Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure to ultraviolet B (UVB) radiation leads to an increased generation of UVB-induced skin damage in humans. The most important UVB-induced side effects are UVB-induced immunosuppression and photocarcinogenesis and there is a large body of evidence that cyclobutane pyrimidine dimers (CPD) induced by UVB radiation play a pivotal role in both processes. The topical application of DNA repair enzymes is a new innovative strategy to reduce the amount of CPDs in human skin. Two different methods have recently been established. The use of T4 endonuclease V was of clinical efficacy in protecting patients with a nucleotide excision repair defect from premalignant and malignant skin lesions. Application of photolyase, a xenogenic enzyme which has been found in different organisms is also capable of removing UVB-induced CPD from normal human skin cells in vivo and appears to be more effective than T4 endonuclease V in damage removal. Photolyase encapsulated in liposomes may have in the near future a broad use as an active ingredient in modern skin care products.
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PMID:Effect of xenogenic repair enzymes on photoimmunology and photocarcinogenesis. 1180 66

The exposure to ultraviolet radiation (UVR) is a major risk factor for skin aging and the development of non-melanoma skin cancer (NMSC). Although traditional sunscreens remain the mainstay for the prevention of UVR-induced skin damage, they cannot ensure a complete protection against the whole spectrum of molecular lesions associated with UVR exposure. The formation of helix-distorting photoproducts such as cyclobutane pyrimidine dimers (CPD), as well as oxidative damage to DNA bases, including the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8OHdG) are among the key DNA lesions associated with photoaging and tumorigenesis. Besides DNA lesions, UVR-induced formation of free radicals can result in protein carbonylation (PC), a major form of irreversible protein damage that inactivates their biological function. This study compares a complex novel topical product (TPF50) consisting of three actives, ie, 1) traditional physical sunscreens (SPF 50), 2) a liposome-encapsulated DNA repair enzymes complex (photolyase, endonuclease, and 8-oxoguanine glycosylase [OGG1]), and 3) a potent antioxidant complex (carnosine, arazine, ergothionine) to existing products. Specifically, we assessed the ability of TFP50 vs those of DNA repair and antioxidant and growth factor topical products used with SPF 50 sunscreens in preventing CPD, 8OHdG, and PC formation in human skin biopsies after experimental irradiations. In head-to-head comparison studies, TPF50 showed the best efficacy in reducing all of the three molecular markers. The results indicated that the three TPF50 components had a synergistic effect in reducing CPD and PC, but not 8OHdG. Taken together, our results indicate that TPF50 improves the genomic and proteomic integrity of skin cells after repeated exposure to UVR, ultimately reducing the risk of skin aging and NMSC.
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PMID:An experimental double-blind irradiation study of a novel topical product (TPF 50) compared to other topical products with DNA repair enzymes, antioxidants, and growth factors with sunscreens: implications for preventing skin aging and cancer. 2480 74

Skin cancer is common in xeroderma pigmentosum (XP) due to a DNA repair mechanisms genetic defect. Ultraviolet (UV) exposure is the main cause of increased incidence of actinic keratosis (AK), basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) observed in XP subjects. Photoprotection is therefore a mandatory strategy in order to reduce skin damage. A topical DNA repair enzyme has been shown to slow down the development of skin lesions in XP. However, there are no data regarding the effects of photoprotection combined with DNA repair strategies in this clinical setting. A film-forming medical device containing the DNA repair enzyme photolyase and very high-protection UV filters (Eryfotona AK-NMSC, Ery) is currently available. We report retrospective data regarding the use of Ery in 8 patients (5 women, 3 men) with a diagnosis of XP treated for at least 12 consecutive months, comparing the rate of new skin lesions (AK, BCC and SCC) during active treatment with Ery and during 12 months just before the use of the product. New AK, BCC and SCC mean lesion numbers during the 1-year Ery treatment were 5, 3 and 0, respectively in comparison with 14, 6.8 and 3 lesions, respectively during the 1-year pre-treatment period. Ery use was associated with a 65% reduction in appearance of new AK lesions and with 56 and 100% reductions in the incidence of new BCC and SCC lesions, respectively. These data suggest that topical use of photoprotection and DNA repair enzyme could help lower skin cancer lesions in XP. Control prospective trials are advisable in this clinical setting.
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PMID:Preventive Long-Term Effects of a Topical Film-Forming Medical Device with Ultra-High UV Protection Filters and DNA Repair Enzyme in Xeroderma Pigmentosum: A Retrospective Study of Eight Cases. 2540 50