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Special Issue "UV-Induced Cell Death 2012"

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 October 2012)

Special Issue Editor

Guest Editor
Dr. Terrence Piva (Website)

School of Health & Biomedical Sciences, RMIT University, PO Box 71 Bundoora, Victoria 3083, Australia
Phone: +61-3-99256503
Fax: +61 3 9925 7063
Interests: cell death; photobiology; photoimmunology; skin cancer; enzymology; cell metabolism; oxidative stress; cancer metabolism; cell signalling; cytokines; inflammation; enzyme kinetics; metal oxide nanoparticles; sunscreens

Keywords

  • ultraviolet light
  • apoptosis
  • necrosis
  • cell membrane
  • caspases
  • nucleus
  • signalling pathways
  • enzyme activation
  • autophagy
  • sunburnt cell

Published Papers (14 papers)

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Research

Jump to: Review

Open AccessArticle Ultraviolet (UV) and Hydrogen Peroxide Activate Ceramide-ER Stress-AMPK Signaling Axis to Promote Retinal Pigment Epithelium (RPE) Cell Apoptosis
Int. J. Mol. Sci. 2013, 14(5), 10355-10368; doi:10.3390/ijms140510355
Received: 24 November 2012 / Revised: 15 April 2013 / Accepted: 2 May 2013 / Published: 17 May 2013
Cited by 17 | PDF Full-text (1801 KB) | HTML Full-text | XML Full-text
Abstract
Ultraviolet (UV) radiation and reactive oxygen species (ROS) impair the physiological functions of retinal pigment epithelium (RPE) cells by inducing cell apoptosis, which is the main cause of age-related macular degeneration (AMD). The mechanism by which UV/ROS induces RPE cell death is [...] Read more.
Ultraviolet (UV) radiation and reactive oxygen species (ROS) impair the physiological functions of retinal pigment epithelium (RPE) cells by inducing cell apoptosis, which is the main cause of age-related macular degeneration (AMD). The mechanism by which UV/ROS induces RPE cell death is not fully addressed. Here, we observed the activation of a ceramide-endoplasmic reticulum (ER) stress-AMP activated protein kinase (AMPK) signaling axis in UV and hydrogen peroxide (H2O2)-treated RPE cells. UV and H2O2 induced an early ceramide production, profound ER stress and AMPK activation. Pharmacological inhibitors against ER stress (salubrinal), ceramide production (fumonisin B1) and AMPK activation (compound C) suppressed UV- and H2O2-induced RPE cell apoptosis. Conversely, cell permeable short-chain C6 ceramide and AMPK activator AICAR (5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide) mimicked UV and H2O2’s effects and promoted RPE cell apoptosis. Together, these results suggest that UV/H2O2 activates the ceramide-ER stress-AMPK signaling axis to promote RPE cell apoptosis. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessArticle Effect of Artocarpus communis Extract on UVB Irradiation-Induced Oxidative Stress and Inflammation in Hairless Mice
Int. J. Mol. Sci. 2013, 14(2), 3860-3873; doi:10.3390/ijms14023860
Received: 15 October 2012 / Revised: 28 January 2013 / Accepted: 28 January 2013 / Published: 12 February 2013
Cited by 6 | PDF Full-text (574 KB) | HTML Full-text | XML Full-text
Abstract
Administration of antioxidants and anti-inflammatory agents is an effective strategy for preventing ultraviolet (UV) irradiation-induced skin damage. Artocarpus communis possesses several pharmacological activities, such as antioxidant, anticancer and anti-inflammation. However, the photoprotective activity of methanol extract of A. communis heartwood (ACM) in [...] Read more.
Administration of antioxidants and anti-inflammatory agents is an effective strategy for preventing ultraviolet (UV) irradiation-induced skin damage. Artocarpus communis possesses several pharmacological activities, such as antioxidant, anticancer and anti-inflammation. However, the photoprotective activity of methanol extract of A. communis heartwood (ACM) in ultraviolet irradiation-induced skin damage has not yet been investigated. The present study was performed using ultraviolet absorption, histopathological observation, antioxidant and anti-inflammation assays to elucidate the mechanism of the photoprotective activity of ACM. Our results indicated that ACM displayed a UVA and UVB absorption effect and then effectively decreased scaly skin, epidermis thickness and sunburn cells during ultraviolet irradiation in hairless mice. ACM not only decreased ultraviolet irradiation-mediated oxidative stress, including lowering the overproduction of reactive oxygen species and lipid peroxidation (p < 0.05), but also reduced the levels of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin 1β. Additionally, ACM can decrease the synthesis of cytosolic phospholipase A2, cyclooxygenase, inducible nitric oxide synthase and vascular cell adhesion molecular-1 via inhibiting TNF-α-independent pathways (p < 0.05) in UVB-mediated inflammation and formation of sunburn cells. Consequently, we concluded that ACM extract has a photoprotective effect against UVB-induced oxidative stress and inflammation due to its sunscreen property, and its topical formulations may be developed as therapeutic and/or cosmetic products in further studies. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessArticle Induction of Heat Shock Protein 70 Ameliorates Ultraviolet-Induced Photokeratitis in Mice
Int. J. Mol. Sci. 2013, 14(1), 2175-2189; doi:10.3390/ijms14012175
Received: 7 November 2012 / Revised: 9 January 2013 / Accepted: 18 January 2013 / Published: 22 January 2013
Cited by 5 | PDF Full-text (3228 KB) | HTML Full-text | XML Full-text
Abstract
Acute ultraviolet (UV) B exposure causes photokeratitis and induces apoptosis in corneal cells. Geranylgeranylacetone (GGA) is an acyclic polyisoprenoid that induces expression of heat shock protein (HSP)70, a soluble intracellular chaperone protein expressed in various tissues, protecting cells against stress conditions. We [...] Read more.
Acute ultraviolet (UV) B exposure causes photokeratitis and induces apoptosis in corneal cells. Geranylgeranylacetone (GGA) is an acyclic polyisoprenoid that induces expression of heat shock protein (HSP)70, a soluble intracellular chaperone protein expressed in various tissues, protecting cells against stress conditions. We examined whether induction of HSP70 has therapeutic effects on UV-photokeratitis in mice. C57 BL/6 mice were divided into four groups, GGA-treated (500 mg/kg/mouse) and UVB-exposed (400 mJ/cm2), GGA-untreated UVB-exposed (400 mJ/cm2), GGA-treated (500 mg/kg/mouse) but not exposed and naive controls. Eyeballs were collected 24 h after irradiation, and corneas were stained with hematoxylin and eosin (H&E) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). HSP70, reactive oxygen species (ROS) production, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and protein kinase B (Akt) expression were also evaluated. Irradiated corneal epithelium was significantly thicker in the eyes of mice treated with GGA compared with those given the vehicle alone (p < 0.01). Significantly fewer TUNEL-positive cells were observed in the eyes of GGA-treated mice than controls after irradiation (p < 0.01). Corneal HSP70 levels were significantly elevated in corneas of mice treated with GGA (p < 0.05). ROS signal was not affected by GGA. NF-κB activation was reduced but phospho-(Ser/Ther) Akt substrate expression was increased in corneas after irradiation when treated with GGA. GGA-treatment induced HSP70 expression and ameliorated UV-induced corneal damage through the reduced NF-κB activation and possibly increased Akt phosphorilation. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessArticle Quantitative Profiling of DNA Damage and Apoptotic Pathways in UV Damaged Cells Using PTMScan Direct
Int. J. Mol. Sci. 2013, 14(1), 286-307; doi:10.3390/ijms14010286
Received: 31 October 2012 / Revised: 4 December 2012 / Accepted: 10 December 2012 / Published: 21 December 2012
Cited by 4 | PDF Full-text (5068 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Traditional methods for analysis of peptides using liquid chromatography and tandem mass spectrometry (LC-MS/MS) lack the specificity to comprehensively monitor specific biological processes due to the inherent duty cycle limitations of the MS instrument and the stochastic nature of the analytical platform. [...] Read more.
Traditional methods for analysis of peptides using liquid chromatography and tandem mass spectrometry (LC-MS/MS) lack the specificity to comprehensively monitor specific biological processes due to the inherent duty cycle limitations of the MS instrument and the stochastic nature of the analytical platform. PTMScan Direct is a novel, antibody-based method that allows quantitative LC-MS/MS profiling of specific peptides from proteins that reside in the same signaling pathway. New PTMScan Direct reagents have been produced that target peptides from proteins involved in DNA Damage/Cell Cycle and Apoptosis/Autophagy pathways. Together, the reagents provide access to 438 sites on 237 proteins in these signaling cascades. These reagents have been used to profile the response to UV damage of DNA in human cell lines. UV damage was shown to activate canonical DNA damage response pathways through ATM/ATR-dependent signaling, stress response pathways and induce the initiation of apoptosis, as assessed by an increase in the abundance of peptides corresponding to cleaved, activated caspases. These data demonstrate the utility of PTMScan Direct as a multiplexed assay for profiling specific cellular responses to various stimuli, such as UV damage of DNA. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessArticle UVA Irradiation of Dysplastic Keratinocytes: Oxidative Damage versus Antioxidant Defense
Int. J. Mol. Sci. 2012, 13(12), 16718-16736; doi:10.3390/ijms131216718
Received: 5 September 2012 / Revised: 13 November 2012 / Accepted: 29 November 2012 / Published: 6 December 2012
Cited by 2 | PDF Full-text (1050 KB) | HTML Full-text | XML Full-text
Abstract
UVA affects epidermal cell physiology in a complex manner, but the harmful effects have been studied mainly in terms of DNA damage, mutagenesis and carcinogenesis. We investigated UVA effects on membrane integrity and antioxidant defense of dysplastic keratinocytes after one and two [...] Read more.
UVA affects epidermal cell physiology in a complex manner, but the harmful effects have been studied mainly in terms of DNA damage, mutagenesis and carcinogenesis. We investigated UVA effects on membrane integrity and antioxidant defense of dysplastic keratinocytes after one and two hours of irradiation, both immediately after exposure, and 24 h post-irradiation. To determine the UVA oxidative stress on cell membrane, lipid peroxidation was correlated with changes in fatty acid levels. Membrane permeability and integrity were assessed by propidium iodide staining and lactate dehydrogenase release. The effects on keratinocyte antioxidant protection were investigated in terms of catalase activity and expression. Lipid peroxidation increased in an exposure time-dependent manner. UVA exposure decreased the level of polyunsaturated fatty acids, which gradually returned to its initial value. Lactate dehydrogenase release showed a dramatic loss in membrane integrity after 2 h minimum of exposure. The cell ability to restore membrane permeability was noted at 24 h post-irradiation (for one hour exposure). Catalase activity decreased in an exposure time-dependent manner. UVA-irradiated dysplastic keratinocytes developed mechanisms leading to cell protection and survival, following a non-lethal exposure. The surviving cells gained an increased resistance to apoptosis, suggesting that their pre-malignant status harbors an abnormal ability to control their fate. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessArticle A Comparative Analysis of the Photo-Protective Effects of Soy Isoflavones in Their Aglycone and Glucoside Forms
Int. J. Mol. Sci. 2012, 13(12), 16444-16456; doi:10.3390/ijms131216444
Received: 19 September 2012 / Revised: 24 November 2012 / Accepted: 29 November 2012 / Published: 4 December 2012
Cited by 8 | PDF Full-text (1035 KB) | HTML Full-text | XML Full-text
Abstract
Isoflavones exist in nature predominantly as glucosides such as daidzin or genistin and are rarely found in their corresponding aglycone forms daidzein and genistein. The metabolism and absorption of isoflavones ingested with food is well documented, but little is known about their [...] Read more.
Isoflavones exist in nature predominantly as glucosides such as daidzin or genistin and are rarely found in their corresponding aglycone forms daidzein and genistein. The metabolism and absorption of isoflavones ingested with food is well documented, but little is known about their use as topical photo-protective agents. The aim of this study was to investigate in a comparative analysis the photo-protective effects of isoflavones in both their aglycone and glucoside forms. In human skin fibroblasts irradiated with 60 mJ/cm2 ultraviolet B (UVB), we measured the expression levels of COX-2 and Gadd45, which are involved in inflammation and DNA repair, respectively. We also determined the cellular response to UVB-induced DNA damage using the comet assay. Our findings suggest that both the isoflavone glucosides at a specific concentration and combination with an aglycone mixture exerted an anti-inflammatory and photo-protective effect that prevented 41% and 71% of UVB-induced DNA damage, respectively. The advantages of using either isoflavone glucosides or an aglycone mixture in applications in the field of dermatology will depend on their properties and their different potential uses. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessArticle Sensing and Responding to UV-A in Cyanobacteria
Int. J. Mol. Sci. 2012, 13(12), 16303-16332; doi:10.3390/ijms131216303
Received: 1 November 2012 / Revised: 27 November 2012 / Accepted: 27 November 2012 / Published: 3 December 2012
Cited by 9 | PDF Full-text (527 KB) | HTML Full-text | XML Full-text
Abstract
Ultraviolet (UV) radiation can cause stresses or act as a photoregulatory signal depending on its wavelengths and fluence rates. Although the most harmful effects of UV on living cells are generally attributed to UV-B radiation, UV-A radiation can also affect many aspects [...] Read more.
Ultraviolet (UV) radiation can cause stresses or act as a photoregulatory signal depending on its wavelengths and fluence rates. Although the most harmful effects of UV on living cells are generally attributed to UV-B radiation, UV-A radiation can also affect many aspects of cellular processes. In cyanobacteria, most studies have concentrated on the damaging effect of UV and defense mechanisms to withstand UV stress. However, little is known about the activation mechanism of signaling components or their pathways which are implicated in the process following UV irradiation. Motile cyanobacteria use a very precise negative phototaxis signaling system to move away from high levels of solar radiation, which is an effective escape mechanism to avoid the detrimental effects of UV radiation. Recently, two different UV-A-induced signaling systems for regulating cyanobacterial phototaxis were characterized at the photophysiological and molecular levels. Here, we review the current understanding of the UV-A mediated signaling pathways in the context of the UV-A perception mechanism, early signaling components, and negative phototactic responses. In addition, increasing evidences supporting a role of pterins in response to UV radiation are discussed. We outline the effect of UV-induced cell damage, associated signaling molecules, and programmed cell death under UV-mediated oxidative stress. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)

Review

Jump to: Research

Open AccessReview Effects of Narrow Band UVB (311 nm) Irradiation on Epidermal Cells
Int. J. Mol. Sci. 2013, 14(4), 8456-8466; doi:10.3390/ijms14048456
Received: 4 February 2013 / Revised: 9 April 2013 / Accepted: 9 April 2013 / Published: 17 April 2013
Cited by 9 | PDF Full-text (1621 KB) | HTML Full-text | XML Full-text
Abstract
Ultraviolet radiation (UVR) is known to be one of the most important environmental hazards acting on the skin. It was revealed that chronic exposure to UVR accelerates skin aging, induces immunosuppression and may lead to the development of skin cancers. On the [...] Read more.
Ultraviolet radiation (UVR) is known to be one of the most important environmental hazards acting on the skin. It was revealed that chronic exposure to UVR accelerates skin aging, induces immunosuppression and may lead to the development of skin cancers. On the other hand, UVR has been shown to be effective in the treatment of numerous skin diseases and thus, various phototherapy modalities have been developed to date. Narrow-band ultraviolet B (NB-UVB) emitting a light with a peak around 311 nm has been demonstrated to be effective in the treatment of various skin disorders; currently it is one of the most commonly used phototherapy devices. Despite NB-UVB has been developed more than 30 years ago, the exact mechanism of its therapeutic action remains poorly understood. To date, most of NB-UVB effects were attributed to its influence on immune cells; however, nearly 90% of NB-UVB irradiation is absorbed by epidermis and keratinocytes seem to be important players in mediating NB-UVB biological activity. Here, we have reviewed the current data about the influence of NB-UVB on epidermal cells, with a special emphasis on cell proliferation and death. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessReview Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy
Int. J. Mol. Sci. 2013, 14(3), 6414-6435; doi:10.3390/ijms14036414
Received: 1 November 2012 / Revised: 13 March 2013 / Accepted: 15 March 2013 / Published: 20 March 2013
Cited by 38 | PDF Full-text (979 KB) | HTML Full-text | XML Full-text
Abstract
The human skin is an integral system that acts as a physical and immunological barrier to outside pathogens, toxicants, and harmful irradiations. Environmental ultraviolet rays (UV) from the sun might potentially play a more active role in regulating several important biological responses [...] Read more.
The human skin is an integral system that acts as a physical and immunological barrier to outside pathogens, toxicants, and harmful irradiations. Environmental ultraviolet rays (UV) from the sun might potentially play a more active role in regulating several important biological responses in the context of global warming. UV rays first encounter the uppermost epidermal keratinocytes causing apoptosis. The molecular mechanisms of UV-induced apoptosis of keratinocytes include direct DNA damage (intrinsic), clustering of death receptors on the cell surface (extrinsic), and generation of ROS. When apoptotic keratinocytes are processed by adjacent immature Langerhans cells (LCs), the inappropriately activated Langerhans cells could result in immunosuppression. Furthermore, UV can deplete LCs in the epidermis and impair their migratory capacity, leading to their accumulation in the dermis. Intriguingly, receptor activator of NF-κB (RANK) activation of LCs by UV can induce the pro-survival and anti-apoptotic signals due to the upregulation of Bcl-xL, leading to the generation of regulatory T cells. Meanwhile, a physiological dosage of UV can also enhance melanocyte survival and melanogenesis. Analogous to its effect in keratinocytes, a therapeutic dosage of UV can induce cell cycle arrest, activate antioxidant and DNA repair enzymes, and induce apoptosis through translocation of the Bcl-2 family proteins in melanocytes to ensure genomic integrity and survival of melanocytes. Furthermore, UV can elicit the synthesis of vitamin D, an important molecule in calcium homeostasis of various types of skin cells contributing to DNA repair and immunomodulation. Taken together, the above-mentioned effects of UV on apoptosis and its related biological effects such as proliferation inhibition, melanin synthesis, and immunomodulations on skin residential cells have provided an integrated biochemical and molecular biological basis for phototherapy that has been widely used in the treatment of many dermatological diseases. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Figures

Open AccessReview Vitamin D and Death by Sunshine
Int. J. Mol. Sci. 2013, 14(1), 1964-1977; doi:10.3390/ijms14011964
Received: 6 December 2012 / Revised: 4 January 2013 / Accepted: 10 January 2013 / Published: 18 January 2013
Cited by 8 | PDF Full-text (425 KB) | HTML Full-text | XML Full-text
Abstract
Exposure to sunlight is the major cause of skin cancer. Ultraviolet radiation (UV) from the sun causes damage to DNA by direct absorption and can cause skin cell death. UV also causes production of reactive oxygen species that may interact with DNA [...] Read more.
Exposure to sunlight is the major cause of skin cancer. Ultraviolet radiation (UV) from the sun causes damage to DNA by direct absorption and can cause skin cell death. UV also causes production of reactive oxygen species that may interact with DNA to indirectly cause oxidative DNA damage. UV increases accumulation of p53 in skin cells, which upregulates repair genes but promotes death of irreparably damaged cells. A benefit of sunlight is vitamin D, which is formed following exposure of 7-dehydrocholesterol in skin cells to UV. The relatively inert vitamin D is metabolized to various biologically active compounds, including 1,25-dihydroxyvitamin D3. Therapeutic use of vitamin D compounds has proven beneficial in several cancer types, but more recently these compounds have been shown to prevent UV-induced cell death and DNA damage in human skin cells. Here, we discuss the effects of vitamin D compounds in skin cells that have been exposed to UV. Specifically, we examine the various signaling pathways involved in the vitamin D-induced protection of skin cells from UV. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessReview UV-Induced Cell Death in Plants
Int. J. Mol. Sci. 2013, 14(1), 1608-1628; doi:10.3390/ijms14011608
Received: 1 November 2012 / Revised: 5 December 2012 / Accepted: 4 January 2013 / Published: 14 January 2013
Cited by 37 | PDF Full-text (1642 KB) | HTML Full-text | XML Full-text
Abstract
Plants are photosynthetic organisms that depend on sunlight for energy. Plants respond to light through different photoreceptors and show photomorphogenic development. Apart from Photosynthetically Active Radiation (PAR; 400–700 nm), plants are exposed to UV light, which is comprised of UV-C (below 280 [...] Read more.
Plants are photosynthetic organisms that depend on sunlight for energy. Plants respond to light through different photoreceptors and show photomorphogenic development. Apart from Photosynthetically Active Radiation (PAR; 400–700 nm), plants are exposed to UV light, which is comprised of UV-C (below 280 nm), UV-B (280–320 nm) and UV-A (320–390 nm). The atmospheric ozone layer protects UV-C radiation from reaching earth while the UVR8 protein acts as a receptor for UV-B radiation. Low levels of UV-B exposure initiate signaling through UVR8 and induce secondary metabolite genes involved in protection against UV while higher dosages are very detrimental to plants. It has also been reported that genes involved in MAPK cascade help the plant in providing tolerance against UV radiation. The important targets of UV radiation in plant cells are DNA, lipids and proteins and also vital processes such as photosynthesis. Recent studies showed that, in response to UV radiation, mitochondria and chloroplasts produce a reactive oxygen species (ROS). Arabidopsis metacaspase-8 (AtMC8) is induced in response to oxidative stress caused by ROS, which acts downstream of the radical induced cell death (AtRCD1) gene making plants vulnerable to cell death. The studies on salicylic and jasmonic acid signaling mutants revealed that SA and JA regulate the ROS level and antagonize ROS mediated cell death. Recently, molecular studies have revealed genes involved in response to UV exposure, with respect to programmed cell death (PCD). Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessReview The Role of Altered Nucleotide Excision Repair and UVB-Induced DNA Damage in Melanomagenesis
Int. J. Mol. Sci. 2013, 14(1), 1132-1151; doi:10.3390/ijms14011132
Received: 31 October 2012 / Revised: 29 November 2012 / Accepted: 26 December 2012 / Published: 9 January 2013
Cited by 25 | PDF Full-text (510 KB) | HTML Full-text | XML Full-text
Abstract
UVB radiation is the most mutagenic component of the UV spectrum that reaches the earth’s surface and causes the development of DNA damage in the form of cyclobutane pyrimidine dimers and 6-4 photoproducts. UV radiation usually results in cellular death, but if [...] Read more.
UVB radiation is the most mutagenic component of the UV spectrum that reaches the earth’s surface and causes the development of DNA damage in the form of cyclobutane pyrimidine dimers and 6-4 photoproducts. UV radiation usually results in cellular death, but if left unchecked, it can affect DNA integrity, cell and tissue homeostasis and cause mutations in oncogenes and tumour-suppressor genes. These mutations, if unrepaired, can lead to abnormal cell growth, increasing the risk of cancer development. Epidemiological data strongly associates UV exposure as a major factor in melanoma development, but the exact biological mechanisms involved in this process are yet to be fully elucidated. The nucleotide excision repair (NER) pathway is responsible for the repair of UV-induced lesions. Patients with the genetic disorder Xeroderma Pigmentosum have a mutation in one of eight NER genes associated with the XP complementation groups XP-A to XP-G and XP variant (XP-V). XP is characterized by diminished repair capacity, as well as a 1000-fold increase in the incidence of skin cancers, including melanoma. This has suggested a significant role for NER in melanoma development as a result of UVB exposure. This review discusses the current research surrounding UVB radiation and NER capacity and how further investigation of NER could elucidate the role of NER in avoiding UV-induced cellular death resulting in melanomagenesis. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessReview Ultraviolet B (UVB) Irradiation-Induced Apoptosis in Various Cell Lineages in Vitro
Int. J. Mol. Sci. 2013, 14(1), 532-546; doi:10.3390/ijms14010532
Received: 31 October 2012 / Revised: 19 December 2012 / Accepted: 21 December 2012 / Published: 27 December 2012
Cited by 15 | PDF Full-text (762 KB) | HTML Full-text | XML Full-text
Abstract
Ultraviolet B (UVB) radiation acts as a strong apoptotic trigger in many cell types, in tumor and normal cells. Several studies have demonstrated that UVB-induced cell death occurs through the generation of reactive oxygen species. The consequent oxidative stress includes the impairment [...] Read more.
Ultraviolet B (UVB) radiation acts as a strong apoptotic trigger in many cell types, in tumor and normal cells. Several studies have demonstrated that UVB-induced cell death occurs through the generation of reactive oxygen species. The consequent oxidative stress includes the impairment of cellular antioxidants, the induction of DNA damage and the occurrence of apoptosis. In this review, we investigated UVB apoptotic action in various cell models by using ultrastructural, molecular and cytofluorimetric techniques. Myeloid leukemia HL-60, T-lymphoblastoid Molt-4 and myelomonocytic U937 human cells, generally affected by apoptotic stimuli, were studied. Human chondrocytes and C2C12 skeletal muscle cells, known to be more resistant to damage, were also considered. All of them, when exposed to UVB radiation, revealed a number of characteristic apoptotic markers. Membrane blebbing, cytoplasm shrinkage and chromatin condensation were detected by means of electron microscopy. DNA cleavage, investigated by using agarose gel electrophoresis and TUNEL reaction, was observed in suspended cells. Differently, in chondrocytes and in skeletal muscle cells, oligonucleosomic DNA fragmentation did not appear, even if a certain TUNEL positivity was detected. These findings demonstrate that UVB radiation appears to be an ideal tool to study the apoptotic behavior. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
Open AccessReview The Role of Photolabile Dermal Nitric Oxide Derivates in Ultraviolet Radiation (UVR)-Induced Cell Death
Int. J. Mol. Sci. 2013, 14(1), 191-204; doi:10.3390/ijms14010191
Received: 26 October 2012 / Revised: 11 December 2012 / Accepted: 12 December 2012 / Published: 21 December 2012
Cited by 2 | PDF Full-text (324 KB) | HTML Full-text | XML Full-text
Abstract
Human skin is exposed to solar ultraviolet radiation comprising UVB (280–315 nm) and UVA (315–400 nm) on a daily basis. Within the last two decades, the molecular and cellular response to UVA/UVB and the possible effects on human health have been investigated [...] Read more.
Human skin is exposed to solar ultraviolet radiation comprising UVB (280–315 nm) and UVA (315–400 nm) on a daily basis. Within the last two decades, the molecular and cellular response to UVA/UVB and the possible effects on human health have been investigated extensively. It is generally accepted that the mutagenic and carcinogenic properties of UVB is due to the direct interaction with DNA. On the other hand, by interaction with non-DNA chromophores as endogenous photosensitizers, UVA induces formation of reactive oxygen species (ROS), which play a pivotal role as mediators of UVA-induced injuries in human skin. This review gives a short overview about relevant findings concerning the molecular mechanisms underlying UVA/UVB-induced cell death. Furthermore, we will highlight the potential role of cutaneous antioxidants and photolabile nitric oxide derivates (NODs) in skin physiology. UVA-induced decomposition of the NODs, like nitrite, leads not only to non-enzymatic formation of nitric oxide (NO), but also to toxic reactive nitrogen species (RNS), like peroxynitrite. Whereas under antioxidative conditions the generation of protective amounts of NO is favored, under oxidative conditions, less injurious reactive nitrogen species are generated, which may enhance UVA-induced cell death. Full article
(This article belongs to the Special Issue UV-Induced Cell Death 2012)

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