Ultraviolet irradiation-induced enhancement of inflammatory potential of polystyrene nano- and microplastics and effects of dispersion on lung clearance

Skin, our first interface to the external environment, is subjected to oxidative stress caused by a variety of factors such as solar ultraviolet, infrared and visible light, environmental pollution, including ozone and particulate matters, and psychological stress. Excessive reactive species, including reactive oxygen species and reactive nitrogen species, exacerbate skin pigmentation and aging, which further lead to skin tone unevenness, pigmentary disorder, skin roughness and wrinkles. Besides these, skin microbiota are also a very important factor ensuring the proper functions of skin. While environmental factors such as UV and pollutants impact skin microbiota compositions, skin dysbiosis results in various skin conditions. In this review, we summarize the generation of oxidative stress from exogenous and endogenous sources. We further introduce current knowledge on the possible roles of oxidative stress in skin pigmentation and aging, specifically with emphasis on oxidative stress and skin pigmentation. Meanwhile, we summarize the science and rationale of using three well-known antioxidants, namely vitamin C, resveratrol and ferulic acid, in the treatment of hyperpigmentation. Finally, we discuss the strategy for preventing oxidative stress-induced skin pigmentation and aging.

Ultraviolet (UV) irradiation regulates UV-responsive genes, including matrix metalloproteinases (MMPs). Moreover, UV-induced MMPs cause connective tissue damage and the skin to become wrinkled and aged. Here, we investigated the effect of eicosapentaenoic acid (EPA), a dietary omega-3 fatty acid, on UV-induced MMP-1 expression in human dermal fibroblasts (HDFs). We found that UV radiation increases MMP-1 expression and that this is mediated by p44 and p42 MAP kinase (ERK) and Jun-N-terminal kinase (JNK) activation but not by p38 activation. Pretreatment of HDFs with EPA inhibited UV-induced MMP-1 expression in a dose-dependent manner and also inhibited the UV-induced activation of ERK and JNK by inhibiting ERK kinase (MEK1) and SAPK/ERK kinase 1 (SEK1) activation, respectively. Moreover, inhibition of ERK and JNK by EPA resulted in the decrease of c-Fos expression and c-Jun phosphorylation/expression induced by UV, respectively, which led to the inhibition of UV-induced activator protein-1 DNA binding activity. This inhibitory effect of EPA on MMP-1 was not mediated by an antioxidant effect. We also found that EPA inhibited 12-O-tetradecanoylphorbol-13-acetate- or tumor necrosis factor-alpha-induced MMP-1 expression in HDFs and UV-induced MMP-1 expression in HaCaT cells. In conclusion, our results demonstrate that EPA can inhibit UV-induced MMP-1 expression by inhibiting the MEK1/ERK/c-Fos and SEK1/JNK/c-Jun pathways. Therefore, EPA is a potential agent for the prevention and treatment of skin aging.

In our previous study, we reported a facile method for preparing cylindrical polymer particles, namely, the stirring method. In this method, spherical polystyrene (PS) particles were just stirred in a poly(vinylpyrrolidone) aqueous solution using a magnetic stirrer for several hours. This study clarified the formation mechanism of cylindrical shapes from spherical particles by varying the combinations of materials [poly(tetrafluoroethylene) (PTFE) and glass] used in a vial and a bar. The Young's modulus values of PTFE and glass are lower and considerably higher, respectively, than that of PS. Cylindrical PS particles were obtained using a glass vial and a PTFE stirring bar or a PTFE vial and a glass stirring bar. In contrast, no deformation was observed in the spherical PS particles after stirring with a PTFE vial and a stirring bar. Thus, the deformation of the PS particles was attributed to the direct mechanical stress between the vial and stirring bar rather than the shear stress of the fluid. In addition, another fabrication method for cylindrical particles involving the application of direct mechanical stress using two plates, that is, the rubbing process, was developed.

Dihydrorhodamine (DHR) 123 is a fluorophore commonly used for measuring reactive oxygen species (ROS), often after exposing cells to ultraviolet (UV) irradiation or oxidative burst inducers such as Phorbol 12‐myristate 13‐acetate (PMA). However, the negative effects of UV irradiation on oxidation of DHR123 itself to green fluorescence rhodamine (R) 123 under different experimental conditions (e.g., different buffers, media, cells, ROS detection techniques) have not been fully appreciated. We determined the effect of UV on DHR123 fluorescence, using a cell‐free system, and A549 epithelial cells, NIH/3T3 fibroblast cells, Jurkat T cells, primary human T cells, HL‐60 neutrophils and primary human neutrophils. We found that UV irradiation rapidly increases green fluorescence of DHR123 in cell‐free solutions. The intensity of green fluorescence increases with increasing amounts of DHR123 and UV exposure. The fluorescence increase was greater in Roswell Park Memorial Institute medium (RPMI) than DMEM media. The presence of DMSO (0–1.25%, v/v) in RPMI further increases the fluorescence signal. Phosphate buffered solution (PBS) and Hanks' Balanced Salt Solution (HBSS) generate considerable background signal with DHR123, and increasing DMSO concentration greatly increases the fluorescence signal in these buffers. However, after UV irradiation the amount of DHR123 that remains unoxidized generates sufficient fluorescence signal to measure the ROS produced by H2O2 and peroxidase in vitro or Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase‐mediated ROS production within HL‐60 neutrophils or primary human neutrophils. We conclude that UV irradiation oxidizes DHR123 to generate Rhodamine 123 (R123) green fluorescence signal, and that the R123 present in the culture supernatant could give erroneous results in plate reader assays. However, flow cytometry and fluorescence microscopy reliably detect ROS in cells such as neutrophils. Overall, avoiding false‐positive results when detecting ROS using DHR123 requires selection of, agonists, the correct buffers, media, cell types, and measurement techniques.

Epidermal Growth Factor Receptor Is a Critical Mediator of Ultraviolet B Irradiation-Induced Signal Transduction in Immortalized Human Keratinocyte HaCaT Cells

As the skin is always in contact with oxygen and is increasingly exposed to environmental and artificial ultraviolet (UV) irradiation the risk of photooxidative damage induced by reactive oxygen species – finally leading to phototoxicity, photoaging and skin cancer – has increased substantially.The term reactive oxygen species (ROS) includes oxygen centered radicals like the superoxide anion radical and the hydroxyl radical, but also non‐radical species such as hydrogen peroxide and singlet oxygen – all being produced in skin upon UV irradiation. In response to the attack of reactive oxygen species the skin has developed a complex antioxidant defense system including enzymatic and non‐enzymatic antioxidants. As a first line of the enzymatic antioxidative defense, superoxide dismutases reduce superoxide anion radicals to hydrogen peroxide which subsequently is detoxified to water by catalase and glutathione peroxidases.We were interested whether the antioxidant enzymes manganese superoxide dismutase (SOD2) and glutathion peroxidase (GPx1) are inducible upon UV irradiation and whether repetitive UV exposure, as practiced for the light‐hardening during phototherapy of photodermatoses, can even enhance the adaptive antioxidant response. To address this question skin fibroblasts and keratinocytes were exposed in vitro to single and repetitive UV low dose irradiation in different time intervals and afterwords challenged by high dose irradiation. The antioxidant response was measured in terms of steady state mRNA levels and activity changes of SOD2 or GPx1 as well as of the viability after challenge with high dose UV‐irradiation.Interstingly, only UVA but not UVB irradiation was able to induce the mRNA steady state levels and the activity of SOD2 in fibroblasts. However, fibroblasts incubated with the supernatants from UVB‐irradiated epidermal cells responded with an increase in SOD2. This increase on mRNA and activity levels was mediated by paracrine acting secreted factors produced by the keratinocytes. If fibroblasts were exposed repetitively to sublethal UVA doses the further up‐regulation of SOD2 correlated with the protection against high UV doses. Importantly, SOD2 basal levels of protein content and activity substantially differed within cultivated cells and skin biopsies from different individuals. These results provide evidence for an adaptive antioxidative UV response of the skin. Interindividual differences might account for differences in the susceptibility to develop photodermatologic disorders related to photosensitivity, photoaging, and skin cancer.

Atmospheric particulate matter (PM) contains various chemicals, some of which generate in vivo reactive oxygen species (ROS). Owing to their high reactivity and oxidation ability, ROS can cause various diseases. To understand how atmospheric PM affects human health, we must clarify the PM components having oxidative potential (OP) leading to ROS production. According to previous studies, OP is exhibited by humic-like substances (HULIS) in atmospheric PM. However, the OP-dependence of the chemical structures of HULIS has not been clarified. Therefore, in this study, humic acid (HA, a model HULIS material) was exposed to ozone and ultraviolet (UV) irradiation, and its OP and structures were evaluated before and after the reactions using dithiothreitol (DTT) assay and Fourier transform infrared (FT-IR), respectively. The OP of HA was more significantly increased by UV irradiation than by ozone exposure. FT-IR analysis showed an increased intensity of the C=O peak in the HA structure after UV irradiation, suggesting that the OP of HA was increased by a chemical change to a more quinone-like structure after irradiation.

Solar UVA, but not UVC, reaches the earth's surface and therefore is an important etiological factor for the induction of human skin cancer. ATM kinase is an important regulator of cell survival and cell cycle checkpoints. Here, we observe that UVA, unlike UVC, triggers ATM kinase activity, and the activation may occur through reactive oxygen species produced after irradiation of cells with UVA. We also show that ATM activation is involved in the apoptotic response to UVA but not UVC. Furthermore, we provide evidence that ATM-dependent p53 and c-Jun N-terminal kinase (JNK) pathways are linked to UVA-induced apoptosis. On the other hand, UVC-induced apoptosis occurs through ATR-dependent p53 phosphorylation as well as the JNK pathway. Therefore, these results suggest that ATM, like p53, is involved in the UVA-induced apoptosis to suppress carcinogenesis.

Development of UV-induced squamous cell carcinomas is suppressed in the absence of SPARC.

A resveratrol-loaded nanostructured lipid carrier hydrogel to enhance the anti-UV irradiation and anti-oxidant efficacy

Low-dose Ultraviolet-A irradiation selectively eliminates nitrite oxidizing bacteria for mainstream nitritation

Lipoteichoic acid isolated from Lactobacillus plantarum down-regulates UV-induced MMP-1 expression and up-regulates type I procollagen through the inhibition of reactive oxygen species generation

Separations of spherical and disc-shaped polystyrene particles and blood components (red blood cells and platelets) using pinched flow fractionation device with a tilted sidewall and vertical focusing channels (t-PFF-v)

Aging is a biologic process characterized by time-dependent functional declines that are influenced by oxidative stress-induced inflammatory reactions. In particular, ultraviolet (UV) irradiation plays a key role in cellular senescence in photo-aged skin. However, the cellular senescence of epidermal keratinocytes and dermal fibroblasts by UV irradiation may differ depending on the exposure time and dosage of UV irradiation. Therefore, the purpose of the study was to evaluate and compare the effects of UV irradiation on cellular senescence in human epidermal keratinocytes (HaCaT) and human dermal fibroblasts (HDFs). After cell viability test, 200 mJ/cm UV irradiation was used in this study. To evaluate the reactive oxygen species and reactive nitrogen species production, the levels of glutathione (GSH) and nitrite (NO2) were measured. We also performed reverse transcription-polymerase chain reaction, Western blot analysis, and senescence-associated beta-galactosidase assay. An overall decrease in GSH and an increase in NO2 were observed in the HaCaT and HDF cells. However, the time-line and dose-dependent effects varied. Higher expressions of tumor necrosis factor-α, inducible nitric oxide synthase, and interleukin-1β than that of the control group were observed in both cells. The HDF cells showed high levels of matrix metallopeptidase 9 and neutral endopeptidase protein but low levels of SIRT1 and procollagen I. The expression of nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) was increased in the HaCaT cells, but not in the HDF cells. The NF-κB peaked at 1 hour after UV irradiation in the HaCaT cells. The "turning-on" signal was faster in the irradiated HaCaT cells.

Photoaging of the Connective Tissue of Skin: Its Prevention and Therapy