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

Oxygen-centred free radicals play an important role in the pathogenesis of acute and chronic UV-induced skin damage as well as in skin aging. In this double-blind randomized study the efficacy of topically applied melatonin (N-acetyl-5-methoxytryptamine), a potent free radical scavenger, in the suppression of UV-induced erythema was assessed. A group of 20 healthy volunteers were irradiated with 0.099 J/cm2 UVB on four 5-cm2 areas on the lower back and topically treated with various concentrations of melatonin (0.05, 0.1, 0.5%) in a nanocolloid gel as carrier or with carrier alone. The UV-induced erythema was examined 8 and 24 h after irradiation by visual scoring and chromametry. A distinct dose response relationship was observed between the topical dose of melatonin and the degree of UV-induced erythema. Significant differences (P < 0.05) were found in redness (chromameter a-value and visual scoring) 8 h after irradiation between the areas treated with melatonin at 0.5% and those treated with melatonin at 0.05% or with the carrier. These results might open a new approach in the prevention and control of free radical-influenced skin diseases.
Arch Dermatol Res 1996 Aug
PMID:Suppression of UV-induced erythema by topical treatment with melatonin (N-acetyl-5-methoxytryptamine). A dose response study. 887 46

Glutathione S-transferases (GSTs) play a primary role in cellular defense against electrophilic chemical species and radical oxygen species. Because free radical attack is one mechanism of UV irradiation-caused skin damage, we investigated whether genetic variation at the GST loci GST T1 and GST M1 influences individual UVB sensitivity. In a double-blind clinical trial, 50 healthy volunteers were evaluated for minimal erythema dose of UVB irradiation, MED (J/cm2), skin types were assigned, and internal standard-controlled polymerase chain reaction (PCR) was used to identify their GST T1 and GST M1 genotypes. The five homozygous carriers of the GST T1 deletion (GST T1*0/0) presented with the most intensive inflammatory reactions after irradiation; they were significantly overrepresented among the highly UVB-sensitive subgroups (p = 0.006). Lack of GST M1 (GST M1*0/0, n = 27) tended to be more frequent only in UVB-sensitive subjects, and the proportion of the active GST M1 allelic variants *A and *B was similar in all UVB sensitivity subgroups. Three subjects with deficiencies in GST T1 and GST M1 had the most intense inflammatory responses. No effect of gender or genetic variations at the MC1R gene locus was established. Thus, heritable GST T1 deficiency may be a genetic determinant of individual skin sensitivity toward UV irradiation.
J Invest Dermatol 1997 Feb
PMID:Deficiency of glutathione S-transferases T1 and M1 as heritable factors of increased cutaneous UV sensitivity. 900 40

Irradiation with ultraviolet (UV) B light results in the formation of apoptotic keratinocytes called sunburn cells (SC). Although generation of SC appears to be one of the most characteristic features of UV-induced skin damage and has been a well-known phenomenon for a long time, the mechanisms involved are not quite clear. Recently, it was demonstrated that tumor necrosis factor alpha (TNF alpha) appears to be involved in the formation of SC since neutralization of TNF alpha both in vitro and in vivo reduced UVB-induced apoptosis of keratinocytes. Pentoxifylline is a methylxanthine derivative suppressing the release of TNF alpha. Therefore, we studied whether PTX is able to prevent the formation of SC. Addition of PTX to UVB-exposed HaCaT cells reduced DNA-fragmentation as examined by nick translation evaluated by flowcytometry. To prove whether PTX also reduces UVB-induced apoptosis in vivo, BALB/c mice were exposed to UVB on their abdomens, skin biopsies performed 24 h later and SC counted. A single dose of 2000 J/m2 caused a significant induction of SC which were remarkably reduced when PTX was injected intraperitoneally 3 h before and 12 h after UVB exposure. In summary, the data demonstrate that PTX can reduce the formation of SC both in vitro and in vivo and thus further support that TNF alpha is involved in UVB-induced apoptosis of keratinocytes.
Exp Dermatol 1997 Feb
PMID:Pentoxifylline reduces the formation of sunburn cells. 906

Congenital erythropoietic porphyria is a rare autosomal-recessive disorder of the porphyrin metabolism caused by the homozygous defect of uroporphyrinogen III cosynthase. High amounts of uroporphyrin I accumulate in all cells and tissues, reflected by an increased erythrocyte porphyrin concentration and excretion of high porphyrin amounts in urine and feces. Dermal deposits of uroporphyrin frequently induce a dramatic phototoxic oxygen-dependent skin damage with extensive ulcerations and mutilations. Splenomegaly and hemolytic anemia are typical internal symptoms. Skeletal changes such as osteolysis and calcifications are frequent. To date 130 cases of congenital erythropoietic porphyria have been published and are summarized here. Splenectomy, erythrocyte transfusions, and bone marrow transplantation have shown some beneficial effect. The best therapy is the avoidance of sunlight. In the two patients with congenital erythropoietic porphyria described here, oral administration of the oxygen quenchers ascorbic acid and alpha-tocopherol resulted in an improvement in the reduced hemoglobin and erythrocyte concentrations.
J Am Acad Dermatol 1997 Apr
PMID:Congenital erythropoietic porphyria. 909 47

Previously we showed a protective role of endogenous glutathione (GSH) in ultraviolet B (UVB) injury. Moderate UVB exposure to hairless mice receiving oral treatment with buthionine sulfoximine (BSO), an inhibitor of GSH synthesis, resulted in a greater number of SBCs in the epidermis. The evidence led to the hypothesis that increasing the level of endogenous GSH in the skin may reduce the skin damage caused by a high dose of UVB irradiation. Since systemic administration of a reduced form of GSH (reduced GSH) is understood to have poor permeability into the cells, in the current study we investigated transportability of esterified GSH and photoprotective effect of reduced GSH and the esterified derivative against UVB injury in vivo. Oral administration of esterified GSH revealed increased cutaneous GSH level more effectively than did reduced GSH. The number of sunburn cells (SBC) formed was significantly depressed in the skin exposed to UVB in mice treated with esterified GSH as compared with non-GSH- or reduced GSH-treated mice. The suppressive effect of esterified GSH was prominent in BSO-treated animals.
J Invest Dermatol 1997 May
PMID:Photoprotective effect of esterified glutathione against ultraviolet B-induced sunburn cell formation in the hairless mice. 912 23

Actinic prurigo is an inflammatory disease of the skin that appears to be mediated by an abnormal immune response. Cell adhesion molecules play a key role in the induction of the immune response as well as in the pathogenesis of inflammation. We investigated the expression of cell adhesion and activation molecules, as well as the density of Langerhans cells in skin from patients with actinic prurigo. Skin biopsies from ultraviolet light-induced lesions, and non-irradiated areas from 10 actinic prurigo patients were studied; in addition, several spontaneous skin lesions were studied. Skin biopsies from normal individuals were used as controls. The expression of ICAM-1, ICAM-3, LFA-3, CD2, LFA-1, VLA-4, CD1a, VCAM-1, CD69, and activated b1 integrins were assessed by immunostaining. An increased expression of LFA-1, LFA-2, ICAM-3, VLA-4, and activated b1 integrins was observed in the cell infiltrate of actinic prurigo lesions and an up-regulated expression of ICAM-1 was detected in keratinocytes from these specimens. Interestingly, the number of Langerhans cells (CD1a + ) in actinic prurigo skin was not significantly affected by ultraviolet irradiation, a phenomenon that was not observed in normal controls. The increased expression of adhesion molecules in the cell infiltrate of actinic prurigo, indicates that these cells are activated and suggests that they are involved in the skin damage seen in these patients. The resistance of Langerhans cells from patients with actinic prurigo to ultraviolet light may have an important role in the pathogenesis of this condition. The involvement of keratinocytes in the pathogenesis of actinic prurigo is suggested by the expression of ICAM-1 on these cells.
Eur J Dermatol
PMID:An immunohistochemical study of UV-induced skin lesions in actinic prurigo. Resistance of langerhans cells to UV light. 964 10

The efficacy of a topical agent in barrier recovery was evaluated after acetone-induced acute water loss barrier disruption in vivo in humans. The upper back of several volunteers was rubbed with acetone-soaked cotton balls until elevated rates of transepidermal water loss (TEWL) occurred (> 20 g/m2h, or greater). The topical agent was then applied to the acetone-treated skin sites once daily for 5 days. Resolution evaluation used TEWL measurements and the data were expressed as the percentage recovery in water barrier function. In comparison with placebo control the topical agent significantly enhanced barrier recovery, especially within the first 72 h (P < 0.05). This model offers a simple method of examining chemicals accelerating (or inhibiting) repair of this form of acute skin damage in man.
Clin Exp Dermatol 1998 Jan
PMID:Human barrier recovery after acute acetone perturbation: an irritant dermatitis model. 966 1

Infant skin differs from adult skin in several ways. These important differences place infants at increased risk for fluid electrolyte imbalance, thermal instability, skin damage, percutaneous infection, and percutaneous toxicity from topically applied agents. This article includes a review of skin development, as well as the details of current skin care practices in the neonatal nursery. A better understanding of the principles of infant skin care and a more uniform approach to skin care in the neonatal nursery can minimize risks and costs to this special population of patients.
Dermatol Clin 1998 Jul
PMID:Neonatal skin and skin care. 970 3

This study was performed as part of PROMETES (Swiss Prospective Metal Worker Eczema Study) to examine the role of atopy as a possible risk factor for the development of hand eczema in trainee metal workers. In a cohort of 201 young men without any skin problems at the start of their apprenticeship, 9.5% developed signs of dermatitis on their hands within a period of 6 months. The 2. 5-year incidence was 23%. We did not find a significantly increased risk for hand eczema in those participants with an atopic skin diathesis according to the atopy score of Diepgen et al. (Dermatosen 1991; 39: 79-83) Analysis of individual atopic signs and symptoms showed reported metal reactivity to have a significant influence on the onset of early skin damage within 6 months, whereas a history of flexural eczema appeared to be significantly related to the overall incidence over 2.5 years.
Br J Dermatol 1999 May
PMID:Role of the atopy score and of single atopic features as risk factors for the development of hand eczema in trainee metal workers. 1035 34

Exposing human skin to ultraviolet radiation causes DNA damage, sunburn, immune alterations, and eventually, skin cancer. We wished to determine whether liposomes containing a DNA repair enzyme could prevent any of the acute effects of irradiation when applied after ultraviolet exposure. Fifteen human patients with a prior history of skin cancer were exposed to two minimal erythema doses of ultraviolet radiation on their buttock skin. Liposomes containing T4 endonuclease V or heat-inactivated enzyme were applied immediately and at 2, 4, and 5 h after ultraviolet irradiation. Transmission electron microscopy after anti-T4 endonuclease V-staining and immunogold labeling on biopsies taken at 6 h after ultraviolet exposure revealed that the enzyme was present within cells in the skin. Immunohistochemical DNA damage studies suggested a trend toward improved DNA repair at the active T4 endonuclease V liposome-treated test sites. Although the active T4 endonuclease V liposomes did not significantly affect the ultraviolet-induced erythema response and microscopic sunburn cell formation, they nearly completely prevented ultraviolet-induced upregulation of interleukin-10 and tumor necrosis factor-alpha RNA message and of interleukin-10 protein. These studies demonstrate that liposomes can be used for topical intracellular delivery of small proteins to human skin and suggest that liposomes containing DNA repair enzymes may provide a new avenue for photoprotection against some forms of ultraviolet-induced skin damage.
J Invest Dermatol 2000 Jan
PMID:Topical treatment with liposomes containing T4 endonuclease V protects human skin in vivo from ultraviolet-induced upregulation of interleukin-10 and tumor necrosis factor-alpha. 1062 Jan 31


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