DNC News

Sunscreen backfires

Jacob Schor, ND

September 19, 2006

 

Last week's issue of New Scientist reports on a rather distressing study regarding sunscreen. If these results are accurate, sunscreen is not protecting the skin as we thought it does. It may be making matters worse.

 

Kerry Hanson and her colleagues at the University of California at Riverside exposed human skin samples grown in the lab to UV radiation while supposedly protected with the chemicals commonly used in sunscreens. One hour later, each compound had soaked into the skin, reducing its protective effect. This finding gave rise to the news reports, you may have seen, suggesting that you need to reapply sunscreen every two hours.

These news stories missed a more important finding. The skin samples that were supposedly protected by sunscreen contained more reactive oxygen species (ROS) than skin with no sunscreen on it. ROS are free radicals that damage skin cells and increase the risk of skin cancer. [i]

If this report is confirmed it would mean that sunscreen not only does not protect us from skin cancer, it increases the risk.

It is possible to prevent the formation of free radicals in skin exposed to UV light by adding antioxidants to the sunscreen formulations. A variety of things have already been studied that will work. Vitamin E has is very protective, especially in combination with selenium. [ii] Green tea extracts also prevent damage. [iii] Actually, quite a few plant extracts appear to be protective. If you are making a list, add milk thistle, [iv] grape seed extracts, [v] pomegranate extracts, [vi] caffeine, [vii] and Cat's Claw. [viii]

This is not the first study to question sunscreen use, it is only the latest. Do not expect things to change soon. Current medical opinion is incredibly invested in selling us the benefits of sunscreen. Changing this idea will be difficult; the Skin Cancer Foundation's response to this most recent study was to simply suggest that we apply the sunscreen more often.

 

References

[i] New Scientist magazine, 09 September 2006 , page 16

 

[ii] J Am Acad Dermatol. 2003 Sep;49(3):458-72.

Effects of topical L-selenomethionine with topical and oral vitamin E on pigmentation and skin cancer induced by ultraviolet irradiation in Skh:2 hairless mice.

 

Burke KE, Clive J, Combs GF Jr, Nakamura RM.

 

Department of Biostatistics, University of Connecticut Health Center , Farmington , USA .

 

BACKGROUND: The antioxidants selenium and vitamin E can be effective in reducing acute and chronic ultraviolet (UV)-induced skin damage. OBJECTIVE: This study investigated whether topical L-selenomethionine with topical RRR-alpha-tocopherol (Eol) or oral RRR-alpha-tocopheryl acetate (Eac) can reduce the incidence of UV-induced skin damage more than treatment with each alone. METHODS: Skh:2 hairless pigmented mice were treated with lotion vehicle, L-selenomethionine lotion, Eol lotion, oral Eac, L-selenomethionine plus Eol lotion, or L-selenomethionine lotion plus oral Eac and exposed to UVB. Skin pigmentation was scored, and the number of skin tumors per animal was counted weekly. RESULTS: Mice treated with selenium and vitamin E had significantly less acute and chronic UV-induced skin damage. CONCLUSION: Topical L-selenomethionine alone and combined with vitamin E gave the best protection against UV-induced blistering and pigmentation. In protecting against skin cancer, topical Eol and topical L-selenomethionine plus oral Eac were best. Significant synergy of L-selenomethionine with vitamin E was not observed.

 

PMID: 12963910 [PubMed - indexed for MEDLINE]

 

[iii] Neoplasia. 2003 Nov-Dec;5(6):555-65.

 

Exceptionally high protection of photocarcinogenesis by topical application of (--)-epigallocatechin-3-gallate in hydrophilic cream in SKH-1 hairless mouse model: relationship to inhibition of UVB-induced global DNA hypomethylation.

 

Mittal A, Piyathilake C, Hara Y, Katiyar SK.

 

Department of Dermatology, University of Alabama at Birmingham , Birmingham , AL 35294 , USA .

 

(--)-Epigallocatechin-3-gallate (EGCG) has been shown to have potent antiphotocarcinogenic activity, but it was required to develop a cream-based formulation for topical application. For topical application, we tested hydrophilic cream as a vehicle for EGCG. Treatment with EGCG ( approximately 1 mg/cm(2) skin area) in hydrophilic cream resulted in exceptionally high protection against photocarcinogenesis when determined in terms of tumor incidence, tumor multiplicity, and tumor size in a SKH-1 hairless mouse model. EGCG also inhibited malignant transformation of ultraviolet B (UVB)-induced papillomas to carcinomas. In order to determine the mechanism of prevention of photocarcinogenesis, we determined the effect of EGCG on global DNA methylation pattern using monoclonal antibodies against 5-methyl cytosine and DNA methyltransferase in the long-term UV-irradiated skin because altered DNA methylation silencing is recognized as a molecular hallmark of human cancer. We found that treatment with EGCG resulted in significant inhibition of UVB-induced global DNA hypomethylation pattern. Long-term application of EGCG did not show any apparent sign of toxicity in mice when determined in terms of skin appearance, lean mass, total bone mineral content, and total bone mineral density but showed reduction in fat mass when analyzed using dual-energy X-ray absorptiometry. These data suggest that hydrophilic cream could be a suitable vehicle for topical application of EGCG, and that EGCG is a promising candidate for future cancer therapies based on its influence on the epigenetic pathway.

 

 

[iv] Carcinogenesis. 2004 Jan;25(1):99-106. Epub 2003 Oct 10.

Dual efficacy of silibinin in protecting or enhancing ultraviolet B radiation-caused apoptosis in HaCaT human immortalized keratinocytes.

 

Dhanalakshmi S, Mallikarjuna GU, Singh RP, Agarwal R.

 

Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Health Sciences Center, Denver , CO 80262 , USA .

 

An increasing incidence of human skin cancer and other adverse effects of solar ultraviolet (UV) radiation enhance the need for novel chemoprevention strategies. Here, we have studied the effect of silibinin on UVB-induced apoptosis in HaCaT cells. Silibinin strongly prevented lower doses (15 and 30 mJ/cm2) of UVB-induced apoptosis, as observed by a reversal in UVB-caused poly(ADP-ribose) polymerase (PARP) cleavage, caspase 9 activation and an increase in apoptotic cells. UVB-induced PARP cleavage was also abolished by all caspase inhibitor, suggesting that it is a caspase-dependent effect. In other studies, silibinin restored UVB-caused depletion of a protein inhibitor of apoptosis, survivin, concomitant with up-regulation of transcription factor nuclear factor kappaB DNA binding activity, without any noticeable effect on UVB-caused activated protein-1 activation. Further, silibinin treatment up-regulated UVB-induced extracellular signal regulated kinase 1/2 phosphorylation, suggesting a possible role as a survival event in the protective effect of silibinin. In other studies, silibinin caused a moderate increase in phospho-Bcl-2, without any noticeable changes in total Bcl-2 levels, and down-regulated bax levels moderately. Silibinin also caused a strong decrease in Bad heterodimerization with Bclx(L), which was consistent with an increased translocation of Bclx(L) to the mitochondria from the cytosol. Consistent with its protective effect on UVB-caused apoptosis, silibinin also increased S phase arrest, possibly providing a prolonged time for efficient DNA repair. Interestingly, the protective effects of silibinin in HaCaT cells were lost at a higher dose of UVB (120 mJ/cm2) and instead it further enhanced UVB-caused apoptosis together with a strong decrease in UVB-caused activated protein-1 activation. Together, these results clearly demonstrate the dual efficacy of silibinin in protecting or enhancing UVB-caused apoptosis in the same cellular system and suggest that silibinin possibly works as a UVB damage sensor to exert its biological action.

 

PMID:

[v] Carcinogenesis. 2003 Aug;24(8):1379-88. Epub 2003 Jun 05.

Dietary feeding of proanthocyanidins from grape seeds prevents photocarcinogenesis in SKH-1 hairless mice: relationship to decreased fat and lipid peroxidation.

 

Mittal A, Elmets CA , Katiyar SK.

 

Department of Dermatology, University of Alabama at Birmingham , Birmingham , AL 35294 , USA .

 

The use of dietary botanicals is receiving considerable interest in the protection of skin from the adverse biological effects of solar ultraviolet (UV) radiation. Dietary feeding of proanthocyanidins extracted from grape seeds (GSP) (0.2 and 0.5%, w/w) in AIN76 control diet to SKH-1 hairless mice resulted in prevention of photocarcinogenesis in terms of tumor incidence (20-95%), tumor multiplicity (46-95%) and tumor size (29-94%) against UVB-induced complete (both initiation + promotion), initiation and promotion stages of photocarcinogenesis. Feeding of GSP (0.5%, w/w) also resulted in prevention of malignant transformation of UVB-induced papillomas to carcinomas in terms of carcinoma incidence (45%), carcinoma multiplicity (61%) and carcinoma size (75%) compared with non-GSP treated mice following UVB-induced complete carcinogenesis protocol at the end of 30 weeks. Biochemical analysis revealed that treatment of GSP in vivo and in vitro systems significantly inhibited UVB- or Fe3+-induced lipid peroxidation by 57-66% (P<0.01) and 41-77% (P< 0.05-0.001), respectively, thus suggesting the antioxidant mechanism of photoprotection by GSP. Long-term feeding of GSP did not show apparent signs of toxicity in mice when determined in terms of body weight, diet consumption and physical characteristics of internal body organs like spleen, liver and kidney. Feeding of GSP also did not show apparent signs of toxicity when determined in terms of total body mass (mass of lean + fat), total bone mineral density and total bone mineral content by employing dual-energy X-ray absorptiometry (DXA). DXA analysis also revealed that feeding of GSP significantly decreased tissue fat level (24-27%, P<0.05) without changing the total body mass of the animals compared with non-GSP-fed animals. This can be attributed to increased lipolysis or decreased synthesis of fat due to administration of GSP. Together, it can be suggested that inhibition of photocarcinogenesis by GSP treatment may be associated with the reduction in UVB-induced oxidative damage and tissue fat content.

 

PMID: 12807737 [PubMed - indexed for MEDLINE]

 

 

[vi] Photochem Photobiol. 2006 Mar-Apr;82(2):398-405.  

Photochemopreventive effect of pomegranate fruit extract on UVA-mediated activation of cellular pathways in normal human epidermal keratinocytes.

•  Syed DN ,

•  Malik A ,

•  Hadi N ,

•  Sarfaraz S ,

•  Afaq F ,

•  Mukhtar H .

Department of Dermatology, University of Wisconsin , Madison , WI , USA .

UVA is the major portion (90-99%) of solar radiation reaching the surface of the earth and has been described to lead to formation of benign and malignant tumors. UVA-mediated cellular damage occurs primarily through the release of reactive oxygen species and is responsible for immunosuppression, photodermatoses, photoaging and photocarcinogenesis. Pomegranate fruit extract (PFE) possesses strong antioxidant and anti-inflammatory properties. Our recent studies have shown that PFE treatment of normal human epidermal keratinocytes (NHEK) inhibits UVB-mediated activation of MAPK and NF-kappaB pathways. Signal transducers and activators of transcription 3 (STAT3), Protein Kinase B/AKT and Map Kinases (MAPKs), which are activated by a variety of factors, modulate cell proliferation, apoptosis and other biological activities. The goal of this study was to determine whether PFE affords protection against UVA-mediated activation of STAT3, AKT and extracellular signal-regulated kinase (ERK1/2). Immunoblot analysis demonstrated that 4 J/cm2 of UVA exposure to NHEK led to an increase in phosphorylation of STAT3 at Tyr705, AKT at Ser473 and ERK1/2. Pretreatment of NHEK with PFE (60-100 microg/mL) for 24 h before exposure to UVA resulted in a dose-dependent inhibition of UVA-mediated phosphorylation of STAT3 at Tyr705, AKT at Ser473 and ERK1/2. mTOR, structurally related to PI3K, is involved in the regulation of p70S6K, which in turn phosphorylates the S6 protein of the 40S ribosomal subunit. We found that UVA radiation of NHEK resulted in the phosphorylation of mTOR at Thr2448 and p70S6K at Thr421/Ser424. PFE pretreatment resulted in a dose-dependent inhibition in the phosphorylation of mTOR at Thr2448 and p70S6K at Thr421/Ser424. Our data further demonstrate that PFE pretreatment of NHEK resulted in significant inhibition of UVA exposure-mediated increases in Ki-67 and PCNA. PFE pretreatment of NHEK was found to increase the cell-cycle arrest induced by UVA in the G1 phase of the cell cycle and the expression of Bax and Bad (proapoptotic proteins), with downregulation of Bcl-X(L) expression (antiapoptotic protein). Our data suggest that PFE is an effective agent for ameliorating UVA-mediated damages by modulating cellular pathways and merits further evaluation as a photochemopreventive agent.

PMID: 16613491 [PubMed - indexed for MEDLINE]

 

[vii] Carcinogenesis. 2006 Jul 24; [Epub ahead of print]  

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

•  Lu YP ,

•  Lou YR ,

•  Xie JG ,

•  Peng QY ,

•  Zhou S ,

•  Lin Y ,

•  Shih WJ ,

•  Conney AH .

Susan Lehman Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854-8020, USA.

Topical application of caffeine sodium benzoate immediately after UVB irradiation of SKH-1 mice enhanced UVB-induced apoptosis by a 2- to 3- fold greater extent than occurred after the topical application of an equimolar amount of caffeine. Although topical application of caffeine sodium benzoate or caffeine enhanced UVB-induced apoptosis, both substances were inactive on non-UVB-treated normal skin. Topical application of caffeine sodium benzoate or caffeine (each has UVB absorption properties) 0.5 hr before irradiation with a high dose of UVB decreased UVB-induced thymine dimer formation and sunburn lesions (sunscreen effect). Caffeine sodium benzoate was more active than an equimolar amount of caffeine in exerting a sunscreen effect. In additional studies, caffeine sodium benzoate strongly inhibited the formation of tumors in UVB-pretreated high risk mice and in tumor-bearing mice, and the growth of UVB-induced tumors was also inhibited. Caffeine sodium benzoate and caffeine are the first examples of compounds that have both a sunscreen effect and enhance UVB-induced apoptosis. Our studies suggest that caffeine sodium benzoate and caffeine may be good agents for inhibiting the formation of sunlight-induced skin cancer. (Supported in part by NIH Grants No. CA80759 and CA88961, as well as a State of New Jersey Commission on Cancer Research Grant 05-1976-CCR-EO).

 

[viii] Phytother Res. 2006 Mar;20(3):178-83.  

A water soluble extract from Uncaria tomentosa (Cat's Claw) is a potent enhancer of DNA repair in primary organ cultures of human skin.

•  Mammone T ,

•  Akesson C ,

•  Gan D ,

•  Giampapa V ,

•  Pero RW .

Laboratory of Skin Biology Group, The Estee Lauder Companies Inc, 125 Pinelawn Road, Melville, NY 11747, USA.

Cat's Claw (Uncaria tomentosa) water extracts, essentially free of oxindole alkaloids, have been shown to possess a broad spectrum of biological activity including DNA repair enhancement and antiinflammatory properties. These two biological mechanisms are key molecular targets to develop treatments that protect skin exposed to ultraviolet light from the sun. Because C-Med-100, a Cat's Claw water extract, is the only documented natural source of components that can up-regulate simultaneously both DNA repair and antiinflammation, its ability to modulate DNA repair in human skin organ cultures was undertaken. For this purpose skin cultures were treated with or without 5 mg/mL C-Med-100, irradiated with 0-100 mJ/cm2 UVB, and microscopically analysed for necrosis as well as the level of pyrimidine dimers using immunofluorescent TT-dimer antibody staining. The data clearly demonstrated that co-incubation with C-Med-100 reduced skin cell death from UV exposure, and this protection was accounted for by a concomitant increase in DNA repair. Based on these results, it was concluded that C-Med-100 was a natural plant extract worthy of further consideration as a sunscreen product. Copyright 2006 John Wiley & Sons, Ltd.

PMID: 16521105 [PubMed - indexed for MEDLINE]

 


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