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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cleanser technology has come a long way from merely cleansing to providing mildness and moisturizing benefits as well. It is known that harsh surfactants in cleansers can cause damage to skin proteins and lipids, leading to after-wash tightness, dryness, barrier damage, irritation, and even itch. In order for cleansers to provide skin-care benefits, they first must minimize surfactant damage to skin proteins and lipids. Secondly, they must deposit and deliver beneficial agents such as occlusives, skin lipids, and humectants under wash conditions to improve skin hydration, as well as mechanical and visual properties. While all surfactants tend to interact to some degree with lipids, their interaction with proteins can vary significantly, depending upon the nature of their functional head group. In vitro, ex vivo, and in vivo studies have shown that surfactants that cause significant skin irritation interact strongly with skin proteins. Based on this understanding, several surfactants and surfactant mixtures have been identified as "less irritating" mild surfactants because of their diminished interactions with skin proteins. Surfactants that interact minimally with both skin lipids and proteins are especially mild. Another factor that can aggravate surfactant-induced dryness and irritation is the pH of the cleanser. The present authors' recent studies demonstrate that high pH (pH 10) solutions, even in the absence of surfactants, can increase stratum corneum (SC) swelling and alter lipid rigidity, thereby suggesting that cleansers with neutral or acidic pH, close to SC-normal pH 5.5, may be potentially less damaging to the skin. Mildness enhancers and moisturizing agents such as lipids, occlusives, and humectants minimize damaging interactions between surfactants, and skin proteins and lipids, and thereby, reduce skin damage. In addition, these agents play an ameliorative role, replenishing the skin lipids lost during the wash period. The present review discusses the benefits of such agents and their respective roles in improving the overall health of the skin barrier.
Dermatol Ther 2004
PMID:Cleansing without compromise: the impact of cleansers on the skin barrier and the technology of mild cleansing. 1472 95

Ultraviolet radiation (UVR) promotes skin cancer development by mutagenic, immunosuppressive, and oxidative-stress-inducing mechanisms; however, certain antioxidants may counteract and prevent UVR-induced photodamage. Lutein is a xanthophyll carotenoid with potent antioxidant activity. Because reactive oxygen species (ROS) are believed to have a role in UVR-induced skin damage, we investigated whether lutein can modify UVR effects including the tissue swelling response to midrange UVR (280-320 nm, ultraviolet B (UVB) radiation) and UVB suppression of contact hypersensitivity (CHS) in both the local and the systemic models of UV-induced immunosuppression. We found that compared to mice fed the standard laboratory diet, mice fed dietary lutein demonstrated significant inhibition of ear swelling owing to UVB radiation. Mice exposed to 1700 J per m2 UVB radiation four times at daily intervals and then sensitized to dinitrofluorobenzene at the site of irradiation showed a decreased CHS response upon challenge. This suppression by UVB radiation was significantly inhibited by lutein feeding. When UVB radiation was given at a single dose of 10,000 J per m2 to inhibit the induction of CHS at a distant, nonirradiated site, no effect of lutein was seen. Finally, lutein accumulated in the skin of mice following diet supplementation and was shown to decrease ROS generation following UVR exposure. Thus, lutein modulates the skin's response to UVR and may contribute to the defense against some of the deleterious effects of solar radiation.
J Invest Dermatol 2004 Feb
PMID:Dietary lutein reduces ultraviolet radiation-induced inflammation and immunosuppression. 1500 38

Ultraviolet A radiation from sunlight is a major human health concern, as it is not absorbed by the ozone layer and can deeply penetrate into the skin causing skin damage. To study the molecular mechanism involved in the ultraviolet A effect, human HaCaT keratinocytes were exposed to ultraviolet A at doses of 10 J per cm2 and 30 J per cm2. Ultraviolet A irradiation caused dose- and time-dependent apoptotic cell death, as evidenced by DNA fragmentation, flow cytometry, and the activation of caspase-3. To study the genes altered by ultraviolet A at an apoptosis-inducing dose (30 J per cm2), cells were harvested immediately after ultraviolet A treatment (0 h), and 6 h and 24 h after ultraviolet A exposure. Total RNA was extracted for microarray and real-time RT-PCR analysis, and cellular proteins were extracted for western blot analysis. Of the selected critical genes/proteins, the induction of c-Jun, c-myc, and p33ING1, and the repression of epidermal growth factor receptor, inhibitor of apoptosis protein, and survivin pathways, could be involved in ultraviolet-A-induced apoptosis. On the other hand, the late induction of cyclin D1 and cyclin-dependent kinase 4 was indicative of possible cell cycle recovery in surviving cells. Real-time RT-PCR analysis confirmed these results and a majority of the protein levels paralleled their corresponding RNA levels. In addition, ultraviolet A treatment altered the expression of genes involved in signal transduction, RNA processing, structural proteins, and metabolism in a time-dependent manner. This initial microarray analysis could advance our understanding of cellular responses to ultraviolet A exposure, and provide a platform from which to further study ultraviolet-A-induced apoptosis and carcinogenesis.
J Invest Dermatol 2004 Feb
PMID:Expression profiling of human keratinocyte response to ultraviolet A: implications in apoptosis. 1500 41

DNA damage caused by ultraviolet (UV) irradiation is considered the main etiologic factor contributing to the development of skin cancer. Systemic or topical application of antioxidants has been suggested as a protective measure against UV-induced skin damage. We investigated the effect of long-term oral administration of a combination of the antioxidants ascorbic acid (vitamin C) and D-alpha-tocopherol (vitamin E) in human volunteers on UVB-induced epidermal damage. The intake of vitamins C and E for a period of 3 mo significantly reduced the sunburn reaction to UVB irradiation. Detection of thymine dimers in the skin using a specific antibody revealed a significant increase of this type of DNA damage following UVB exposure. After 3 mo of antioxidant administration, significantly less thymine dimers were induced by the UVB challenge, suggesting that antioxidant treatment protected against DNA damage.
J Invest Dermatol 2005 Feb
PMID:Ultraviolet B-induced DNA damage in human epidermis is modified by the antioxidants ascorbic acid and D-alpha-tocopherol. 1567 47

Cutaneous aging is characterized by a decline in cellular energy metabolism, which is mainly caused by detrimental changes in mitochondrial function. The processes involved seem to be predominantly mediated by free radicals known to be generated by exogenous noxes, e.g., solar ultraviolet (UV) radiation. Basically, skin cells try to compensate any loss of mitochondrial energetic capacity by extra-mitochondrial pathways such as glycolysis or the creatine kinase (CK) system. Recent studies reported the presence of cytosolic and mitochondrial isoenzymes of CK, as well as a creatine transporter in human skin. In this study, we analyzed the cutaneous CK system, focusing on those cellular stressors known to play an important role in the process of skin aging. According to our results, a stress-induced decline in mitochondrial energy supply in human epidermal cells correlated with a decrease in mitochondrial CK activity. In addition, we investigated the effects of creatine supplementation on human epidermal cells as a potential mechanism to reinforce the endogenous energy supply in skin. Exogenous creatine was taken up by keratinocytes and increased CK activity, mitochondrial function and protected against free oxygen radical stress. Finally, our new data clearly indicate that human skin cells that are energetically recharged with the naturally occurring energy precursor, creatine, are markedly protected against a variety of cellular stress conditions, like oxidative and UV damage in vitro and in vivo. This may have further implications in modulating processes, which are involved in premature skin aging and skin damage.
J Invest Dermatol 2005 Feb
PMID:The creatine kinase system in human skin: protective effects of creatine against oxidative and UV damage in vitro and in vivo. 1567 66

The Skin Cancer Foundation is the only national and international organization devoted exclusively to malignancies of the skin. It conducts public and medical education programs andprovides support for research and professional training to reduce the incidence, morbidity, and mortality of skin cancers. The following article is reprinted from The Melanoma Letter, Vol. 22, No. 3. Outstanding articles from the Foundation's award-winning publications, The Skin Cancer Foundation Journal, The Melanoma Letter, and Sun & Skin News will regularly appear here in upcoming issues. The Skin Cancer Foundation Journal, published annually, is a major part of the Foundation's professional and public education programs. Directed primarily to dermatologists, it also has an extensive readership among the general public. The Melanoma Letter, a widely respected quarterly newsletter for clinicians and researchers, focuses on the diagnosis, treatment, and prevention of the deadliest form of skin cancer. Sun & Skin News, a quarterly newsletter for the lay public, covers a broad range of topics related to skin health, including prevention and treatment of skin cancers and other sun-induced skin damage, the effectiveness of new sunscreen formulas, sunglasses, and the danger of tanning parlors.
J Drugs Dermatol
PMID:Consideration of statins for chemoprevention of cutaneous melanoma. 1569 98

The p38 mitogen-activated protein kinase (MAPK) signaling pathway is activated by numerous inflammatory mediators and environmental stresses. We assessed the effects of ultraviolet B (UVB) on the p38 MAPK pathway and determined whether cyclooxygenase (COX)-2 expression is downstream of this kinase in the skin of UVB-irradiated SKH-1 mice. SKH-1 mice were irradiated with a single dose of UVB (360 mJ per cm2), and activation of the epidermal p38 MAPK pathway was assessed. UVB-induced phosphorylation of p38 MAPK occurred in a time-dependent manner. Phosphorylation of MAPK-activated protein kinase-2 (MAPKAPK-2) also was detected and correlated with an increase in its kinase activity. Phosphorylation of heat shock protein 27 (HSP27), a substrate for MAPKAPK-2, also was detected post-irradiation. Oral administration of the p38 inhibitor, SB242235, prior to UVB irradiation, blocked activation of the p38 MAPK cascade, and abolished MAPKAPK-2 kinase activity and phosphorylation of HSP27. Moreover, SB242235 inhibited expression of the pro-inflammatory cytokines interleukin (IL)-6 and KC (murine IL-8) and COX-2. Our data demonstrate that UVB irradiation of murine skin activates epidermal p38 MAPK signaling and induces a local pro-inflammatory response. Blockade of the p38 MAPK pathway may offer an effective approach to reducing or preventing skin damage resulting from acute solar radiation.
J Invest Dermatol 2005 Jun
PMID:Role of p38 MAPK in UVB-induced inflammatory responses in the skin of SKH-1 hairless mice. 1595 10

Whereas in Australia the high incidence of UV-induced skin cancer and chronic UV-damage is epidemiologically well proved, comparable figures in Europe and particularly in Germany are missing. Presumably, the prevalence and incidence of actinic keratoses, basal cell carcinoma and squamous cell carcinoma are significantly underestimated. The importance of chronic skin damage is discussed in accordance with new epidemiologic studies recently published in international journals. Since the percentage of older people is increasing in Germany the therapeutic importance of UV-damage and its relevance for preventive medicine will be of increasing importance in the next years.
J Dtsch Dermatol Ges 2005 Sep
PMID:[Epidemiology of chronic UV-damage]. 1611 42

Protection against ultraviolet (UV) irradiation prevents from the development of acute skin damage such as erythema formation and chronic skin changes such as premature skin ageing. Especially those sunscreens with higher sun protection factors do not only protect against solar dermatitis but also inhibit UV-induced immunosuppression by blocking the release of immunosuppressive mediators from UV-exposed epidermis. In particular, the protection against UV-induced immunosuppression by sunscreens is supposed to reduce the development of UV-induced skin cancer. Besides immunosuppression UV-irradiation is also able to induce "UV signature" mutations within UV-exposed DNA. Topical application of DNA repair enzymes induces nucleotide excision repair and corrections of DNA damages. Thereby, the risk to develop UV-induced skin malignancies is markedly reduced. Accordingly, future perspectives in the development of sunscreens include DNA repair enzymes or factors, which can induce the endogenous cellular DNA repair system. Until these developments come to practice reasonable sun protection according to the skin complexion is of primary importance.
J Dtsch Dermatol Ges 2005 Sep
PMID:[Sunprotection: possibilities and limitations]. 1611 44

The effectiveness of a sunscreen product can be reduced by sweating, friction, water immersion, or any other force that has the potential to remove the product from the surface of the skin. Substantivity (resistance to removal by water or sweat) along with durability (resistance to removal by wear) during physical activity are important aspects of sunscreen performance along with the fundamental protection provided against sunburn and ultraviolet-induced skin damage. Standards for measuring substantivity and other performance characteristics are available in regulations or guidelines around the world, but these regulations vary concerning the labeling and communication of product performance to consumers. Sunscreens alone should not be relied on to prevent all of the possible harmful effects of sun exposure. Variation between individuals, the substantivity and durability of products, and exposure conditions all play a role in the performance of sunscreens.
Dermatol Clin 2006 Jan
PMID:Water resistance and extended wear sunscreens. 1631 Nov 69


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