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      Prospects on the nano-plastic particles internalization and induction of cellular response in human keratinocytes

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          Abstract

          Background

          Today, cosmetic products are very popular with both men and women to improve their appearance and increase their social acceptability.

          Results

          In this study, nano-sized (30–300 nm) plastic particles were isolated from the commercial face-scrubs and treated on the human keratinocytes. The observed adherence of polyethylene nano-plastics (PENPs), polystyrene NPs (PSNPs), and face-scrubs isolated nano-plastics (NPs) on the keratin layer reveals a significant attachment of NPs from the cosmetics that are applied on the skin for a short duration. This attachment property could facilitate further adherence of protein molecules on NPs and the protein-corona formation. The protein-corona mimics protein aggregates, thereby triggers macropinocytosis, followed by the macropinolysosomal process in the cell. These internalized NPs induced the concentration-dependent cytotoxic, cytostatic and cytoprotective activity in keratinocytes. Both single dose and chronic long-term exposure of lethal and sub-lethal concentrations of NPs resulted in oxidative stress-mediated down-regulation of cell growth and proliferation inhibition. Autophagic structures and premature aging were also observed using an electron microscopy and a senescence marker, respectively in the NPs internalized HaCaT cells incubated in a fresh, NPs-free medium.

          Conclusion

          Though 2D culture models have many limitations, it produces significant conceptual advancements. This work provides an insight into the NPs concentration-dependent regulatory, cytoprotective, and cytotoxic effects in HaCaT cells. However, 3D model studies are required to identify the detailed mechanisms of NPs toxicity and cytoprotective events in cells at the molecular level.

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          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12989-021-00428-9.

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          Most cited references92

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          Autophagy fights disease through cellular self-digestion.

          Autophagy, or cellular self-digestion, is a cellular pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. For example, autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection and ageing. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health.
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            The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase.

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              Oxidative stress and autophagy: the clash between damage and metabolic needs

              Autophagy is a catabolic process aimed at recycling cellular components and damaged organelles in response to diverse conditions of stress, such as nutrient deprivation, viral infection and genotoxic stress. A growing amount of evidence in recent years argues for oxidative stress acting as the converging point of these stimuli, with reactive oxygen species (ROS) and reactive nitrogen species (RNS) being among the main intracellular signal transducers sustaining autophagy. This review aims at providing novel insight into the regulatory pathways of autophagy in response to glucose and amino acid deprivation, as well as their tight interconnection with metabolic networks and redox homeostasis. The role of oxidative and nitrosative stress in autophagy is also discussed in the light of its being harmful for both cellular biomolecules and signal mediator through reversible posttranslational modifications of thiol-containing proteins. The redox-independent relationship between autophagy and antioxidant response, occurring through the p62/Keap1/Nrf2 pathway, is also addressed in order to provide a wide perspective upon the interconnection between autophagy and oxidative stress. Herein, we also attempt to afford an overview of the complex crosstalk between autophagy and DNA damage response (DDR), focusing on the main pathways activated upon ROS and RNS overproduction. Along these lines, the direct and indirect role of autophagy in DDR is dissected in depth.
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                Author and article information

                Contributors
                ravanan@cutn.ac.in
                nchandrasekaran@vit.ac.in , nchandra40@hotmail.com
                Journal
                Part Fibre Toxicol
                Part Fibre Toxicol
                Particle and Fibre Toxicology
                BioMed Central (London )
                1743-8977
                8 September 2021
                8 September 2021
                2021
                : 18
                : 35
                Affiliations
                [1 ]GRID grid.412813.d, ISNI 0000 0001 0687 4946, Centre for Nanobiotechnology, , Vellore Institute of Technology (VIT), Tamil Nadu, ; Vellore, 632 014 India
                [2 ]GRID grid.412813.d, ISNI 0000 0001 0687 4946, Apoptosis and Cell Survival Research Lab, Department of Biosciences, School of Biosciences and Technology, , VIT University, ; Vellore, Tamil Nadu 632 014 India
                [3 ]GRID grid.448768.1, ISNI 0000 0004 1772 7660, Department of Microbiology, School of Life Sciences, , Central University of Tamil Nadu, ; Thiruvarur, Tamil Nadu 610 104 India
                [4 ]GRID grid.11201.33, ISNI 0000 0001 2219 0747, Faculty of Science and Environment, , Plymouth University, ; Plymouth, PL4 8AA UK
                Article
                428
                10.1186/s12989-021-00428-9
                8424902
                34496914
                f4eba0e9-f765-4358-a961-8d78a209d91d
                © The Author(s) 2021

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 22 April 2021
                : 31 August 2021
                Categories
                Research
                Custom metadata
                © The Author(s) 2021

                Toxicology
                nano-plastics,keratinocytes,human keratin,protein-corona,macropinocytosis,oxidative stress,autophagy,senescence

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