidase 4 (NOX4) expression and decreased superoxide dismutase 1 (SOD1), SOD2, and catalase (CAT) activities, whereas malondialdehyde (MDA) levels remained unchanged, indicating a state of chronic, low-level oxidative stress. Mitochondrial respiratory chain activities, including nicotinamide adenine dinucleotide cytochrome c reductase (NCCR) and succinate cytochrome c reductase (SCCR), were significantly reduced. Ultrastructural analysis revealed mitochondrial swelling and cristae disruption. In parallel, mitochondrial biogenesis-related proteins, including peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), nuclear respiratory factor 1 (NRF-1), and mitochondrial transcription factor A (TFAM), were downregulated, while mitophagy markers, including PTEN-induced kinase 1 (PINK1), Parkin RBR E3 ubiquitin protein ligase (Parkin), microtubule-associated protein 1 light chain 3 (LC3), and sequestosome 1 (p62), were upregulated. Notably, most significant alterations were primarily observed in the high-dose group. Furthermore, the aorta showed increased oxidative stress markers without overt structural remodeling. These findings suggest that repeated exposure to PSMP is associated with subclinical cardiac redox–mitochondrial dysregulation, potentially involving redox imbalance, impaired mitochondrial respiratory chain activity, reduced mitochondrial biogenesis, and altered mitochondrial quality-control markers. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Micro(Nano)plastics)
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23 pages, 10270 KB  
Article
Polystyrene Nanoplastics Induce Early Mitochondrial Dysfunction in H9c2 Cardiomyoblasts Without Substantial Cell Damage
by Ming-Hung Shen, Pei-Hsuan Lu, Ting-Yu Tsai, Eddy Owaga, Yi-Sheng Tsai, Chia-Wen Chen and Rong-Hong Hsieh
Antioxidants 2026, 15(7), 801; https://doi.org/10.3390/antiox15070801 - 26 Jun 2026
Viewed by 373
Abstract
Global plastic production has led to widespread contamination by micro- and nanoplastics, with polystyrene nanoplastics (PSNPs) increasingly being detected in human biological samples, including blood and cardiac tissue. Given the critical role of mitochondria in cardiac energy metabolism, this study investigated whether 100 [...] Read more.
Global plastic production has led to widespread contamination by micro- and nanoplastics, with polystyrene nanoplastics (PSNPs) increasingly being detected in human biological samples, including blood and cardiac tissue. Given the critical role of mitochondria in cardiac energy metabolism, this study investigated whether 100 nm PSNPs interact with mitochondria and affect mitochondrial function in H9c2 cardiomyoblasts. Cellular uptake and intracellular distribution were examined, followed by an evaluation of mitochondrial ultrastructure, intracellular and mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential, mitochondrial dynamics and mitophagy-related gene expression, mitochondrial DNA copy number, and metabolic function. PSNPs were internalized but did not directly localize to mitochondria within 24 h. No significant cytotoxicity, increase in intracellular or mitochondrial ROS production, or alteration in basal metabolic activity was observed. However, PSNP exposure resulted in intracellular accumulation, an altered mitochondrial ultrastructure characterized by crista loosening and vacuole-like structural changes. These changes were accompanied by reduced mitochondrial membrane potential; the upregulation of mitochondrial dynamics-related genes, including optic atrophy 1 (Opa1) and dynamin-related protein 1 (Drp1); the suppression of PTEN-induced kinase 1 (PINK1)/Parkin RBR E3 ubiquitin protein ligase (Parkin)-mediated mitophagy-related genes; and decreased maximal respiratory capacity. Lactate production and the extracellular acidification rate remained unchanged, suggesting that compensatory glycolysis was not activated. These findings indicate that PSNP exposure induces early mitochondrial structural and functional alterations without substantial cell damage, suggesting a potential reduction in cardiac adaptive capacity under PSNP-induced stress conditions. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Micro(Nano)plastics)
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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 1029
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
Cited by 2 | Viewed by 1654
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 21 | Viewed by 10092
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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