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Radiation-Induced Damage to Human Skin: Biological and Medical Implications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2024) | Viewed by 2345

Special Issue Editors

Department of Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, Jagiellońska 4, 41-200 Sosnowiec, Poland
Interests: lomefloxacin; melanoma; oxidative stress; DNA fragmentation; apoptosis
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Guest Editor
Department of Pharmaceutical Chemistry, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia in Katowice, Jagiellońska 4, 41-200 Sosnowiec, Poland
Interests: eumelanin; pyrrole-2,3,5-tricarboxylic acid; Auricularia auricula-judae
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The skin is the largest organ of the human body. Its unique and complex structure provides effective protection of other tissues and organs against the harmful effects of external factors: chemical, biological, and physical. The skin also performs many other functions, including thermoregulatory and immunological. It also enables the reception of stimuli and participates in water–mineral as well as redox balance.

Due to their location, skin cells are exposed to radiation that reaches the Earth's surface. On the one hand, this provides some beneficial effects, such as the stimulation of melanogenesis or vitamin D synthesis. However, it can also contribute to damage to skin cells at the genetic and molecular levels. The result of such changes is numerous cytophysiological and biochemical disorders, which are responsible for the loss of basic functions of skin cells and the appearance of clinical symptoms. It should be noted that radiation-induced adverse skin reactions may be aggravated by photosensitizing substances, including drugs. Damage to skin cells can also accompany various therapies that use radiation in the treatment of dermatological or cancer diseases. Considering the functions of the skin as well as the medical and biological consequences of its damage, the importance and value of research in this area should be emphasized. This Special Issue focuses on presenting the latest discoveries regarding the impact of different types and ranges of radiation on the skin, taking into account medical aspects and environmental exposure.

Dr. Jakub Rok
Prof. Dr. Dorota Wrześniok
Guest Editors

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Keywords

  • irradiation
  • photosensitizer
  • photobiology
  • phototherapy
  • radiobiology
  • free radicals
  • UV radiation
  • oxidative stress
  • skin cells
  • phototoxicity
  • photoallergy
  • cell damage

Published Papers (2 papers)

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Research

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17 pages, 2926 KiB  
Article
Amaranthus cruentus L. Seed Oil Counteracts UVA-Radiation-Induced Inhibition of Collagen Biosynthesis and Wound Healing in Human Skin Fibroblasts
by Katarzyna Wolosik, Magda Chalecka, Jerzy Palka, Blanka Mitera and Arkadiusz Surazynski
Int. J. Mol. Sci. 2024, 25(2), 925; https://doi.org/10.3390/ijms25020925 - 11 Jan 2024
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Abstract
The effect of Amaranthus cruentus L. seed oil (AmO) on collagen biosynthesis and wound healing was studied in cultured human dermal fibroblasts exposed to UVA radiation. It was found that UVA radiation inhibited collagen biosynthesis, prolidase activity, and expression of the β1-integrin receptor, [...] Read more.
The effect of Amaranthus cruentus L. seed oil (AmO) on collagen biosynthesis and wound healing was studied in cultured human dermal fibroblasts exposed to UVA radiation. It was found that UVA radiation inhibited collagen biosynthesis, prolidase activity, and expression of the β1-integrin receptor, and phosphorylated ERK1/2 and TGF-β, while increasing the expression of p38 kinase. The AmO at 0.05–0.15% counteracted the above effects induced by UVA radiation in fibroblasts. UVA radiation also induced the expression and nuclear translocation of the pro-inflammatory NF-κB factor and enhanced the COX-2 expression. AmO effectively suppressed the expression of these pro-inflammatory factors induced by UVA radiation. Expressions of β1 integrin and IGF-I receptors were decreased in the fibroblasts exposed to UVA radiation, while AmO counteracted the effects. Furthermore, AmO stimulated the fibroblast’s migration in a wound healing model, thus facilitating the repair process following exposure of fibroblasts to UVA radiation. These data suggest the potential of AmO to counteract UVA-induced skin damage. Full article
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Review

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14 pages, 2288 KiB  
Review
Radiation Dermatitis: Radiation-Induced Effects on the Structural and Immunological Barrier Function of the Epidermis
by Claudia E. Rübe, Benjamin M. Freyter, Gargi Tewary, Klaus Roemer, Markus Hecht and Christian Rübe
Int. J. Mol. Sci. 2024, 25(6), 3320; https://doi.org/10.3390/ijms25063320 - 15 Mar 2024
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Abstract
An important hallmark of radiation dermatitis is the impairment of the mitotic ability of the stem/progenitor cells in the basal cell layers due to radiation-induced DNA damage, leading to suppressed cell renewal in the epidermis. However, this mechanism alone does not adequately explain [...] Read more.
An important hallmark of radiation dermatitis is the impairment of the mitotic ability of the stem/progenitor cells in the basal cell layers due to radiation-induced DNA damage, leading to suppressed cell renewal in the epidermis. However, this mechanism alone does not adequately explain the complex pathogenesis of radiation-induced skin injury. In this review, we summarize the latest findings on the complex pathogenesis of radiation dermatitis and correlate these with the clinical features of radiation-induced skin reactions. The current studies show that skin exposure to ionizing radiation induces cellular senescence in the epidermal keratinocytes. As part of their epithelial stress response, these senescent keratinocytes secrete pro-inflammatory mediators, thereby triggering skin inflammation. Keratinocyte-derived cytokines and chemokines modulate intercellular communication with the immune cells, activating skin-resident and recruiting skin-infiltrating immune cells within the epidermis and dermis, thereby orchestrating the inflammatory response to radiation-induced tissue damage. The increased expression of specific chemoattractant chemokines leads to increased recruitment of neutrophils into the irradiated skin, where they release cytotoxic granules that are responsible for the exacerbation of an inflammatory state. Moreover, the importance of IL-17-expressing γδ-T cells to the radiation-induced hyperproliferation of keratinocytes was demonstrated, leading to reactive hyperplasia of the epidermis. Radiation-induced, reactive hyperproliferation of the keratinocytes disturbs the fine-tuned keratinization and cornification processes, leading to structural dysfunction of the epidermal barrier. In summary, in response to ionizing radiation, epidermal keratinocytes have important structural and immunoregulatory barrier functions in the skin, coordinating interacting immune responses to eliminate radiation-induced damage and to initiate the healing process. Full article
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