Caffeine and caffeine sodium benzoate have a sunscreen effect, enhance UVB-induced apoptosis, and inhibit UVB-induced skin carcinogenesis in SKH-1 mice

Lu, Yao-Ping; Lou, You-Rong; Xie, Jun; Peng, Qingyun; Zhou, Sherry; Lin, Yong; Shih, Weichung Joe; Conney, Allan H.

doi:10.1093/carcin/bgl112

Cited by 77 publications

(67 citation statements)

References 26 publications

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“…In recent studies, we identified caffeine sodium benzoate as a complex of caffeine and sodium benzoate that is more active than caffeine at enhancing UVB-induced apoptosis (27). Our hypothesis predicts that administration of caffeine or caffeine sodium benzoate will inhibit UVB-induced activation of the ATR/Chk1 pathway by inhibiting the phosphorylation of Chk1 at Ser 345 , thereby leading to increased cyclin B1, premature chromatin condensation, premature mitosis, and cell death in DNA-damaged cells (see Fig.…”

Section: Resultsmentioning

confidence: 89%

“…Studies from our laboratory showed that administration of caffeine or caffeine sodium benzoate has sunscreen activity, increases the elimination of DNA-damaged cells by apoptosis, and inhibits UVB-induced carcinogenesis in SKH-1 mice (3,4,7,8,27,42). Topical applications of caffeine or caffeine sodium benzoate to UVBpretreated high-risk mice inhibited carcinogenesis in the absence of further UVB treatment (4,27,42), and administration of caffeine also enhanced apoptosis in the tumors (42). The results of these studies suggest that caffeine and caffeine sodium benzoate may be mechanistically novel agents for inhibiting sunlight-induced skin cancer.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Caffeine on the ATR/Chk1 Pathway in the Epidermis of UVB-Irradiated Mice

et al. 2008

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Administration of caffeine was shown in earlier studies to enhance UVB-induced apoptosis and inhibit UVB-induced carcinogenesis in hairless SKH-1 mice. Here, we describe a potential mechanism for these in vivo effects. A single irradiation of mouse skin with UVB activated the ataxiatelangiectasia mutated-and Rad3-related (ATR) pathway, causing a severalfold increase in keratinocytes with phosphoChk1 (Ser 345 ) and a marked decrease in mitotic keratinocytes with cyclin B1 compared with baseline. When given in the drinking water for 1 to 2 weeks before UVB, caffeine (0.4 mg/mL) markedly inhibited the UVB-induced phosphorylation of Chk1 on Ser 345 and caused premature expression of cyclin B1 in the epidermis. Normal keratinocytes had delayed mitotic entry for >10 h following UVB. Caffeine administration reduced this mitotic delay to only 4 h and caused markedly increased apoptosis by 6 to 10 h after UVB. p53 knockout mice were used to determine the role of p53 in these processes. Irradiation with UVB markedly decreased the number of mitotic keratinocytes with cyclin B1 in p53 knockout mice, and topical caffeine immediately after UVB abrogated this response and increased UVB-induced apoptosis severalfold. These effects of caffeine in knockout mice were substantially greater than in wild-type mice. The ability of caffeine to promote the deletion of p53 À/À keratinocytes may be relevant to its inhibitory effect on UVB-induced skin cancer. Our studies indicate that administration of caffeine enhances the removal of DNA-damaged cells by inhibiting the ATRmediated phosphorylation of Chk1 and prematurely increasing the number of cyclin B1-containing cells that undergo lethal mitosis. [Cancer Res 2008;68(7):2523-9]

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Section: Resultsmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Effect of Caffeine on the ATR/Chk1 Pathway in the Epidermis of UVB-Irradiated Mice

et al. 2008

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“…Along with its role as an antioxidant (17), recent studies have shown additional anticarcinogenic properties of caffeine, that include antimetastatic effects (30), the ability to inhibit cell proliferation (31), and enhance apoptosis (32). With respect to mammary tumorigenesis, one group reported that chronic caffeine exposure prior to the appearance of the tumor was associated with a significant reduction in tumor burden and metastasis in a transgenic mouse model (33).…”

Section: Discussionmentioning

confidence: 99%

The CYP1A2 Genotype Modifies the Association Between Coffee Consumption and Breast Cancer Risk Among BRCA1 Mutation Carriers

Kotsopoulos

Ghadirian²,

El-Sohemy

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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We have recently reported that, among BRCA1 mutation carriers, the consumption of caffeinated coffee was associated with a significant reduction in breast cancer risk. Because the metabolism of caffeine is primarily by CYP1A2, we examined whether or not the CYP1A2 genotype modifies the association between a history of coffee consumption and the risk of breast cancer. A common A to C polymorphism in the CYP1A2 gene is associated with decreased enzyme inducibility and impaired caffeine metabolism. Information regarding coffee consumption habits and the CYP1A2 genotype was available for 411 BRCA1 mutation carriers (170 cases and 241 controls). We estimated the odds ratios (ORs) and 95% confidence intervals (95% CIs) for breast cancer associated with the CYP1A2 genotype and a history of coffee consumption before age 35, adjusting for potential confounders. The CYP1A2 genotype did not affect breast cancer risk. Among women with at least one variant C allele (AC or CC), those who consumed coffee had a 64% reduction in breast cancer risk, compared with women who never consumed coffee (OR, 0.36; 95% CI, 0.18-0.73). A significant protective effect of coffee consumption was not observed among women with the CYP1A2 AA genotype (OR, 0.93; 95% CI,). Similar results were obtained when the analysis was restricted to caffeinated coffee. This study suggests that caffeine protects against breast cancer in women with a BRCA1 mutation and illustrates the importance of integrating individual genetic variability when assessing diet-disease associations. (Cancer Epidemiol Biomarkers Prev 2007;16(5):912 -6)

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“…This active shows potential anticancer effects upon oral and topical administration, and is able to protect the skin from ultraviolet (UV) light induced skin cancer (Dias et al, 1999;Koo et al, 2007;Lu et al, 2007;Roure et al, 2011;Gee et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Design of solid lipid nanoparticles for caffeine topical administration

et al. 2014

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Caffeine is an interesting compound showing anticancer and protective effects upon topical administration, although its penetration through the skin is compromised by its hydrophilicity. Materials and methods: SLN-CAF were formulated by using a modification of the quasi-emulsion solvent diffusion technique (QESD) and characterized by PCS and DSC analyses. In vitro percutaneous absorption studies were effected using excised human skin membranes (i.e. Stratum Corneum Epidermis or SCE).Results: SLN-CAF were in a nanometric range (182.6 ± 8.4 nm) and showed an interesting payload value (75% ± 1.1). DSC studies suggest the presence of a well-defined system and the successful drug incorporation. Furthermore, SLN-CAF generated a significantly faster permeation than a control formulation over 24 h of monitoring. Discussion and conclusions: SLN-CAF were characterized by valid dimensions and a good encapsulation efficiency, although the active to incorporate showed a hydrophilic character. This result confirms the suitability of the formulation strategy employed in the present work. Furthermore, the in vitro evidence outline the key role of lipid nanoparticles in enhancing caffeine permeation through the skin.

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Caffeine and caffeine sodium benzoate have a sunscreen effect, enhance UVB-induced apoptosis, and inhibit UVB-induced skin carcinogenesis in SKH-1 mice

Cited by 77 publications

References 26 publications

Effect of Caffeine on the ATR/Chk1 Pathway in the Epidermis of UVB-Irradiated Mice

Effect of Caffeine on the ATR/Chk1 Pathway in the Epidermis of UVB-Irradiated Mice

The CYP1A2 Genotype Modifies the Association Between Coffee Consumption and Breast Cancer Risk Among BRCA1 Mutation Carriers

Design of solid lipid nanoparticles for caffeine topical administration

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