Photoaging and oxidative stress

Nishigori, Chikako; Hattori, Yukari; Arima, Yusuke; Miyachi, Yoshiki

doi:10.1034/j.1600-0625.12.s2.3.x

Cited by 56 publications

(51 citation statements)

References 15 publications

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“…This is consistent with the yield of UV-induced 8-OHdG in cultured cells [~ 3/10 9 dG/J/m 2 (65)] considering the transmission of UV-B as ~10%. Next, we studied the relation between the method of UV exposure and the induced oxidative stress by irradiating mice with UV-B using different protocols: mice were irradiated with a single dose of UV-B at 2 minimal erythema doses (MED)/time or 10 MED/time, three times per week for 1-4 weeks ( Table 2) (32,65). Repeated UV-B exposure at a physiologically relevant dose (2 or 10 MED) generated 8-OHdG in the mouse skin tissue.…”

Section: Detection Of 8-ohdg In Mouse Skin Irradiated With Uv-bsupporting

confidence: 86%

Role of Reactive Oxygen Species in Skin Carcinogenesis

Nishigori

Hattori²,

Toyokuni³

2004

Antioxidants & Redox Signaling

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243

174

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Reactive oxygen species (ROS) are associated not only with initiation, but also with promotion and progression in the multistage carcinogenesis model. In the present review, we will focus on the involvement of ROS in skin carcinogenesis, especially that induced by ultraviolet (UV) radiation. UV-specific DNA damage has been well studied thus far. However, recent reports have revealed the previously unknown participation of oxidative stress in UV-induced skin carcinogenesis. Indeed, in addition to transition-type mutations at dipyrimidine sites, G:C to T:A transversions, which may be induced by the presence of 8-oxoguanine during DNA replication, are frequently observed in the ras oncogene and p53 tumor suppressor gene in human skin cancers of sun-exposed areas and in UV-induced mouse skin cancers. Recent studies have shown that not only UV-B, but also UV-A is involved in UV-induced carcinogenesis. A wide variety of biological phenomena other than direct influence by UV, such as inflammatory and immunological responses and oxidative modifications of DNA and proteins, appear to play roles in UV-induced skin carcinogenesis. Furthermore, it has become clear that genetic diseases such as xeroderma pigmentosum show deficient repair of oxidatively modified DNA lesions. The involvement of ROS in skin carcinogeneisis caused by arsenic and chemical carcinogens will also be discussed.

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Section: Detection Of 8-ohdg In Mouse Skin Irradiated With Uv-bsupporting

confidence: 86%

Role of Reactive Oxygen Species in Skin Carcinogenesis

Nishigori

Hattori²,

Toyokuni³

2004

Antioxidants & Redox Signaling

Self Cite

243

174

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“…UVR-driven generation of reactive oxygen species (ROS) may originate from endogenous non-DNA photosensitizers and other molecular sources including NAD(P)H oxidase and mitochondrial electron leakage [7–10]. Oxidative stress is now widely considered as a key mechanism contributing to the detrimental effects of acute and chronic UVR exposure, and both the UVB (290–320 nm) and UVA (320–400 nm) spectral regions have been shown to cause skin oxidative damage through structural and functional alterations of critical molecular targets [11–15]. …”

Section: Introductionmentioning

confidence: 99%

Malondialdehyde-derived epitopes in human skin result from acute exposure to solar UV and occur in nonmelanoma skin cancer tissue

Williams

Bermudez

Park

et al. 2014

Journal of Photochemistry and Photobiology B: Biology

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Cutaneous exposure to solar ultraviolet radiation (UVR) is a causative factor in photoaging and photocarcinogenesis. In human skin, oxidative stress is widely considered a key mechanism underlying the detrimental effects of acute and chronic UVR exposure. The lipid peroxidation product malondialdehyde (MDA) accumulates in tissue under conditions of increased oxidative stress, and the occurrence of MDA-derived protein epitopes, including dihydropyridine-lysine (DHP), has recently been substantiated in human skin. Here we demonstrate for the first time that acute exposure to sub-apoptogenic doses of solar simulated UV light (SSL) causes the formation of free MDA and protein-bound MDA-derived epitopes in cultured human HaCaT keratinocytes and healthy human skin. Immunohistochemical staining revealed that acute exposure to SSL is sufficient to cause an almost twenty-fold increase in general MDA- and specific DHP-epitope content in human skin. When compared to dose-matched solar simulated UVA, complete SSL was more efficient generating both free MDA and MDA-derived epitopes. Subsequent tissue microarray (TMA) analysis revealed the prevalence of MDA- and DHP-epitopes in nonmelanoma skin cancer (NMSC). In squamous cell carcinoma tissue, both MDA- and DHP-epitopes were increased more than three-fold as compared to adjacent normal tissue. Taken together, these date demonstrate the occurrence of MDA-derived epitopes in both solar UVR-exposed healthy human skin and NMSC TMA tissue; however, the potential utility of these epitopes as novel biomarkers of cutaneous photodamage and a functional role in the process of skin photocarcinogenesis remain to be explored.

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“…The most common negative effect is acute sunburn or erythema, but UV insults can also lead to premature photoaging [17][18][19][20][21][22] and carcinogenesis [23][24][25][26][27][28][29]. The identification of novel treatments to increase skin resistance to UV induced damage without the limitations of traditional methods would prove particularly useful.…”

Section: Discussionmentioning

confidence: 99%

LED photoprevention: Reduced MED response following multiple LED exposures

Barolet

Boucher²

2008

Lasers Surg Med

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Background and Objectives: As photoprotection with traditional sunscreen presents some limitations, the use of non-traditional treatments to increase skin resistance to ultraviolet (UV) induced damage would prove particularly appealing. The purpose of this pilot study was to test the potential of non-thermal pulsed light-emitting diode (LED) treatments (660 nm) prior to UV exposure in the induction of a state of cellular resistance against UV-induced erythema. Study Design/Materials and Methods: Thirteen healthy subjects and two patients with polymorphous light eruption (PLE) were exposed to 5, 6, or 10 LED treatments (660 nm) on an EXPERIMENTAL anterior thigh region. Individual baseline minimal erythema doses (MED) were then determined. UV radiation was thereafter performed on the LED EXPERIMENTAL and CONTROL anterior thigh areas. Finally, 24 hours post-UV irradiation, LED pre-treated MED responses were compared to the nontreated sites. Results: Reduction of erythema was considered significant when erythema was reduced by > 50% on the LED-treated side as opposed to CONTROL side. A significant LED treatment reduction in UV-B induced erythema reaction was observed in at least one occasion in 85% of subjects, including patients suffering from PLE. Moreover, there was evidence of a dose-related pattern in results. Finally, a sun protection factor SPF-15-like effect and a reduction in post-inflammatory hyperpigmentation were observed on the LED pre-treated side. Conclusions: Results suggest that LED based therapy prior to UV exposure provided significant protection against UV-B induced erythema. The induction of cellular resistance to UV insults may possibly be explained by the induction of a state a natural resistance to the skin via specific cell signaling pathways and without the drawbacks and limitations of traditional sunscreens. These results represent an encouraging step towards expanding the potential applications of LED therapy and could be useful in the treatment of patients with anomalous reactions to sunlight.

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Photoaging and oxidative stress

Cited by 56 publications

References 15 publications

Role of Reactive Oxygen Species in Skin Carcinogenesis

Role of Reactive Oxygen Species in Skin Carcinogenesis

Malondialdehyde-derived epitopes in human skin result from acute exposure to solar UV and occur in nonmelanoma skin cancer tissue

LED photoprevention: Reduced MED response following multiple LED exposures

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