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

Less than 20 of the hundreds of carotenoids found in nature are found in the human body. These carotenoids are present in the body from the foods or dietary supplements that humans consume. The body does not synthesize them. Among the carotenoids present in the body, only lutein and its coexistent isomer, zeaxanthin, are found in that portion of the eye where light is focused by the lens, namely, the macula lutea. Numerous studies have shown that lutein and zeaxanthin may provide significant protection against the potential damage caused by light striking this portion of the retina. In the eye, lutein and zeaxanthin have been shown to filter high-energy wavelengths of visible light and act as antioxidants to protect against the formation of reactive oxygen species and subsequent free radicals. Human studies have demonstrated that lutein and zeaxanthin are present in the skin, and animal studies have provided evidence of significant efficacy against light-induced skin damage, especially the ultraviolet wavelengths. Little was known about the protective effects of these carotenoids in human skin until recently. This article reviews the scientific literature pertaining to the effects that lutein and zeaxanthin exhibit in the human eye and skin.
Clin Dermatol
PMID:Lutein and zeaxanthin in eye and skin health. 1916

About half of people with cancer are treated with radiation therapy; however, normal tissue toxicity still remains a dose-limiting factor for this treatment. The skin response to ionizing radiation may involve multiple inflammatory outbreaks. The endothelium is known to play a critical role in radiation-induced vascular injury. Furthermore, endothelial dysfunction reflects a decreased availability of nitric oxide. Statins have been reported to preserve endothelial function through their antioxidant and anti-inflammatory activities. In this study, wild type and endothelial nitric oxide synthase (eNOS)(-/-) mice were subjected to dorsal skin irradiation and treated with pravastatin for 28 days. We demonstrated that pravastatin has a therapeutic effect on skin lesions and abolishes radiation-induced vascular functional activation by decreasing interactions between leukocytes and endothelium. Pravastatin limits the radiation-induced increase of blood CCL2 and CXCL1 production expression of inflammatory adhesion molecules such as E-selectin and intercellular adhesion molecule-1, and inflammatory cell migration in tissues. Pravastatin limits the in vivo and in vitro radiation-induced downregulation of eNOS. Moreover, pravastatin has no effect in eNOS(-/-) mice, demonstrating that eNOS plays a key role in the beneficial effect of pravastatin in radiation-induced skin lesions. In conclusion, pravastatin may be a good therapeutic approach to prevent or reduce radiation-induced skin damage.
J Invest Dermatol 2009 May
PMID:Pravastatin limits radiation-induced vascular dysfunction in the skin. 1921 44

The secondary skin malignancies arising in seborrheic keratosis (SK) are uncommon, and the causal association between the pre-existing lesion and subsequent malignant transformation remains uncertain. Among these enigmatic conditions, trichilemmal differentiation and/or neoplasms in SK have rarely been reported thus far. Herein, we describe a case of invasive trichilemmal carcinoma arising in a long-standing SK of the abdominal skin, and clinicopathologically review this rare complication with a computerized medical published work search (PubMed) and citations from earlier reports. To our knowledge, only four cases of trichilemmal tumors arising in SK have been observed, and, interestingly, all cases, including ours, were Japanese. Four of five cases (80%) developed the tumors in non-sun-exposed SK, and indeed had no apparent actinic damage in the histology. The pre-existing SK itself is more likely to act as the primary pathogenic event for developing the secondary trichilemmal tumors than a coincidental phenomenon and a consequence of skin damage by cumulative sun exposure.
J Dermatol 2008 Dec
PMID:Trichilemmal carcinoma arising in seborrheic keratosis: a case report and published work review. 1923 59

It is recognized that reactive oxygen species (ROS) are responsible for skin damage due to UVB-radiation (UVB-R). However, the triggering substance(s) for ROS generation after UVB-R is uncertain with respect to the activation of NADPH oxidase (Nox), xanthine oxidase (XOD), and respiratory chain-chain reactions in mitochondria. As a first step in identifying the trigger(s) for UVB-induced ROS generation, we examined the relationship between Ca(2+) levels and ROS generation in HaCaT keratinocytes. UVB-R exposure of HaCaT keratinocytes resulted in an immediate elevation of ROS that recurred 7 hours later. This was accompanied by immediately elevated intracellular Ca(2+) . A Ca(2+) chelating agent, BAPTA, abolished the elevation of ROS after UVB-R completely. In addition, exogenous H(2)O(2) did not increase intracellular Ca(2+) levels. This suggests that intracellular Ca(2+) is the first trigger for UVB-induced ROS generation.Journal of Investigative Dermatology Symposium Proceedings (2009) 14, 50-52; doi:10.1038/jidsymp.2009.12.
J Investig Dermatol Symp Proc 2009 Aug
PMID:Reactive oxygen species in HaCaT keratinocytes after UVB irradiation are triggered by intracellular Ca(2+) levels. 1967 53

The sun emits different types of ultraviolet (UV) light. Our skin is a natural target of UV radiation which is involved in vitamin D3 production in our body. UV radiation at high doses is an environmental carcinogen which can elicit skin damage as well as inducing skin cancer. It can mediate inflammatory and immunological reactions through activation of receptors, DNA/RNA damage and production of reactive oxygen species. It is also involved in the release of pro-inflammatory cytokines, of which TNFalpha has been implicated in tumorigenic activities. In order to mediate its effects, UV radiation is known to activate multiple signalling cascades such as the p38 MAPK, Jun N-terminal kinase, extracellular signal-regulated kinase 1/2 and NFkappaB pathways in skin cells. The role each of these pathways plays in mediating the release of cytokines such as TNFalpha remains to be fully characterized. Once the function of these pathways is known, this information may provide for the formulation of therapy which will prevent the release of immunosuppressive cytokines resulting in a reduction in skin cancer formation.
Arch Dermatol Res 2010 Jan
PMID:The UV response of the skin: a review of the MAPK, NFkappaB and TNFalpha signal transduction pathways. 1975 72

In western societies, casual consumption of alcohol during such outdoor activities as barbecuing and sunbathing is common. The current literature shows that alcohol drinkers have increased episodes of sunburn and a higher prevalence of skin cancer. Moreover, recent evidence suggests that the combination of subcarcinogenic (minimal) ultraviolet (UV) exposure with other behavioural, environmental and xenobiotic factors has resulted in increased incidents of skin-related health problems that also result in skin-cancer formation. We hypothesize that the combination of alcohol consumption with UV radiation can potentiate the skin carcinogenic effects through the intermediate biproducts or metabolites of alcohol, which serve as the photosensitizers, consequently enhancing the cellular damage. We have proposed a mechanism that explains the combined alcohol-UV radiation carcinogenicity and its potential involvement in enhancing skin damage in the multistep skin carcinogenesis process. Previous literature has explored this mutual effect but no studies have definitively ascribed the reasons for increased skin cancer prevalence among alcohol drinkers. Nevertheless, the preceding epidemiological data and clinical studies recognize this matter, making the further testing of this hypothesis necessary.
Clin Exp Dermatol 2010 Jan
PMID:Induction of skin carcinogenicity by alcohol and ultraviolet light. 2050 May 19

Solar radiation is a very important exogenous factor in skin pathogenesis and can lead to the development of a number of skin disorders. UVB irradiation is known to induce oxidative stress, inflammation and especially DNA lesions in exposed cells. It is important, therefore, to identify agents that can offer protection against UVB-caused skin damage. Natural compounds have been studied for their possible ability to control/modulate various lifestyle-related diseases. The application of plant compounds/extracts with screening, antioxidant and anti-inflammatory activities may also successfully protect the skin against UV-caused injury. We assessed the potency of Prunella vulgaris extract (PVE) and its main phenolic acid component, rosmarinic acid (RA), to suppress UVB-induced (295-315 nm) alterations to human keratinocytes HaCaT using a solar simulator. Pre- and post-treatment of HaCaT cells with PVE (5-50 mg/l) and RA (0.18-1.8 mg/l) reduced breakage together with the apoptotic process. PVE and RA also significantly eliminated ROS production and diminished IL-6 release. Taken together, both PVE and RA prevent UVB-caused injury to keratinocytes. However their efficacy needs to be demonstrated in vivo.
Arch Dermatol Res 2010 Apr
PMID:Prunella vulgaris extract and rosmarinic acid prevent UVB-induced DNA damage and oxidative stress in HaCaT keratinocytes. 1986 37

Due to its rapidly proliferating matrix keratinocytes, the hair follicle is highly sensitive to ionizing irradiation (IR)-induced skin damage and thus an instructive and clinically relevant model organ for investigating the effects of IR on rapidly dividing epithelial-mesenchymal interaction systems. Here, we have assessed the impact of IR on organ-cultured human scalp hair follicles. We show that IR significantly inhibits the proliferation and induces apoptosis of hair follicle matrix keratinocytes, disrupts normal hair follicle pigmentation, and upregulates a number of quantitative toxicity and viability markers (oxidative stress indicators, DNA oxidative damage, LDH release). This introduces human hair follicle organ culture as an excellent novel research tool for radiobiology and invites exploitation as a preclinical assay system for testing candidate radioprotectants.
Exp Dermatol 2010 Aug
PMID:A simple assay for the study of human hair follicle damage induced by ionizing irradiation. 1992 37

Incontinence-associated dermatitis (IAD), sometimes referred to as perineal dermatitis, is an inflammation of the skin associated with exposure to urine or stool. Elderly adults, and especially those in long-term care facilities, are at risk for urinary or fecal incontinence and IAD. Traditionally, IAD has received little attention as a distinct disorder, and it is sometimes confused with stage I or II pressure ulcers. However, a modest but growing body of research is beginning to provide insights into the epidemiology, etiology, and pathophysiology of IAD. In addition, recent changes in reimbursement policies from the US Center for Medicare and Medicaid Services regarding pressure ulcer prevention has focused attention on the differential diagnosis of IAD versus pressure ulcer, and its influence on pressure ulcer risk. Color, location, depth, and the presence or absence of necrotic tissue are visual indicators used to differentiate IAD from pressure-related skin damage. Prevention is based on avoiding or minimizing exposure to stool or urine combined with a structured skin-care program based on principles of gentle cleansing, moisturization, preferably with an emollient, and application of a skin protectant. Treatment of IAD focuses on three main goals: (i) removal of irritants from the affected skin; (ii) eradication of cutaneous infections such as candidiasis; and (iii) containment or diversion of incontinent urine or stool.
Am J Clin Dermatol 2010
PMID:Optimal management of incontinence-associated dermatitis in the elderly. 2013 23

Botanical extracts and single compounds are increasingly used in cosmetics but also in over-the-counter drugs and food supplements. The focus of the present review is on controlled clinical trials with botanicals in the treatment of acne, inflammatory skin diseases, skin infections, UV-induced skin damage, skin cancer, alopecia, vitiligo, and wounds. Studies with botanical cosmetics and drugs are discussed, as well as studies with botanical food supplements. Experimental research on botanicals was considered to a limited extent when it seemed promising for clinical use in the near future. In acne therapy, Mahonia, tea tree oil, and Saccharomyces may have the potential to become standard treatments. Mahonia, Hypericum, Glycyrrhiza and some traditional Chinese medicines appear promising for atopic dermatitis. Some plant-derived substances like dithranol and methoxsalen (8-methoxypsoralen) [in combination with UVA] are already accepted as standard treatments in psoriasis; Mahonia and Capsicum (capsaicin) are the next candidates suggested by present evidence. Oral administration and topical application of antioxidant plant extracts (green and black tea, carotenoids, coffee, and many flavonoids from fruits and vegetables) can protect skin from UV-induced erythema, early aging, and irradiation-induced cancer. Hair loss and vitiligo are also traditional fields of application for botanicals. According to the number and quality of clinical trials with botanicals, the best evidence exists for the treatment of inflammatory skin diseases, i.e. atopic dermatitis and psoriasis. However, many more controlled clinical studies are needed to determine the efficacy and risks of plant-derived products in dermatology. Safety aspects, especially related to sensitization and photodermatitis, have to be taken into account. Therefore, clinicians should not only be informed of the beneficial effects but also the specific adverse effects of botanicals used for dermatologic disorders and cosmetic purposes.
Am J Clin Dermatol 2010
PMID:Botanicals in dermatology: an evidence-based review. 2050 19


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