Oral administration of Polypodium leucotomos delays skin tumor development and increases epidermal p53 expression and the anti‐oxidant status of UV‐irradiated hairless mice
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Chronic exposure to ultraviolet radiation (UVR) induces skin tumors in hairless mice. Daily oral administration of a Polypodium leucotomos (PL) extract significantly delayed tumor development in PL‐treated versus non‐PL‐treated mice. UVR and/or PL treatment modified several oxidative stress markers. In all irradiated mice, erythrocytic glutathione S‐transferase (GST) activity and glutathione disulphide (GSSG) content increased and in all PL‐treated mice GSSG content decreased, specially in non‐irradiated animals, and total plasma anti‐oxidant capacity (ORAC) increased. In dorsolateral non‐tumoral skin of all irradiated mice, glutathione reductase (GR) and glutathione peroxidase (GP x) activities increased and GSSG decreased in non‐irradiated PL‐treated animals. UVR induced a steep increase of p53 expression in epidermal cells. In non‐tumoral skin, this increase was significantly higher in PL‐treated animals than in non‐treated mice and can contribute in delaying tumor development, either by repairing the damaged DNA or by increasing apoptosis. These results reinforce the usefulness of PL as systemic photoprotective agent, especially in patients highly sensitive to UVR.
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Oral administration of Polypodium leucotomos delays skin tumor development in hairless mice possibly through improvement in antioxidant defense status.
“Furthermore, the mechanisms by which oral administration of Polypodium leucotomos delayed skin tumor development in hairless mice might involve improvement in antioxidant defense status [161].”
From Ultraviolet Radiation‐Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging (2016) · cites this paper as [161]
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Botanical antioxidants in the prevention of photocarcinogenesis and photoaging
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Oral Polypodium leucotomos extract decreases ultraviolet-induced damage of human skin
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DNA repair is activated in early stages of p53-induced apoptosis
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Self-citationCrosstalk among p53 family members in cutaneous carcinoma
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Panich, U., Sittithumcharee, G., Rathviboon, N., & Jirawatnotai, S. (2016) · Stem Cells International · doi:10.1155/2016/7370642 · Cited by 374 · see citing works
Subhadarshani, S., Athar, M., & Elmets, C. A. (2020) · Current Dermatology Reports · doi:10.1007/s13671-020-00307-0 · Cited by 21 · see citing works
- Authors
- Rodríguez‐Yanes, E., Cuevas, J., González, S., & Mallol, J.
- Affiliations
- Department of Pharmacology School of Medicine Reus Spain
- Hospital Universitario de Guadalajara (ES)
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Mallol, Jordi
- ORCID
- González, Salvador
- Venue
- Experimental Dermatology
- Publisher
- Wiley
- Published
- 2014-07
- Volume
- 23
- Issue
- 7
- Pages
- 526-528
- ISSN
- 0906-6705 (ISSN-L)
- 1600-0625
- OpenAlex
- W1972164633
- Cited by
- 25
- References
- 16
- Citations by year
- 2026: 2 · 2025: 1 · 2023: 4 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 4 · 2017: 1 · 2016: 4 · 2015: 3 · 2014: 1
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Experimental Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
- Health Sciences › Medicine › Biochemistry › Phytochemicals and Antioxidant Activities
- Keywords
- Polypodium leucotomos, ultraviolet radiation, skin tumors, photoprotection, p53 expression, oxidative stress, glutathione disulfide, glutathione reductase, glutathione peroxidase, glutathione S-transferase, antioxidant capacity, epidermis, hairless mice, apoptosis, DNA repair
- MeSH terms
- Administration, Oral, Animals, Antioxidants, Female, Glutathione Peroxidase, Glutathione Transferase, Immunosuppression Therapy, Light, Neoplasms, Radiation-Induced, Plant Extracts, Skin, Skin Neoplasms, Ultraviolet Rays, Tumor Suppressor Protein p53, Apoptosis, Oxidative Stress, Glutathione Disulfide, Polypodium, Mice, Keratosis, Actinic
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