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WIREs Nanomed Nanobiotechnol
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Understanding engineered nanomaterial skin interactions and the modulatory effects of ultraviolet radiation skin exposure

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The study of engineered nanomaterials for the development of technological applications, nanomedicine, and nano‐enabled consumer products is an ever‐expanding discipline as is the concern over the impact of nanotechnology on human environmental health and safety. In this review, we discuss the current state of understanding of nanomaterial skin interactions with a specific emphasis on the effects of ultraviolet radiation (UVR) skin exposure. Skin is the largest organ of the body and is typically exposed to UVR on a daily basis. This necessitates the need to understand how UVR skin exposure can influence nanomaterial skin penetration, alter nanomaterial systemic trafficking, toxicity, and skin immune function. We explore the unique dichotomy that UVR has on inducing both deleterious and therapeutic effects in skin. The subject matter covered in this review is broadly informative and will raise awareness of potential increased risks from nanomaterial skin exposure associated with specific occupational and life style choices. The UVR‐induced immunosuppressive response in skin raises intriguing questions that motivate future research directions in the nanotoxicology and nanomedicine fields. WIREs Nanomed Nanobiotechnol 2014, 6:61–79. doi: 10.1002/wnan.1244 This article is categorized under: Therapeutic Approaches and Drug Discovery > Emerging Technologies Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials

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Transmission electron micrographs illustrating unique features of skin. (a) The stratum corneum (SC) is comprised of multiple layers of enucleated and elongated corneocytes each defined by a dense cornified envelope indicated by the black arrows. The cells in the stratum granulosum (SG) are distinguished by the presence of a nucleus (N) and a high density of keratohyalin granules (K). (Reprinted with permission from Ref . Copyright 1988 Nature Publishing Group). (b) Electron micrograph of a corneocyte cytosol illustrating the nanoscale organization of keratin intermediate filaments. The subfilamentous molecular architecture appears as groups of electron dense spots surrounding a central dense dot. The keratin filaments are ˜7.8 nm wide with a center‐to‐center distance of ˜16 nm. Inset box scale bar is 10 nm. (Reprinted with permission from Ref . Copyright 2004 Nature Publishing Group). (c) Corneocytes in the SC are bound by corneodesmosome tight junctions indicated by black arrows. Racial differences exist in the density of corneodesmosomes. Scale bar is 1 µm. (Reprinted with permission from Ref . Copyright 2009 Nature Publishing Group). (d) Electron micrograph illustrating the lipid lamellar bilayers in the intercellular space between corneocytes. (Reprinted with permission from Ref . Copyright 1999 Nature Publishing Group)
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Schematic of human skin structure and constituent cell types. Skin is stratified epithelium composed of the epidermis and dermis. The epidermis is mainly comprised of keratinocytes. Basal keratinocytes undergo terminal differentiation to form the stratum spinosum, stratum granulosum, and stratum corneum (SC) barrier. Stratum lucidum is an additional layer present under the SC in areas of thick skin like palms of the hands and soles of the feet. Pigment producing melanocytes and antigen‐presenting Langerhans cells are also present in the epidermis. The dermis is a layer rich in connective tissue and is divided into the papillary and reticular regions. The dermis contains many cell types including fibroblasts that make collagen and other extracellular matrix molecules that provide skin mechanical toughness. Adipocytes, macrophage, mast cells, plasmatoid dendritic cells (pDCs), CD4+ T cells, CD8+ T cells, T regulatory cells (Tregs), and natural killer T cells also abundantly present in the dermis apart from other structures including pilosebaceous unit, sweat glands, nerves, blood, and lymphatic vessels.
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Cadmium tissue level in distal organs following 24 h quantum dot (QD) nanoparticle application to SHK mice as a function of ultraviolet radiation (UVR). Liver results show that QD exposure to control mice (no UVR) does not significantly increase Cd level. Application of QDs to UVR‐exposed mice did statistically increase liver Cd relative to controls (no UVR with or without QD). Lymph node results show that the background Cd level was below the limit of quantification (<LOQ) in vehicle‐treated animals with and without UVR exposure. Unexpectedly, application of QDs to control mice (no UVB) produced a high Cd level in the lymph nodes suggesting QDs penetrated intact mouse skin. QD application to UVR‐exposed mice produced lower Cd level suggesting a UVR‐dependent cellular transport of QD mechanism to lymph node. Each value is reported as the mean ± SEM (n = 5, *P < 0.05). (Reprinted with permission from Ref . Copyright 2013 Informa Health Care)
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Dependence of ultraviolet (UV)–visible light attenuation on TiO2 nanoparticle aggregate size. With decreasing particle size, UV protection shifts to shorter wavelengths. Blue line, 20 nm; green line, 50 nm; and red line, 100 nm. Particles with average aggregate size of ˜50 nm offer high UVB attenuation and lower visible light scattering but less UVA absorption. (Reprinted with permission from Ref . Copyright 2011 Elsevier Inc)
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Transmission electron microscopy (TEM) imaging of mouse skin sections suggesting quantum dot nanoparticles penetrate intercellularly between corneocytes. (a) The penetration pathway through the stratum corneum is between corneocytes, which is shown in more detail in (b) where the large dark spots are quantum dots. (c) Another skin section demonstrating the penetration pathway showing quantum dot present in the stratum granulosum. (d) A negative control (no quantum dots). (Reprinted with permission from Ref . Copyright 2008 American Chemical Society Publications)
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The effect of ultraviolet radiation (UVR) on SKH mouse skin barrier function as measured by transepidermal water loss (TEWL). UVR exposure increases the barrier defect in a UVB dose‐ (0–360 mJ/cm2UVB) and time‐dependent manner. A statistically significant increase in TEWL is observed for all exposures with the peak defect ranging from 3 to 6 days post‐UVR exposure. Each value is reported as the mean ± SEM (n = 4, *P < 0.05, **P < 0.01, ***P < 0.001). (Reprinted with permission from Ref . Copyright 2013 Informa Health Care)
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Characterization of ultraviolet radiation (UVR)‐induced epidermal injury in SKH‐1 mice. Hematoxylin and eosin‐stained photomicrographs of normal dorsal mouse skin (N) and of skin 24, 72, 96, or 168 h after UVR (180 mJ/cm2UVB) irradiation. Note the epidermal hyperplasia (black arrow), hyperkeratosis (white arrow), and the perivascular inflammation (arrowheads) present 72 h after UVR irradiation. At 168 h post‐UVR irradiation, the epidermis has returned to near normal. Scale bar: 50 µm. (Reprinted with permission from Ref . Copyright 2003 Nature Publishing Group)
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E‐cadherin expression in primary mouse keratinocytes (PMK) after acute ultraviolet radiation (UVR) exposure. PMKs were harvested at the times indicated post‐UVR (40 mJ/cm2UVB). Unirradiated PMKs were included as controls. Densitometric analysis of Western data for relative E‐cadherin levels normalized to GAPDH. E‐cadherin levels were significantly different from control at 6, 24, and 72 h (n = 3). ***P < 0.001. Inset, a representative Western blot for E‐cadherin from one of three separate experiments. Equal loading of protein was verified by GAPDH staining. (Reprinted with permission from Ref . Copyright 2007 American Association for Cancer Research, Inc)
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Formation of bipyrimidine photoproducts within human skin exposed to UVB radiation. (a) Photoproduct formation is linear with respect to the applied UVB dose (0–0.2 J/cm2). The results are expressed in lesions per 106 bases and are the average ± SD. (b) A similar distribution of bipyrimidine photoproducts is produced in human skin and in cultured primary keratinocytes isolated from the same donor following UVB. (Reprinted with permission from Ref . Copyright 2006 United States National Academy of Sciences)
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Schematic of the human hair follicle in late anagen phase. The bulge, outer root sheath, hair bulb, and follicle papilla are responsible for hair growth.
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Langerhans cell localization pattern around the hair follicle. Immunofluorescent staining of human skin epidermis with anti‐CD207‐Alexa 488 (Langerin) specific for Langerhans cells showing their distribution around the hair follicle infundibulum, scale bar = 50 µm. Inset shows the base of the hair follicle, scale bar = 10 µm.
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Therapeutic Approaches and Drug Discovery > Emerging Technologies
Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials

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