Next Article in Journal
The Level of Remnant Cholesterol and Implications for Lipid-Lowering Strategy in Hospitalized Patients with Acute Coronary Syndrome in China: Findings from the Improving Care for Cardiovascular Disease in China—Acute Coronary Syndrome Project
Next Article in Special Issue
Neurodegeneration, Mitochondria, and Antibiotics
Previous Article in Journal
Three New Compounds, Licopyranol A–C, Together with Eighteen Known Compounds Isolated from Glycyrrhiza glabra L. and Their Antitumor Activities
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Metabolites
Volume 12
Issue 10
10.3390/metabo12100897
metabolites-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

Impact of Micro- and Nanoplastics on Mitochondria

by
Seung Eun Lee
1,
Yoojung Yi
2,
Sangji Moon
2,
Hyunkyung Yoon
2 and
Yong Seek Park
1,*
1
Department of Microbiology, School of Medicine, Kyung Hee University, #26 Kyungheedae-gil, Dongdaemun-gu, Seoul 02447, Korea
2
Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul 02447, Korea
*
Author to whom correspondence should be addressed.
Metabolites 2022, 12(10), 897; https://doi.org/10.3390/metabo12100897
Submission received: 30 August 2022 / Revised: 16 September 2022 / Accepted: 22 September 2022 / Published: 23 September 2022
(This article belongs to the Special Issue The Role of Mitochondria in Metabolic Health and Disease)
Browse Figures
Versions Notes

Abstract

:
Mitochondria are highly dynamic cellular organelles that perform crucial functions such as respiration, energy production, metabolism, and cell fate decisions. Mitochondrial damage and dysfunction critically lead to the pathogenesis of various diseases including cancer, diabetes, and neurodegenerative and cardiovascular disorders. Mitochondrial damage in response to environmental contaminant exposure and its association with the pathogenesis of diseases has also been reported. Recently, persistent pollutants, such as micro- and nanoplastics, have become growing global environmental threats with potential health risks. In this review, we discuss the impact of micro- and nanoplastics on mitochondria and review current knowledge in this field.

1. Introduction

Mitochondria originated in specialized eukaryotic cells that engulfed endosymbiotic prokaryotes approximately two billion years ago [1,2,3]. Mitochondria have been referred to as energy-producing organelles or “power plants” of cells that supply over 90% of adenosine triphosphate (ATP) to support cell metabolism [4]. Mitochondria are also involved in the regulation of redox status, ion homeostasis, cell signaling, and cell growth; thus, they play crucial roles in cell survival and cell death mechanisms [5,6,7]. Because of their central roles in cell survival and death, dysfunctional mitochondria contribute to the pathogenesis and progression of various diseases, such as metabolic diseases, neurological diseases, and cancers [8,9,10,11].
Mitochondria produce most of the cellular energy in the form of ATP through the oxidative phosphorylation of carbohydrates and fatty acids. Metabolites produced by ATP synthesis, including nucleic acids, lipids, and proteins, are used for macromolecule biosynthesis. Mitochondria also provide the majority of reactive oxygen species (ROS), and the bulk of mitochondrial ROS is produced in the electron transport chain (ETC) [12,13,14]. Therefore, dysfunctional mitochondria act as harmful ROS generators, causing oxidative stress and triggering apoptosis and cell damage. Upon stress, mitochondrial damage or loss of mitochondrial membrane integrity results in the release of apoptotic factors and the associated caspase activation [15].
Mitochondria contain their own DNA and a unique genetic code that is maternally inherited and differs from that of nuclear DNA. However, most mitochondrial proteins are generated by nuclear DNA translation [16]. The maintenance of mitochondrial DNA (mtDNA) is essential for preventing abnormal mitochondrial function and plays an important role in the pathogenesis of mitochondria-related disorders [17,18]. Additionally, mtDNA mutations and mitochondrial dysfunction have been associated with several diseases such as metabolic syndrome, cancer, neurodegeneration, and diabetes [19,20].
Exposure to external stimuli, such as multiple environmental contaminants, affects the normal structure and function of the mitochondria, leading to metabolic and functional diseases [21,22]. Recent studies have provided insights into the involvement of mitochondrial function defects that are induced by the toxicity of environmental contaminants [23,24,25] (Figure 1).

2. Environmental Contaminants: Plastics in the Environment

Fossil-based plastics are durable, lightweight, inexpensive, resistant to degradation, and possess thermal and electrical insulation properties [26]. Therefore, global plastic production has increased from 1.5 million tons in the 1950s to approximately 367 million tons in 2020 [27], and this trend is assumed to continue in the coming years. The supply chain of fossil-based plastics, including production, use, management, and waste generation, results in severe environmental problems [28,29]. Among plastic wastes, biodegradable plastics are more susceptible to physical fragmentation (disintegration) than mineralization (degradation); thus, it does not undergo complete biodegradation, which results in smaller sizes of plastic pollutants [30].

2.1. Micro- and Nanoplastics

The hazards of micro- and nanoplastics (MNPs) were first discussed in 2004, and their potentially harmful effects on living organisms have recently attracted significant attention [31,32,33,34]. Microplastics (MPs) are artificial polymer particles with sizes less than or equal to 5 mm and are not the end products of plastic waste as they degrade into nanoplastics [35]. Nanoplastics are defined as particles with sizes ranging from 1 nm to 1 μm [36].
MNPs can be classified into two types based on their source of origin: primary MNPs originate from pre-production plastic pellets in manufacturing industries, scrubbers, plastic resin flakes, plastic powder, commercial cleaning abrasives, or fluff used to produce plastic goods [37]. Secondary MNPs originate from the breakdown of larger plastic materials [38], and the frequency of fragmentation depends on the environmental conditions. MNPs penetrate the environment through land-based sources, atmospheric deposition, air transportation, textiles, and aquaculture (Figure 2). In addition, certain degradations, including UV and bacterial, degrade plastics that enter the environment into micro-nanosizes [39]. MNPs comprise the vast majority of plastic contaminants and have become abundant in the global environment [40,41,42].

2.2. Environmental Pollution with Microplastics

Globally, over 360 million tons of plastic are produced annually, and it is estimated that more than 8 million tons of plastic are dumped into the oceans annually [43]. The abundance of MPs is approximately 103–104 particles/m3 in tidal sediments, 0.1–1 particles/m3 in surface waters, and over 104 particles/m3 in deep-sea sediments [44]. Rivers are the foremost route for transporting plastic waste from land to sea. The concentration of MPs varies from 0.16 to 3438 particles/m3 in North and South American freshwater reservoirs, 0.28 to 1265 particles/m3 in European rivers, and 293 to 19,860 particles/m3 in Asian water bodies [45].
MPs are ubiquitously found in soil environments such as farmlands, greenhouses, home gardens, and floodplain soils [46]. Sewage irrigation is also among several sources of MPs in soil; in the floodplain soils of Spain, the abundance of MPs was higher in sewage-irrigated agricultural fields (5190 particles/kg) than in non-sewage-irrigated agricultural fields (2030 particles/kg) [47].
Airborne MPs have been detected in Shanghai, Paris, and London [48,49,50]. Atmospheric MPs originate from textiles, whereas non-fibrous particles mostly originate from the decomposition of packaging materials.

2.3. Microplastics in the Food Chains and Food

Current food production systems use large amounts of plastic materials for food packaging. Considerable use of plastics has resulted in the penetration of MPs into the food chain, resulting in high exposure to consumers. For example, the abundance of MPs in terrestrial food chains has been reported in chicken stomachs (5.1 particles/g), feces (105 particles/g) [34,51], and sheep feces (1000 particles/g) [52]. Studies have shown the presence of MPs in water, honey, beer, seafood, and sugar [53].

3. Toxicities of Micro- and Nanoplastics on Mitochondria

3.1. Toxicities in Human Cells

The exposure routes of MNPs to humans include inhalation of plastic-contaminated air or ingestion of plastic-contaminated food and water [54,55]. Thus, the respiratory and digestive systems are the first sites of contact for MNPs. MNPs induce systemic toxicity by penetrating cell membranes and internalizing into cells.
The cytotoxicity of MNPs has been evaluated by analyzing cell viability, intracellular ROS levels, mitochondrial membrane potential levels, and apoptosis in human pulmonary cells [56]. The major mechanism of the toxic effect of MNPs on cells may be the increase in ROS caused by oxidative stress, which in turn leads to a decrease in mitochondrial membrane potential. This study provides information on the toxicity of MNPs at environmental concentrations in human pulmonary cells, which helps to improve the risk cognition of MNPs in the respiratory system.
MNPs cause NADPH oxidase 4 (NOX4)-mediated mitochondrial dysfunction, as demonstrated by membrane potential changes and impaired cellular energy metabolism in the respiratory epithelium [57]. This suggests that MNPs induce epithelial-to-mesenchymal transition in human lung adenocarcinoma A549 cells via multiple mechanisms and that NOX4 is a vital mediator in this process. These findings contribute to our understanding of the toxicological mechanisms of MNPs in the respiratory system.
Lin et al. identified that human liver and lung cells exposed to MNPs experienced mitochondrial damage, as evidenced by the overgeneration of mitochondrial ROS, alterations in the mitochondrial membrane potential, and repression of mitochondrial respiration [58]. This study revealed the MNP-evoked mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing new insights into the possibility of adverse outcomes in human health.
A recent study suggested that MNP exposure directly augments mitochondrial damage and dysfunction and that mitochondrial breakdown results in mtDNA release into the cytoplasm. Accumulation of MNPs in hepatocytes was detected in vivo and in vitro. MNPs lead to nuclear DNA and mtDNA damage, and subsequent activation of the cGAS/STING signaling pathway was involved in mediating liver fibrosis. This study provides valuable insights into the potential risks and mechanisms of MNP-induced hepatic toxicity and fibrosis [59].
Wu et al. investigated whether exposure to MNPs alters mitochondrial depolarization and ATP synthesis, thereby inhibiting ATP-binding cassette transporter activity and enhancing toxicity in Caco-2 cells [60]. This study provides basic information on the toxicity of MNPs in human intestinal cells, which is useful for assessing the risk posed by MNPs in humans. Similarly, Wang et al. provided evidence that uptake of the MNPs was related to increased cellular oxidative stress and mitochondrial depolarization [61].
A recent study suggested that MNPs may cause changes in mitochondrial ROS, BCL2-associated agonist of cell death proteins, endoplasmic reticulum stress-related proteins, inflammation-related proteins, and autophagy-related proteins, leading to kidney damage and protein leakage [62]. These results suggest that exposure to MNPs may be a risk factor for poor kidney health.
Florance et al. revealed that MNP-enhanced lipid accumulation is accompanied by mitochondrial oxidative stress and loss of mitochondrial membrane potential, which is presumably restored in human macrophages [63]. This study demonstrated that MNPs induce lipid accumulation in macrophages accompanied by acute oxidative stress and induce macrophage foam cell formation, a characteristic feature observed in the pathology of atherosclerosis.
MNPs cause endothelial cell dysfunction by diminishing mitochondrial function and increasing pro-inflammatory cytokines, thereby triggering apoptosis [64]. This study also revealed differences in gene expression and metabolite levels between MNP-treated endothelial cells.
MNPs augment neurotoxicity in SHSY-5Y cells through the activation of autophagy and mitochondrial dysfunction, which are modulated by mitochondrial oxidative stress. Hence, mitochondrial damage caused by oxidative stress may be involved in the pathological mechanisms of MNP-evoked neurodegenerative diseases [65].
Salimi et al. revealed that MNPs are toxic to human lymphocytes, owing to excessive ROS formation, lysosomal/mitochondrial damage, lipid peroxidation, and glutathione depletion, ultimately resulting in cytotoxicity [66]. This study showed that human lymphocytes are more sensitive to MNP toxicity than fish lymphocytes.

3.2. Toxicities in Other Animal Cells

Liu et al. demonstrated the mitochondrial toxicity of MNPs, thus providing a basis for understanding the causes of sperm damage caused by MNPs. MNPs can damage the mitochondrial structure of GC-2 cells, a mouse spermatocyte line, decrease ATP content, diminish membrane potential, and destroy the integrity of the mitochondrial genome, leading to an imbalance in mitochondrial dynamic homeostasis, which induces mitochondrial autophagy. This study explored the effects of MNPs on the mitochondria of germ cell lines, providing support for further research on the effects of MNPs on reproductive health [67].
The exposure of rat basophilic leukemia RBL-2H3 cells to MNPs resulted in severe mitochondrial damage and apoptosis. Eventually, MNPs induce oxidative stress, damage organelles, and trigger apoptosis by augmenting the modulator of apoptosis-1 expression. Consequently, MNP-induced oxidative stress, organelle damage, cell cycle arrest, and apoptosis are correlated events [68].
MNPs can decrease cell viability, induce cell apoptosis, upregulate apoptosis-related protein expression, elicit ROS production, alter mitochondrial membrane potential, and dysregulate mitochondrial function in murine splenic lymphocytes [69].
MNP-exposed macrophages revealed a decrease in mitochondrial membrane potential, which suggests that phagocytosis of MNPs by murine macrophages can induce an immunometabolic active state [70]. These findings suggest a significant impact of alterations in macrophage metabolism caused by MNP exposure on immunity and inflammation.
Zhang et al. demonstrated that MNPs lead to changes in mitochondrial function and glycogen synthase kinase-3β (GSK-3β) and its associated gene expression in mice via the PI3K/AKT pathway, which eventually leads to the apoptosis of neurons [71]. This finding facilitates the understanding of the neurotoxic effects of MNPs on neurons in the cerebra of mice and helps distinguish the important role of maintaining normal mitochondrial function in protecting cerebrum health.
Liang et al. applied single-nucleus RNA sequencing (snRNA-seq) to mouse brains to examine the transcriptional changes at the single-cell level. Furthermore, to confirm the snRNA-seq findings, the misfolded protein levels, inflammation levels, and ATP content in different regions of the mouse brain were evaluated. MNPs may primarily induce mitochondrial dysfunction and energy metabolism disorders in neurons, particularly in excitatory neurons. Additionally, MNPs may cause disorders of ATP metabolism and mitochondrial and synaptic function regulation in astrocytes and may be involved in neurodegeneration [72].
A recent study revealed that MNPs might suppress antioxidative reactions and induce oxidative stress, leading to mitochondrial damage and cell death in ionocytes, ultimately impairing skin functions such as ion uptake, pH regulation, and ammonia excretion in zebrafish embryos [73]. This study expands our knowledge of the potential toxicity of MNPs in aquatic animals.
MNPs can induce neurodevelopmental toxicity depending on particle size, which is mediated by mitochondrial damage and dopamine reduction. Data from the mutant test demonstrated that improved expression of sel-12 and hop-1 is involved in the regulation of MNP-induced oxidative stress, mitochondrial damage, and neurodevelopmental toxicity in Caenorhabditis elegans [74].
Recently, MNPs, which have emerged as a serious issue in the field of environment and food safety, have been known to induce cell damage and affect cell survival, death, inflammation, and immune responses. Therefore, this review focuses on the association between mitochondria that are closely related to cell growth, survival, and death with various abnormalities induced by MNPs and diseases caused by mitochondrial dysfunction (summarized in Table 1). These findings and their implications should be discussed in the broadest possible contexts, including genomics and epi-genomics, in future research.

4. Conclusions

Mitochondria are eukaryotic cellular organelles that play a chief role in cells by metabolizing nutrients and producing the “universal energy currency”, ATP, and are responsible for various processes such as biosynthesis, bioenergetics, and signaling [75,76]. Dysregulated function of mitochondria has been proved to be essential for the pathogenesis and development of various diseases. Mitochondria are the main source of ROS production, redox molecule generation, and calcium storage; hence, mitochondria function as regulators of multiple related signaling pathways that contribute to a range of pathologies [77,78]. Mitochondrial structural and functional modifications have also been reported to be involved in cancer, metabolic syndromes, aging, and other diseases, such as stroke, ischemia, diabetes, obesity, heart disease, and neurodegenerative diseases.
Numerous studies have shown that exposure to environmental contaminants leads to impairment of mitochondrial function and disruption of mitochondrial dynamics (Figure 3). However, mitochondria-dependent mechanisms associated with MNPs exposure are still poorly understood.
This review focuses on understanding the effects of MNPs to the structure and functions of mitochondria and its impact in the pathogenesis of various diseases. A better understanding of the role of mitochondria after exposure to MNPs will provide a broader understanding of cellular systems.

Author Contributions

Conceptualization, S.E.L. and Y.S.P.; writing—original draft preparation, S.E.L.; writing—review and editing, S.E.L., Y.Y., S.M., H.Y. and Y.S.P.; funding acquisition, Y.S.P. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by the National Research Foundation of Korea (NRF) (grant number NRF-2020R1A2C1011704) and the Ministry of Health & Welfare, Republic of Korea (grant number: HV22C0160).

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not applicable.

Acknowledgments

This study was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (Grant No.: NRF-2020R1A2C1011704) and the Korean Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HV22C0160).

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Archibald, J.M. Endosymbiosis and Eukaryotic Cell Evolution. Curr. Biol. 2015, 25, R911–R921. [Google Scholar] [CrossRef] [PubMed]
  2. Gray, M.W. Mitochondrial evolution. Cold Spring Harb. Perspect. Biol. 2012, 4, a011403. [Google Scholar] [CrossRef] [PubMed]
  3. Kurland, C.G.; Andersson, S.G.E. Origin and evolution of the mitochondrial proteome. Microbiol. Mol. Biol. Rev. 2000, 64, 786–820. [Google Scholar] [CrossRef] [PubMed]
  4. Javadov, S.; Kozlov, A.V.; Camara, A.K.S. Mitochondria in Health and Diseases. Cells 2020, 9, 1177. [Google Scholar] [CrossRef]
  5. Kroemer, G.; Galluzzi, L.; Brenner, C. Mitochondrial membrane permeabilization in cell death. Physiol. Rev. 2007, 87, 99–163. [Google Scholar] [CrossRef]
  6. Zhou, R.; Yazdi, A.S.; Menu, P.; Tschopp, J. A role for mitochondria in NLRP3 inflammasome activation. Nature 2011, 469, 221–225. [Google Scholar] [CrossRef]
  7. Bock, F.J.; Tait, S.W.G. Mitochondria as multifaceted regulators of cell death. Nat. Rev. Mol. Cell Bio. 2020, 21, 85–100. [Google Scholar] [CrossRef]
  8. Wallace, D.C. A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: A dawn for evolutionary medicine. Ann. Rev. Genet. 2005, 39, 359–407. [Google Scholar] [CrossRef]
  9. Coskun, P.; Wyrembak, J.; Schriner, S.E.; Chen, H.W.; Marciniack, C.; LaFerla, F.; Wallace, D.C. A mitochondrial etiology of Alzheimer and Parkinson disease. Biochim. Biophys. Acta-Gen. Subj. 2012, 1820, 553–564. [Google Scholar] [CrossRef]
  10. Brandon, M.; Baldi, P.; Wallace, D.C. Mitochondrial mutations in cancer. Oncogene 2006, 25, 4647–4662. [Google Scholar] [CrossRef] [Green Version]
  11. Mercer, J.R.; Cheng, K.K.; Figg, N.; Gorenne, I.; Mahmoudi, M.; Griffin, J.; Vidal-Puig, A.; Logan, A.; Murphy, M.P.; Bennett, M. DNA Damage Links Mitochondrial Dysfunction to Atherosclerosis and the Metabolic Syndrome. Circ. Res. 2010, 107, 1021–1031. [Google Scholar] [CrossRef] [PubMed]
  12. Hansford, R.G.; Hogue, B.A.; Mildaziene, V. Dependence of H2O2 formation by rat heart mitochondria on substrate availability and donor age. J. Bioenerg. Biomembr. 1997, 29, 89–95. [Google Scholar] [CrossRef] [PubMed]
  13. Li, X.Y.; Fang, P.; Mai, J.T.; Choi, E.T.; Wang, H.; Yang, X.F. Targeting mitochondrial reactive oxygen species as novel therapy for inflammatory diseases and cancers. J. Hematol. Oncol. 2013, 6, 1–19. [Google Scholar] [CrossRef] [PubMed]
  14. Galluzzi, L.; Kepp, O.; Trojel-Hansen, C.; Kroemer, G. Mitochondrial Control of Cellular Life, Stress, and Death. Circ. Res. 2012, 111, 1198–1207. [Google Scholar] [CrossRef]
  15. Jeong, S.Y.; Seol, D.W. The role of mitochondria in apoptosis. Bmb Rep. 2008, 41, 11–22. [Google Scholar] [CrossRef]
  16. Ott, M.; Amunts, A.; Brown, A. Organization and Regulation of Mitochondrial Protein Synthesis. Ann. Rev. Biochem. 2016, 85, 77–101. [Google Scholar] [CrossRef]
  17. Kaarniranta, K.; Pawlowska, E.; Szczepanska, J.; Jablkowska, A.; Blasiak, J. Role of Mitochondrial DNA Damage in ROS-Mediated Pathogenesis of Age-Related Macular Degeneration (AMD). Int. J. Mol. Sci. 2019, 20, 2374. [Google Scholar] [CrossRef]
  18. Caston, R.A.; Demple, B. Risky repair: DNA-protein crosslinks formed by mitochondrial base excision DNA repair enzymes acting on free radical lesions. Free Radic. Biol. Med. 2017, 107, 146–150. [Google Scholar] [CrossRef]
  19. Taylor, R.W.; Turnbull, D.M. Mitochondrial DNA mutations in human disease. Nat. Rev. Genet. 2005, 6, 389–402. [Google Scholar] [CrossRef]
  20. Filograna, R.; Mennuni, M.; Alsina, D.; Larsson, N.G. Mitochondrial DNA copy number in human disease: The more the better? FEBS Lett. 2021, 595, 976–1002. [Google Scholar] [CrossRef]
  21. Duarte-Hospital, C.; Tete, A.; Brial, F.; Benoit, L.; Koual, M.; Tomkiewicz, C.; Kim, M.J.; Blanc, E.B.; Coumoul, X.; Bortoli, S. Mitochondrial Dysfunction as a Hallmark of Environmental Injury. Cells 2022, 11, 110. [Google Scholar] [CrossRef]
  22. Peters, A.; Nawrot, T.S.; Baccarelli, A.A. Hallmarks of environmental insults. Cell 2021, 184, 1455–1468. [Google Scholar] [CrossRef] [PubMed]
  23. Roubicek, D.A.; de Souza-Pinto, N.C. Mitochondria and mitochondrial DNA as relevant targets for environmental contaminants. Toxicology 2017, 391, 100–108. [Google Scholar] [CrossRef] [PubMed]
  24. Dreier, D.A.; Mello, D.F.; Meyer, J.N.; Martyniuk, C.J. Linking Mitochondrial Dysfunction to Organismal and Population Health in the Context of Environmental Pollutants: Progress and Considerations for Mitochondrial Adverse Outcome Pathways. Environ. Toxicol. Chem. 2019, 38, 1625–1634. [Google Scholar] [CrossRef] [PubMed]
  25. Sharma, J.; Parsai, K.; Raghuwanshi, P.; Ali, S.A.; Tiwari, V.; Bhargava, A.; Mishra, P.K. Emerging role of mitochondria in airborne particulate matter-induced immunotoxicity. Environ. Pollut. 2021, 270, 116242. [Google Scholar] [CrossRef]
  26. Andrady, A.L.; Neal, M.A. Applications and societal benefits of plastics. Philos. T R Soc. B 2009, 364, 1977–1984. [Google Scholar] [CrossRef]
  27. PlasticsEurope. Annual Production of Plastics Worldwide from 1950 to 2020 (in Million Metric Tons). Statista 2021. Available online: https://www.statista.com/statistics/282732/global-production-of-plastics-since-1950/ (accessed on 23 August 2022).
  28. Batel, A.; Linti, F.; Scherer, M.; Erdinger, L.; Braunbeck, T. Transfer of benzo[a]pyrene from microplastics to Artemia nauplii and further to zebrafish via a trophic food web experiment: CYP1A induction and visual tracking of persistent organic pollutants. Environ. Toxicol. Chem. 2016, 35, 1656–1666. [Google Scholar] [CrossRef]
  29. Schirinzi, G.F.; Perez-Pomeda, I.; Sanchis, J.; Rossini, C.; Farre, M.; Barcelo, D. Cytotoxic effects of commonly used nanomaterials and microplastics on cerebral and epithelial human cells. Environ. Res. 2017, 159, 579–587. [Google Scholar] [CrossRef]
  30. Whitacre, D.M. Preface. In Reviews of Environmental Contamination and Toxicology Volume 228; Springer: Cham, Switzerland, 2014. [Google Scholar] [CrossRef]
  31. Lebordais, M.; Gutierrez-Villagomez, J.M.; Gigault, J.; Baudrimont, M.; Langlois, V.S. Molecular impacts of dietary exposure to nanoplastics combined with arsenic in Canadian oysters (Crassostrea virginica) and bioaccumulation comparison with Caribbean oysters (Isognomon alatus). Chemosphere 2021, 277, 130331. [Google Scholar] [CrossRef]
  32. Ricciardi, M.; Pironti, C.; Motta, O.; Miele, Y.; Proto, A.; Montano, L. Microplastics in the Aquatic Environment: Occurrence, Persistence, Analysis, and Human Exposure. Water 2021, 13, 973. [Google Scholar] [CrossRef]
  33. Matthews, S.; Mai, L.; Jeong, C.B.; Lee, J.S.; Zeng, E.Y.; Xu, E.G. Key mechanisms of micro- and nanoplastic (MNP) toxicity across taxonomic groups. Comp. Biochem. Physiol. C Toxicol. Pharmacol. 2021, 247, 109056. [Google Scholar] [CrossRef] [PubMed]
  34. Zolotova, N.; Kosyreva, A.; Dzhalilova, D.; Fokichev, N.; Makarova, O. Harmful effects of the microplastic pollution on animal health: A literature review. PeerJ 2022, 10, e13503. [Google Scholar] [CrossRef] [PubMed]
  35. Karlsson, T.M.; Arneborg, L.; Brostrom, G.; Almroth, B.C.; Gipperth, L.; Hassellov, M. The unaccountability case of plastic pellet pollution. Mar. Pollut. Bull. 2018, 129, 52–60. [Google Scholar] [CrossRef] [PubMed]
  36. Gigault, J.; ter Halle, A.; Baudrimont, M.; Pascal, P.Y.; Gauffre, F.; Phi, T.L.; El Hadri, H.; Grassl, B.; Reynaud, S. Current opinion: What is a nanoplastic? Environ. Pollut. 2018, 235, 1030–1034. [Google Scholar] [CrossRef] [PubMed]
  37. Lambert, S.; Sinclair, C.; Boxall, A. Occurrence, degradation, and effect of polymer-based materials in the environment. Rev. Environ. Contam. Toxicol. 2014, 227, 1–53. [Google Scholar] [CrossRef] [PubMed]
  38. Lamichhane, G.; Acharya, A.; Marahatha, R.; Modi, B.; Paudel, R.; Adhikari, A.; Raut, B.K.; Aryal, S.; Parajuli, N. Microplastics in environment: Global concern, challenges, and controlling measures. Int. J. Environ. Sci. Technol. 2022, 1–22. [Google Scholar] [CrossRef] [PubMed]
  39. Lee, H.; Shim, W.J.; Kwon, J.H. Sorption capacity of plastic debris for hydrophobic organic chemicals. Sci. Total Environ. 2014, 470–471, 1545–1552. [Google Scholar] [CrossRef]
  40. Alimi, O.S.; Farner Budarz, J.; Hernandez, L.M.; Tufenkji, N. Microplastics and Nanoplastics in Aquatic Environments: Aggregation, Deposition, and Enhanced Contaminant Transport. Environ. Sci. Technol. 2018, 52, 1704–1724. [Google Scholar] [CrossRef] [PubMed]
  41. Enders, K.; Lenz, R.; Stedmon, C.A.; Nielsen, T.G. Abundance, size and polymer composition of marine microplastics ≥10 μm in the Atlantic Ocean and their modelled vertical distribution. Mar. Pollut. Bull. 2015, 100, 70–81. [Google Scholar] [CrossRef]
  42. Llorca, M.; Farre, M. Current Insights into Potential Effects of Micro-Nanoplastics on Human Health by in-vitro Tests. Front. Toxicol 2021, 3, 752140. [Google Scholar] [CrossRef]
  43. Jambeck, J.R.; Geyer, R.; Wilcox, C.; Siegler, T.R.; Perryman, M.; Andrady, A.; Narayan, R.; Law, K.L. Plastic waste inputs from land into the ocean. Science 2015, 347, 768–771. [Google Scholar] [CrossRef] [PubMed]
  44. Erni-Cassola, G.; Zadjelovic, V.; Gibson, M.I.; Christie-Oleza, J.A. Distribution of plastic polymer types in the marine environment; A meta-analysis. J. Hazard. Mater. 2019, 369, 691–698. [Google Scholar] [CrossRef] [PubMed]
  45. Sarijan, S.; Azman, S.; Said, M.I.M.; Jamal, M.H. Microplastics in freshwater ecosystems: A recent review of occurrence, analysis, potential impacts, and research needs. Environ. Sci. Pollut. R 2021, 28, 1341–1356. [Google Scholar] [CrossRef] [PubMed]
  46. Hirt, N.; Body-Malapel, M. Immunotoxicity and intestinal effects of nano- and microplastics: A review of the literature. Part. Fibre Toxicol. 2020, 17, 1–22. [Google Scholar] [CrossRef] [PubMed]
  47. van den Berg, P.; Huerta-Lwanga, E.; Corradini, F.; Geissen, V. Sewage sludge application as a vehicle for microplastics in eastern Spanish agricultural soils. Environ. Pollut. 2020, 261, 114198. [Google Scholar] [CrossRef] [PubMed]
  48. Liu, K.; Wang, X.H.; Fang, T.; Xu, P.; Zhu, L.X.; Li, D.J. Source and potential risk assessment of suspended atmospheric microplastics in Shanghai. Sci. Total Environ. 2019, 675, 462–471. [Google Scholar] [CrossRef]
  49. Dris, R.; Gasperi, J.; Rocher, V.; Saad, M.; Renault, N.; Tassin, B. Microplastic contamination in an urban area: A case study in Greater Paris. Environ. Chem 2015, 12, 592–599. [Google Scholar] [CrossRef]
  50. Wright, S.L.; Ulke, J.; Font, A.; Chan, K.L.A.; Kelly, F.J. Atmospheric microplastic deposition in an urban environment and an evaluation of transport. Environ. Int. 2020, 136, 105411. [Google Scholar] [CrossRef]
  51. Lwanga, E.H.; Vega, J.M.; Quej, V.K.; Chi, J.D.; del Cid, L.S.; Chi, C.; Segura, G.E.; Gertsen, H.; Salanki, T.; van der Ploeg, M.; et al. Field evidence for transfer of plastic debris along a terrestrial food chain. Sci. Rep. 2017, 7, 1–7. [Google Scholar] [CrossRef] [Green Version]
  52. Beriot, N.; Peek, J.; Zornoza, R.; Geissen, V.; Huerta Lwanga, E. Low density-microplastics detected in sheep faeces and soil: A case study from the intensive vegetable farming in Southeast Spain. Sci. Total Environ. 2021, 755, 142653. [Google Scholar] [CrossRef]
  53. Karbalaei, S.; Hanachi, P.; Walker, T.R.; Cole, M. Occurrence, sources, human health impacts and mitigation of microplastic pollution. Environ. Sci. Pollut. Res. Int. 2018, 25, 36046–36063. [Google Scholar] [CrossRef] [PubMed]
  54. Zhang, Q.; Xu, E.G.; Li, J.; Chen, Q.; Ma, L.; Zeng, E.Y.; Shi, H. A Review of Microplastics in Table Salt, Drinking Water, and Air: Direct Human Exposure. Environ. Sci. Technol. 2020, 54, 3740–3751. [Google Scholar] [CrossRef]
  55. Sivagami, M.; Selvambigai, M.; Devan, U.; Velangani, A.A.J.; Karmegam, N.; Biruntha, M.; Arun, A.; Kim, W.; Govarthanan, M.; Kumar, P. Extraction of microplastics from commonly used sea salts in India and their toxicological evaluation. Chemosphere 2021, 263, 128181. [Google Scholar] [CrossRef] [PubMed]
  56. Zhang, H.; Zhang, S.; Duan, Z.; Wang, L. Pulmonary toxicology assessment of polyethylene terephthalate nanoplastic particles in vitro. Environ. Int 2022, 162, 107177. [Google Scholar] [CrossRef] [PubMed]
  57. Halimu, G.; Zhang, Q.R.; Liu, L.; Zhang, Z.C.; Wang, X.J.; Gu, W.; Zhang, B.W.; Dai, Y.M.; Zhang, H.W.; Zhang, C.G.; et al. Toxic effects of nanoplastics with different sizes and surface charges on epithelial-to-mesenchymal transition in A549 cells and the potential toxicological mechanism. J. Hazard. Mater. 2022, 430, 128485. [Google Scholar] [CrossRef] [PubMed]
  58. Lin, S.; Zhang, H.; Wang, C.; Su, X.L.; Song, Y.; Wu, P.; Yang, Z.; Wong, M.H.; Cai, Z.; Zheng, C. Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells. Environ. Sci. Technol. 2022. [Google Scholar] [CrossRef]
  59. Shen, R.; Yang, K.R.; Cheng, X.; Guo, C.L.; Xing, X.Q.; Sun, H.N.; Liu, D.S.; Liu, X.W.; Wang, D.G. Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway. Environ. Pollut. 2022, 300, 118986. [Google Scholar] [CrossRef]
  60. Wu, B.; Wu, X.M.; Liu, S.; Wang, Z.Z.; Chen, L. Size-dependent effects of polystyrene microplastics on cytotoxicity and efflux pump inhibition in human Caco-2 cells. Chemosphere 2019, 221, 333–341. [Google Scholar] [CrossRef]
  61. Wang, Q.; Bai, J.; Ning, B.; Fan, L.; Sun, T.; Fang, Y.; Wu, J.; Li, S.; Duan, C.; Zhang, Y.; et al. Effects of bisphenol A and nanoscale and microscale polystyrene plastic exposure on particle uptake and toxicity in human Caco-2 cells. Chemosphere 2020, 254, 126788. [Google Scholar] [CrossRef]
  62. Wang, Y.L.; Lee, Y.H.; Hsu, Y.H.; Chiu, I.J.; Huang, C.C.; Huang, C.C.; Chia, Z.C.; Lee, C.P.; Lin, Y.F.; Chiu, H.W. The Kidney-Related Effects of Polystyrene Microplastics on Human Kidney Proximal Tubular Epithelial Cells HK-2 and Male C57BL/6 Mice. Environ. Health Perspect. 2021, 129, 57003. [Google Scholar] [CrossRef]
  63. Florance, I.; Chandrasekaran, N.; Gopinath, P.M.; Mukherjee, A. Exposure to polystyrene nanoplastics impairs lipid metabolism in human and murine macrophages in vitro. Ecotoxicol. Environ. Saf. 2022, 238, 113612. [Google Scholar] [CrossRef] [PubMed]
  64. Zhang, M.; Shi, J.; Huang, Q.; Xie, Y.; Wu, R.H.; Zhong, J.Y.; Deng, H.P. Multi-omics analysis reveals size-dependent toxicity and vascular endothelial cell injury induced by microplastic exposure in vivo and in vitro. Environ. Sci.-Nano. 2022, 9, 663–683. [Google Scholar] [CrossRef]
  65. Tang, Q.S.; Li, T.W.; Chen, K.Z.; Deng, X.Y.; Zhang, Q.; Tang, H.L.; Shi, Z.F.; Zhu, T.M.; Zhu, J.H. PS-NPs Induced Neurotoxic Effects in SHSY-5Y Cells via Autophagy Activation and Mitochondrial Dysfunction. Brain Sci. 2022, 12, 952. [Google Scholar] [CrossRef] [PubMed]
  66. Salimi, A.; Alavehzadeh, A.; Ramezani, M.; Pourahmad, J. Differences in sensitivity of human lymphocytes and fish lymphocytes to polyvinyl chloride microplastic toxicity. Toxicol. Ind. Health 2022, 38, 100–111. [Google Scholar] [CrossRef]
  67. Liu, T.; Hou, B.L.; Wang, Z.P.; Yang, Y.L. Polystyrene microplastics induce mitochondrial damage in mouse GC-2 cells. Ecotoxicol. Environ. Saf. 2022, 237, 113520. [Google Scholar] [CrossRef] [PubMed]
  68. Liu, L.; Liu, B.Y.; Zhang, B.W.; Ye, Y.Y.; Jiang, W. Polystyrene micro(nano)plastics damage the organelles of RBL-2H3 cells and promote MOAP-1 to induce apoptosis. J. Hazard. Mater. 2022, 438, 129550. [Google Scholar] [CrossRef]
  69. Li, Y.Q.; Xu, M.K.; Zhang, Z.C.; Halimu, G.; Li, Y.Q.; Li, Y.S.; Gu, W.; Zhang, B.W.; Wang, X.J.; Rocha-Santos, T.A.P. In vitro study on the toxicity of nanoplastics with different charges to murine splenic lymphocytes. J. Hazard. Mater. 2022, 424, 127508. [Google Scholar] [CrossRef]
  70. Merkley, S.D.; Moss, H.C.; Goodfellow, S.M.; Ling, C.L.; Meyer-Hagen, J.L.; Weaver, J.; Campen, M.J.; Castillo, E.F. Polystyrene microplastics induce an immunometabolic active state in macrophages. Cell Biol. Toxicol. 2022, 38, 31–41. [Google Scholar] [CrossRef]
  71. Zhang, W.; Sun, X.; Qi, X.; Liu, X.; Zhang, Y.; Qiao, S.; Lin, H. Di-(2-Ethylhexyl) Phthalate and Microplastics Induced Neuronal Apoptosis through the PI3K/AKT Pathway and Mitochondrial Dysfunction. J. Agric. Food Chem. 2022. [Google Scholar] [CrossRef]
  72. Liang, B.X.; Huang, Y.J.; Zhong, Y.Z.; Li, Z.M.; Ye, R.Y.; Wang, B.; Zhang, B.L.; Meng, H.; Lin, X.; Du, J.X.; et al. Brain single-nucleus transcriptomics highlights that polystyrene nanoplastics potentially induce Parkinson’s disease-like neurodegeneration by causing energy metabolism disorders in mice. J. Hazard. Mater. 2022, 430, 128459. [Google Scholar] [CrossRef]
  73. Kantha, P.; Liu, S.T.; Horng, J.L.; Lin, L.Y. Acute exposure to polystyrene nanoplastics impairs skin cells and ion regulation in zebrafish embryos. Aquat. Toxicol. 2022, 248, 106203. [Google Scholar] [CrossRef] [PubMed]
  74. Liu, Q.Y.; Chen, C.X.; Li, M.T.; Ke, J.; Huang, Y.C.; Bian, Y.F.; Guo, S.F.; Wu, Y.; Han, Y.; Liu, M.Y. Neurodevelopmental Toxicity of Polystyrene Nanoplastics in Caenorhabditis elegans and the Regulating Effect of Presenilin. ACS Omega 2020, 5, 33170–33177. [Google Scholar] [CrossRef] [PubMed]
  75. Kim, J.A.; Wei, Y.Z.; Sowers, J.R. Role of mitochondrial dysfunction in insulin resistance. Circ. Res. 2008, 102, 401–414. [Google Scholar] [CrossRef]
  76. Halliwell, B.; Gutteridge, J.M.C. Free Radicals in Biology and Medicine, 4th ed.; Oxford University Press: Oxford, UK; New York, NY, USA, 2007; p. xxxvi. 851p. [Google Scholar]
  77. Murphy, M.P. How mitochondria produce reactive oxygen species. Biochem. J. 2009, 417, 1–13. [Google Scholar] [CrossRef]
  78. Mailloux, R.J.; McBride, S.L.; Harper, M.E. Unearthing the secrets of mitochondrial ROS and glutathione in bioenergetics. Trends Biochem. Sci. 2013, 38, 592–602. [Google Scholar] [CrossRef]
Metabolites 12 00897 g001 550
Figure 1. Environmental contaminant-induced mitochondrial dysfunction may lead to various diseases.
Figure 1. Environmental contaminant-induced mitochondrial dysfunction may lead to various diseases.
Metabolites 12 00897 g001
Metabolites 12 00897 g002 550
Figure 2. Sources of micro- and nanoplastics in the environment.
Figure 2. Sources of micro- and nanoplastics in the environment.
Metabolites 12 00897 g002
Metabolites 12 00897 g003 550
Figure 3. Role of mitochondria in response to micro- and nanoplastics toxicity.
Figure 3. Role of mitochondria in response to micro- and nanoplastics toxicity.
Metabolites 12 00897 g003
Table
Table 1. Summary of micro- and nanoplastic (MNP) toxicity on mitochondria.
Table 1. Summary of micro- and nanoplastic (MNP) toxicity on mitochondria.
ModelsMechanismReferences
A549 (human alveolar epithelial cells)Disruption of mitochondrial membrane potentialZhang et al., 2022 [56]
Alteration of mitochondrial dysfunctionHalimu et al., 2022 [57]
L02 (human hepatic cells) and BEAS-2B (human lung epithelial cells)Alteration of mitochondrial dysfunction (disruption of mitochondrial membrane potential and suppression of mitochondrial respiration)Lin et al., 2022 [58]
Human liver and mice liver cellsInduction of mtDNA damageShen et al., 2022 [59]
Caco-2 (human colon adenocarcinoma cells)Induction of mitochondrial depolarizationWu et al., 2019 [60]
Induction of mitochondrial depolarizationWang et al., 2020 [61]
HK-2 (human kidney proximal tubular epithelial cells) and in the kidneys of miceAlteration of mitochondrial dysfunctionWang et al., 2021 [62]
Human and murine macrophagesDisruption of mitochondrial membrane potential and induction of mitochondrial oxidative stressFlorance et al., 2022 [63]
HUVECs (human umbilical vein endothelial cells)Alteration of mitochondrial dysfunctionZhang et al., 2022 [64]
SHSY-5Y (human neuroblastoma cells)Alteration of mitochondrial dysfunctionTang et al., 2022 [65]
Human lymphocytesInduction of mitochondrial damageSalimi et al., 2022 [66]
GC-2 (mouse spermatocyte cells)Induction of mitochondrial damageLiu et al., 2022 [67]
RBL-2H3 (rat basophilic leukemia cells)Induction of mitochondrial damageLiu et al., 2022 [68]
Murine splenic lymphocytesDisruption of mitochondrial membrane potential Li et al., 2022 [69]
Murine macrophagesReduction in mitochondrial respirationMerkley et al., 2022 [70]
NS20Y (mouse neuroblastoma cells)Alteration of mitochondrial dysfunctionZhang et al., 2022 [71]
Mouse brainAlteration of mitochondrial dysfunctionLiang et al., 2022 [72]
Zebrafish embryosInduction of mitochondrial damageKantha et al., 2022 [73]
Caenorhabditis elegansInduction of mitochondrial damageLiu et al., 2020 [74]
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Lee, S.E.; Yi, Y.; Moon, S.; Yoon, H.; Park, Y.S. Impact of Micro- and Nanoplastics on Mitochondria. Metabolites 2022, 12, 897. https://doi.org/10.3390/metabo12100897

AMA Style

Lee SE, Yi Y, Moon S, Yoon H, Park YS. Impact of Micro- and Nanoplastics on Mitochondria. Metabolites. 2022; 12(10):897. https://doi.org/10.3390/metabo12100897

Chicago/Turabian Style

Lee, Seung Eun, Yoojung Yi, Sangji Moon, Hyunkyung Yoon, and Yong Seek Park. 2022. "Impact of Micro- and Nanoplastics on Mitochondria" Metabolites 12, no. 10: 897. https://doi.org/10.3390/metabo12100897

APA Style

Lee, S. E., Yi, Y., Moon, S., Yoon, H., & Park, Y. S. (2022). Impact of Micro- and Nanoplastics on Mitochondria. Metabolites, 12(10), 897. https://doi.org/10.3390/metabo12100897

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop