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Results for “Sunburn”

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At least 19 recordsLinked to original sources

PubMed1979

Decreased DNA repair activity in sunburn cells. A possible pathogenetic factor of the epidermal sunburn reaction.

The pathogenesis of the formation of sunburn cells is unknown. Based on autoradiographic methods the unscheduled DNA repair synthesis of UV-induced thymin dimers was investigated in vivo in sunburn cells and in irradiated but histologically normal stratum spinosum cells. The results show a significant lower number of sparsly labeled cells in the sunburn cell-population (13.2 +/- 2.5; mean) when compared to the population of normal stratum spinosum cells (57.8 +/- 7.5; mean). These data indicate that the population of those epidermal cells, which become manifest as sunburn cells 24 h after UV exposure exhibit a reduced DNA repair of UV induced thymine dimers immediately after UV irradiation. Nuclear factors thus seem to play at least some role in the origin of sunburn cells.

DNA Repair↗

PubMed1992

Melanoma prevention: behavioral and nonbehavioral factors in sunburn among an Australian urban population.

BACKGROUND: To determine the independent contribution of behavioral factors to the occurrence of sunburn, sun protection behavior was assessed over 13 successive summer weekends in a total of 1,655 adults in Melbourne, Australia. METHODS: Telephone survey respondents provided detailed accounts of activities engaged in, time spent outside, and hat, clothing, and sunscreen coverage in the 4 hr around the solar midday on both weekend days, as well as skin type, sociodemographic descriptors, and degree of sunburn experienced. Independent measures of atmospheric temperature and ambient ultraviolet radiation (UVR) were added to individual records. RESULTS: The (mostly recreational) weekend sunburn in this urban sample was strongly associated with UVR, as expected. Temperature at 3 PM, sensitive skin type, youthfulness, and being male were also independently associated with sunburn. After all other predictors were controlled for, the body exposure index (which took into account time outside and hat, clothing, and sunscreen coverage) made a strong independent contribution to the explanation of sunburn (P < 0.001). CONCLUSION: It was concluded that behavior change strategies to prevent malignant melanoma of the skin are warranted.

Adolescent↗

PubMed1990

Malignant melanoma in England: risks associated with naevi, freckles, social class, hair colour, and sunburn.

In a case-control study in the Midlands of England, 195 subjects with superficial spreading or nodular melanoma were compared to age- and sex-matched controls chosen from all inpatients or outpatients in hospitals serving the defined source population. Significant increases in melanoma risk, after adjustment for other factors, were seen in association with total naevi on the arms (odds ratio (OR), for 15+ naevi compared to none = 3.8), intense freckling as an adult (OR = 6.2), and as a child (OR = 6.0), and higher social class (OR = 2.4). Positive single factor associations were also seen with light or red hair colour, tendency to sunburn easily, and a history of sunburn at ages 8-12, although these were not significant when adjusted for the other factors. No significant effect was seen with naevi greater than 6 mm, or with raised naevi, when adjusted for total number of naevi. Total arm naevi and density of freckling had independent effects, consistent with a multiplicative effect, the OR in those with 10+ naevi and heavy freckling being 20.8. The risk associated with red hair was independent of naevi, but associated with freckling. The strongest association with sunburn history was seen with a history of sunburn in childhood, with sunburn at later times, having smaller effects, or none. These results shows that freckling and social class as well as naevi are strong and independent risk indicators for melanoma. These associations were generally consistent by type of melanoma, sex, age, and extent of regular exposure of the body site affected, although the social class gradient was observed neither for nodular melanoma nor for melanomas occurring on the most exposed body sites.

Adult↗

PubMed1988

Effect of hypoxia on sunburn cell formation and inflammation induced by ultraviolet radiation.

Oxygen intermediates are responsible for a number of ultraviolet (UV) radiation effects. To test the hypothesis that UV-induced formation of sunburn cells and skin edema (ear swelling) result from oxidative damage, we examined the effect of hypoxia tissue responses to UV in the mouse ear. Hypoxia resulting from vascular occlusion by ear clamping, either before or after UVB exposure, decreased formation of sunburn cells. Ear clamping alone caused significant ear swelling, which was enhanced when combined with UVB exposure. Using topical 8-methoxypsoralen + UVA (PUVA), increased sunburn cells were observed when ears were clamped for 10 min prior to UVA exposure, but not following exposure. Ear swelling caused by PUVA was also enhanced when ears were clamped during exposure. These results suggest that induction of sunburn cells by UVB is dependent on oxygen, and that UVB and PUVA induce sunburn cell formation by distinct mechanisms.

Animals↗

PubMed1992

Topical tocopherol acetate reduces post-UVB, sunburn-associated erythema, edema, and skin sensitivity in hairless mice.

Exposure of the skin of the back of skh-1 hairless mice to UVB (310 nm peak) irradiation at doses of 0.115-0.23 J/cm2 results after 24-48 h in an erythema which can be quantified using an erythema meter, providing a useful model of sunburn. Application of pure d-alpha-tocopherol acetate, a thick oil, to the skin immediately following the exposure to UVB significantly reduces the increase in erythema index, by 40-55%. At the lower dose (0.115 J/cm2), skin thickness (associated with edematous swelling of the sunburned skin) was measured by a novel non-invasive technique not previously reported for this purpose--magnetic resonance imaging (MRI). In two experiments the UVB-induced increase in skin thickness was significantly reduced at 24 hr by 29 and 54%, and at 48 hr by 26 and 61%. After 8 days the untreated irradiated mouse skin still showed a significant increase in thickness (24%) compared to the untreated unirradiated control, while the treated irradiated control was not significantly thicker than the unexposed control. Skin sensitivity was tested using a modification of the technique of esthesiometry, by observing rapid avoidance responses of the mouse to a pressure of 0.96 g/cm2 exerted by applying to the skin the tip of a nylon esthesiometer fiber extended to 60 mm in length. The untreated irradiated mice were more sensitive (p less than 0.07, Wilcoxon test) than the treated irradiated mice, and also significantly different from the untreated unirradiated control mice (p less than 0.04, Wilcoxon test), but the treated irradiated mice were not significantly differently sensitive when compared to the unirradiated controls (p less than 0.32). Taken together these data indicate that the erythema, edema, and skin sensitivity commonly associated with UVB-induced sunburn are significantly reduced by topical application of tocopherol acetate even after the exposure has occurred. This observation suggests that treatment of sunburn may be possible even after the irradiation has stopped, by a derivative of d-alpha-tocopherol which is stable to autooxidation.

Animals↗

PubMed1992

Cutaneous melanoma and sunburns in childhood in a southern European population.

A population-based case-control study of 260 patients (74 males and 186 females, mean age = 56) with cutaneous malignant melanoma and 416 controls (211 males and 205 females, mean age = 55) was conducted in Turin, north-west Italy, to examine the relation between timing of sunburns and sun exposure and melanoma risk within a southern European population, which is still relatively little investigated. Particularly elevated risk was associated with history of sunburns in childhood [odds ratio 5.9; 95% confidence interval (CI) 3.6-9.5], and such risk elevation persisted after allowance for other major melanoma risk covariates. Conversely, risk increase from history of severe sunburns lifelong was lower (odds ratio = 1.7; 95% CI: 1.1-2.4) and was eliminated by allowance for type of skin reaction to sun exposure and history of sunburns in childhood. A significant increase in the risk of cutaneous malignant melanoma was also associated with number of weeks spent on holiday at the beach not only as an adult, but also as a child.

Adolescent↗

PubMedDate not supplied

[Reactivation of sunburn by methotrexate].

For B-All, we treated a five-year-old boy with a combination chemotherapy course including intermediate-dose methotrexate (MTX) with citrovorum factor rescue (CF) two days after a mild sunburn. The insolation inflammation vanished completely, but was reactivated after three days much more severely than the original sunburn, and healed slowly over three weeks. The reactivation phenomenon has previously been described in man and in the guinea pig. It differs substantially from "radiation recall" caused by other cytostatic drugs, as sunburn is not enhanced by MTX applied simultaneously with insolation and is not reactivated if MTX is given more than a week later. Previously irradiated skin regions are spared from the reactivation. Although the phenomenon is not prevented by CF, it can probably be understood as enhanced MTX toxicity to the hyperproliferating basal cell layer of skin after insolation damage. MTX should therefore not be applied for one week after sunburn.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1979

The influence of longwave ultraviolet radiation on sunburn cell production by UVB.

The potentiation of sunburn by longwave ultraviolet radiation (photoaugmentation) has been examined with regard to the influence of these waves on sunburn cell production in human skin. It was found that UVA did not enhance sunburn cell production. Photoaugmentation is limited to the erythemal component of the sunburn reaction.

Adolescent↗

PubMed1988

Effects of UVB irradiation on epidermal adenylate cyclase responses in vitro: its relation to sunburn cell formation.

UVB irradiation augmented the beta-adrenergic adenylate cyclase response of pig skin epidermis in vitro. The effect was observed 2-4 h following the irradiation and lasted at least for 48 h. There was no significant difference in cyclic AMP phosphodiesterase activity between control and UVB-irradiated epidermis at lower irradiation dose (150 mJ/cm2), which is the dose of the most marked beta-adrenergic augmentation effect. The augmentation effect was specific to the beta-adrenergic system; adenosine and histamine adenylate cyclase responses were unchanged or decreased depending on the irradiation dose. Histologically, marked sunburn-cell formation was observed following the UVB irradiation. It has been suggested that oxygen intermediates generated by ultraviolet radiation participate in sunburn-cell formation. The addition of superoxide dismutase (SOD) in the incubation medium significantly inhibited sunburn-cell formation. On the other hand, the beta-adrenergic augmentation effect was not affected by the addition of SOD. Other scavengers of oxygen intermediates (catalase, catalase + SOD, xanthine, or mannitol) did not inhibit the UVB-induced beta-adrenergic augmentation effect. Further, superoxide-anion generating systems (hypoxanthine-xanthine oxidase system and acetaldehyde-xanthine oxidase system) revealed no stimulatory effect on the beta-adrenergic response of epidermis. These results indicate that (a) the UVB-induced beta-adrenergic augmentation effect is inherent to skin and does not depend on systemic factors such as inflammatory infiltrates following UVB irradiation; (b) in contrast to sunburn-cell formation, induction of the beta-adrenergic adenylate cyclase response is not directly associated with oxygen intermediates generated by UVB irradiation.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1992

Human thermoregulatory responses during heat exposure after artificially induced sunburn.

Thermoregulatory responses in the heat (ambient temperature 49 degrees C, 20% relative humidity, 1 m/s wind) were investigated in 10 unacclimated men during 50 min of cycle ergometer exercise (approximately 53% of maximal aerobic power) after a 10-min rest before as well as 24 h and 1 wk after twice the minimal erythemal dose of UV-B radiation that covered approximately 85% of the body surface area. In 7 subjects esophageal temperature (Tes) was recorded while in all 10 subjects five-site skin and rectal temperatures, heart rate, and back, left forearm, and shielded (12 cm2 area) right forearm sweating rates (msw) were recorded at 15-s intervals. Venous blood was collected before and after exercise-heat stress. Mean skin temperature, Tes, rectal temperature, heart rate, and total body sweating rate were not significantly (P greater than 0.05) affected by sunburn. Pre- and postexercise values of hematocrit, hemoglobin, plasma protein, plasma volume, and plasma osmolality were also not affected (P greater than 0.05) by sunburn. Analysis of presunburn and post-sunburn data showed that the Tes intercept for sweating (degrees C) was unaffected (P greater than 0.05), but msw/Tes and final msw from the left forearm (msw/Tes 0.24 +/- 0.02 vs. 0.17 +/- 0.01 mg.cm-2.min-1. degrees C-1, P less than 0.05; msw 0.60 +/- 0.05 vs. 0.37 +/- 0.02, mg.cm-2.min-1, P less than 0.05) and back (msw/Tes 0.43 +/- 0.03 vs. 0.36 +/- 0.01 mg.cm-2.min-1. degrees C-1, P = 0.052; msw 1.08 +/- 0.09 vs. 0.74 +/- 0.05 mg.cm-2.min-1, P less than 0.05) were significantly reduced 24 h postsunburn.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1977

New concepts in prevention and treatment of sunburn.

Effective topical sunscreens are available in Australasia, but are some more effective and acceptable than others? For those who demand an early tan and longer protection there still remains some hope that effective topical applications may become available. Acute sunburn must be assessed from a general medical viewpoint. Severe sunburn requires a short "dermatological" course of systemic steroids. Prostaglandins and antiprostaglandins may have a role in the future treatment of sunburn.

4-Aminobenzoic Acid↗

PubMed1987

The sunburn cell.

The sunburn cell, with its pyknotic nucleus and eosinophilic cytoplasm, is characteristic of mammalian epidermis after exposure to UVC and UVB radiation or UVA radiation in the presence of psoralens. The photochemical events that lead to its formation are not known, but there is good evidence that damage to DNA is an important factor. The fate of the sunburn cell, a keratinocyte which shows abnormal and premature keratinization, is not known. Desquamation and/or phagocytosis seem probable. Sunburn cells may be regarded as examples of apoptosis: controlled individual cell death.

Animals↗

PubMed1978

Sunburn protection by longwave ultraviolet radiation-induced pigmentation.

The role of melanin pigment in sunburn protection was investigated. Deep tans were induced over the backs of volunteers with repeated exposure to longwave ultraviolet radiation (UV-A). Melanogenesis was stimulated without an appreciable thickening of the stratum corneum. Two to three times the minimal erythema dose was required to produce redness in UV-A-tanned skin. Transmission studies through isolated corneum sheets revealed that specimens from tanned skin were about twice as efficient in filtering sunburn rays as stratum corneum from untanned skin. Tanning with UV-A does not provide a substantial resistance against sunburn.

Adult↗

PubMed1978

Effect of topical corticosteroids on symptoms of clinical sunburn.

Topical corticosteroids have been advocated in the treatment of sunburn. This therapy was evaluated by means of a random, double-blind study in which subjects who had acquired acute natural sunburn served as their own controls. Subjects applied fluocinolone cream to an acutely exposed area of their body and the inert carrier base to a symmetrical, similarly exposed area twice a day for five days while avoiding further exposure. The subjects recorded by means of a rating scale the progression, at both sites, of redness, pain, blistering, swelling, and peeling. The natural course of mild to moderate sunburn to symptomatic resolution was observed to be about three to five days. There was no significant difference in response between the steroid-treated area and the inert-base-treated area.

Administration, Topical↗

PubMed1976

Effect of topical indomethacin on UVR-induced redness and prostaglandin E levels in sunburned guinea pig skin.

Prostaglandin E (PGE) levels in the skin have been shown to be elevated during the 24 hr. period following exposure of guinea pig skin to ultraviolet radiation from 280-320 nm in the so-called UVB or "sunburn spectrum". The development of increased PGE levels paralleled the development of the delayed phase of erythema. When applied immediately after UVB exposure, one topical application of 2.5% Indomethacin (IM) simultaneously decreased the redness and PGE levels in the skin to near normal within one hr. of treatment. The IM effect persisted for approximately 24 hrs. By 48 hrs. the PGE level in the sunburned skin was near normal whether or not the skin had been treated with IM. The redness which was evident at 48 hrs. did not respond to additional topical IM treatment. This suggests that a substance(s) other than PGE may be involved in this latter portion of UVB-induced erythema. A major role for PGE as an early mediator or potentiator of UVB-induced erythema has been deomonstrated. Any involvement of PGE with UVB-induced cell death or alterations in DNA synthesis seems unlikely.

Administration, Topical↗

PubMed1976

The influence of corticosteroids and topical indomethacin on sunburn erythema.

The extent to which topical and intradermal corticosteroids and topical indomethacin suppress sunburn erythema was investigated in human volunteers. Both agents retarded the onset and decreased the magnitude of delayed erythema. Suppression by corticosteroids was not demonstrable with ultraviolet doses larger than 2 MEDs (minimal erythema dose). Below 2 MEDs, topical betamethasone valerate produced a dose-related suppression of erythema. Indomethacin was more effective and produced a measurable dose-dependent suppression against 3 and 6 MEDs. Despite significant inhibition of erythema, sunburn damage to epidermal cells was not altered by these drugs.

Administration, Topical↗

PubMed1992

Human thermoregulatory responses during cold water immersion after artificially induced sunburn.

Thermoregulatory responses during cold-water immersion (water temperature 22 degrees C) were compared in 10 young men before as well as 24 h and 1 wk after twice the minimal erythemal dose of ultraviolet-B radiation that covered approximately 85% of the body surface area. After 10 min of seated rest in cold water, the mean exercised for 50 min on a cycle ergometer (approximately 51% of maximal aerobic power). Rectal temperature, regional and mean heat flow (hc), mean skin temperature from five sites, and hearrt rate were measured continuously for all volunteers while esophageal temperature was measured for six subjects. Venous blood samples were collected before and after cold water immersion. The mean skin temperature was higher (P less than 0.05) throughout the 60-min cold water exposure both 24 h and 1 wk after sunburn compared with before sunburn. Mean hc was higher (P less than 0.05) after 10 min resting immersion and during the first 10 min of exercise when 24 h postsunburn was compared with presunburn, with the difference attributed primarily to higher hc from the back and chest. While rectal temperature and heart rate did not differ between conditions, esophageal temperature before immersion and throughout the 60 min of cold water immersion was higher (P less than 0.05) when 24 h postsunburn was compared with presunburn. Plasma volume increased (P less than 0.05) after 1 wk postsunburn compared with presunburn, whereas plasma protein concentration was reduced (P less than 0.05). After exercise cortisol was greater (P less than 0.05) 24 h postsunburn compared with either presunburn or 1 wk postsunburn.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Temperature↗

PubMed1992

Infrared radiation suppresses ultraviolet B-induced sunburn-cell formation.

Sunburn cell (SC) formation, a quantifiable measure of epidermal cell injury induced in mouse ear skin by ultraviolet-B (UVB) radiation (290-320 nm), was significantly decreased by pre-exposure to infrared radiation (IR), which elevated the surface temperature of ear lobes to 37-42 degrees C. An autoradiographic study demonstrated that the basal cell labelling indices were significantly reduced in a surface temperature-dependent manner by pre-exposure to IR. Taken together with our previous findings that SC formation depends upon the ratio of cycling to non-cycling cells, the present findings suggest that IR retards the cell cycle and, as a result, decreases SC formation. SC counts were not altered by post-UVB exposure to IR. The effect of IR or the IR-induced increase in surface temperature should be considered when studying cutaneous damage by UVB and sunlight.

Animals↗