Preventive effect of antioxidant on ultraviolet-induced skin cancer in mice

Ichihashi, Masamitsu; Ahmed, N. U.; Budiyanto, Arief; Wu, An‐Bang; Bito, Toshinori; Ueda, Masato; Osawa, Toshihiko

doi:10.1016/s0923-1811(00)00083-9

Cited by 82 publications

(55 citation statements)

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“…Many other laboratories around the world also reported the protective effects of GTPs against the harmful effects of UV radiations including photocarcinogenesis [22][23][24]. In several published studies, oral consumption of green tea, black tea, decaffeinated green and black teas by mice was found to prevent skin cancer induction by chemical carcinogens and UV radiation [25].…”

Section: Tea and Prevention Of Photocarcinogenesis In Mouse Modelsmentioning

confidence: 99%

Cutaneous Photochemoprotection by Green Tea: A Brief Review

Ahmad

Mukhtar²

2001

Skin Pharmacol Physiol

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Alarmingly increasing incidences of skin cancer are being reported from many countries where the majority of the population is Caucasian. According to projected estimates by the American Cancer Society, approximately 1.3 million cases of basal-cell and squamous-cell cancers, grouped together as nonmelanoma skin cancers, are diagnosed annually in the USA alone. It is clear that excessive exposure of the skin to solar radiation, particularly the UVB component, is responsible for these cancers. It is also important to mention here that among all the cancers, skin cancer is believed to be one of the most preventable and curable cancer types. While the surgical therapy for these skin cancers is highly effective, because of their recurrence and many other reasons, these cancers cause significant morbidity to the patients. One way to reduce the occurrence of these cancers is through chemoprevention. For the chemoprevention of photodamage and thus for photocarcinogenesis, we will use the term ‘photochemoprotection’. In recent years, the naturally occurring compounds, especially the antioxidants, present in the common diet and beverages consumed by the human population have gained considerable attention as chemopreventive agents for potential human benefit. Many such agents have found a place in skin care products. Green tea, rich in polyphenolic antioxidants, is gaining increasing attention as a supplement in skin care products. In this short review, we will discuss the chemopreventive potential of green tea polyphenols against skin cancer, especially photocarcinogenesis. We advocate that the use of skin care products supplemented with agents such as green tea in conjunction with the use of sunscreens and educational efforts may be an effective strategy for reducing UV-induced photodamage and skin cancer in humans.

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Section: Tea and Prevention Of Photocarcinogenesis In Mouse Modelsmentioning

confidence: 99%

Cutaneous Photochemoprotection by Green Tea: A Brief Review

Ahmad

Mukhtar²

2001

Skin Pharmacol Physiol

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“…The ratio of Py-Py dimers to 8-OH-dG formation in cellular DNA after UVB irradiation is 80 -100:1, (19,24) while the ratio of psoralen-adducts to 8-OH-dG formation by PUVA treatment is 25:1. (25) Although UVB and PUVA treatments induce PyPy dimers and psoralen-DNA adducts, respectively, as major cellular DNA modifications, our study focused on the analysis of 8-OH-dG as a marker of cellular oxidative stress for the following reasons: (1) not only initiation but also chronic inflammation-induced promotion and progression may be involved in UVB-induced skin carcinogenesis; (26,27) (2) antioxidants inhibit both UVB-induced 8-OH-dG formation and carcinogenesis in mouse skin; (28,29) and (3) in Ogg1 (8-OHGua glycosylase) knockout mice, UVB irradiation induced both 8-OH-dG formation and an increase in skin tumors, suggesting that 8-OH-dG is involved in UVB-induced skin carcinogenesis. (30) The purpose of the present study was to assess the oxidative stress induced by clinically used UV wavelengths, doses and apparatus.…”

mentioning

confidence: 99%

Formation of 8‐hydroxy‐2′‐deoxyguanosine in the DNA of cultured human keratinocytes by clinically used doses of narrowband and broadband ultraviolet B and psoralen plus ultraviolet A

et al. 2006

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Psoralen plus ultraviolet A (PUVA) and narrowband ultraviolet B (UVB) are widely used in skin disease phototherapy. Recently, the efficacy of UVB therapy has been greatly improved by narrowband UVB, compared to conventional broadband UVB. The objectives of the current study were to evaluate the influence of UVB-induced and PUVA-induced oxidative stress on cultured keratinocytes. We analyzed 8-hydroxy-2′ ′ ′ ′-deoxyguanosine (8-OH-dG) in human keratinocytes (HaCaT cell line) using a highperformance liquid chromatography system equipped with an electrochemical detector. Non-irradiated human keratinocytes contained a baseline of 1.48 ± ± ± ± 0.22 (mean ± ± ± ± SD) 8-OH-dG per 10 6 deoxyguanosine (dG) residues in cellular DNA, which increased linearly with higher doses of UVB. When their abilities to induce 8-OH-dG were compared to each other, based on the minimal erythemal and therapeutically used doses, by irradiating them with broadband UVB at 100 mJ/cm 2 , the amount of 8-OH-dG increased to 3.42 ± ± ± ± 0.46 residues per 10 6 dG, while a narrowband UVB treatment at 1000 mJ/cm 2 , with biological effects comparable to those elicited by 100 mJ/cm 2 broadband UVB, increased it to 2.06 ± ± ± ± 0.31 residues per 10 6 dG. PUVA treatment, with 100 ng/mL 8-methoxypsoralen and 5000 mJ/cm 2 UVA, increased the 8-OH-dG level to 4.52 ± ± ± ± 0.42 residues per 10 6 dG. When HaCaT cells treated with 2000 mJ/cm 2 narrowband UVB were cultured and the amount of 8-OH-dG was monitored in the living cells, 65.6% of the residues were repaired 24 h after treatment. Our study provides a warning that widely used narrowband UVB and PUVA induce cellular oxidative DNA damage at the therapeutically used doses, although to a lesser degree than broadband UVB with the same clinically effective dose. (Cancer Sci 2006; 97: 99 -105) E ight-hydroxy-2′-deoxyguanosine (8-OH-dG), also known as 7,8-dihydro-8-oxo-deoxyguanosine (8-oxo-dG), (1) has been proposed as a key biomarker of oxidative DNA damage relevant to carcinogenesis (1,2) and pathogenesis of autoimmune disorders. (3,4) This DNA damage is induced by the reactions of reactive oxygen species (ROS), such as hydrogen peroxide (H 2 O 2 ), superoxide anions ( ), singlet oxygen and hydroxyl radicals (·OH).Human skin is constantly exposed to environmental stresses, and is vulnerable to the effects of ROS generated by exposure to ultraviolet (UV) radiation.(5) Yamamoto et al. (6) reported that the formation of 8-OH-dG in DNA might be one of the mechanisms of daylight-induced mutagenesis. In fact, irradiation with a fluorescent sun lamp or with UVB does induce 8-OH-dG in the epidermis of hairless mice. (7,8) Parrish and Jaenicke (9) found that 313 nm UVB radiation is the most effective wavelength for the treatment of psoriasis. This finding provided the impetus for developing the Philips TL-01 fluorescent bulb, a narrowband UVB light source that produces a spectral emission between 310 and 315 nm. Narrowband UVB phototherapy has thus significantly improved the therapeutic efficacy of conventional br...

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“…Olive oil phenolic compounds reduce ROS generated both during metabolism of fatty acids (Mataix et al, 1993;Owen et al, 2000a) and cancer cells (Owen et al, 2000b), or by the action of exogenous agents like UV-light and ionizing radiation Ichihashi et al, 2000;Awad et al, 2003a).…”

Section: Potential Anticancer Activity Of Olive Oil Phenolic Compoundsmentioning

confidence: 99%