Dataset Information

Ultraviolet Radiation-Induced Cytogenetic Damage in White, Hispanic and Black Skin Melanocytes: A Risk for Cutaneous Melanoma.

ABSTRACT: Cutaneous Melanoma (CM) is a leading cause of cancer deaths, with reports indicating a rising trend in the incidence rate of melanoma among Hispanics in certain U.S. states. The level of melanin pigmentation in the skin is suggested to render photoprotection from the DNA-damaging effects of Ultraviolet Radiation (UVR). UVR-induced DNA damage leads to cytogenetic defects visualized as the formation of micronuclei, multinuclei and polymorphic nuclei in cells, and a hallmark of cancer risk. The causative relationship between Sun exposure and CM is controversial, especially in Hispanics and needs further evaluation. This study was initiated with melanocytes from White, Hispanic and Black neonatal foreskins which were exposed to UVR to assess their susceptibility to UVR-induced modulation of cellular growth, cytogenetic damage, intracellular and released melanin. Our results show that White and Hispanic skin melanocytes with similar levels of constitutive melanin are susceptible to UVR-induced cytogenetic damage, whereas Black skin melanocytes are not. Our data suggest that the risk of developing UVR-induced CM in a skin type is correlated with the level of cutaneous pigmentation and its ethnic background. This study provides a benchmark for further investigation on the damaging effects of UVR as risk for CM in Hispanics.

SUBMITTER: Dasgupta A

PROVIDER: S-EPMC4586785 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature

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Ultraviolet Radiation-Induced Cytogenetic Damage in White, Hispanic and Black Skin Melanocytes: A Risk for Cutaneous Melanoma.

Dasgupta Amrita A Katdare Meena M

Cancers 20150814 3

Cutaneous Melanoma (CM) is a leading cause of cancer deaths, with reports indicating a rising trend in the incidence rate of melanoma among Hispanics in certain U.S. states. The level of melanin pigmentation in the skin is suggested to render photoprotection from the DNA-damaging effects of Ultraviolet Radiation (UVR). UVR-induced DNA damage leads to cytogenetic defects visualized as the formation of micronuclei, multinuclei and polymorphic nuclei in cells, and a hallmark of cancer risk. The cau ...[more]

PMID: 26287245

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Project description:New findingsWhat is the central question of this study? Does cutaneous sensory nerve-mediated vasodilatation differ between non-Hispanic Black and White young adults? What is the main finding and its importance? The magnitude of cutaneous reactive hyperaemia is lower in non-Hispanic Black relative to non-Hispanic White young adults, but the overall sensory nerve contribution is the same, suggesting that sensory nerve function is similar in both non-Hispanic Black and White young adults.AbstractThe aim of this study was to assess cutaneous sensory nerve function, independent of nitric oxide, in non-Hispanic Black and White young adults. We tested the hypothesis that cutaneous reactive hyperaemia and sensory nerve-mediated vasodilatation would be lower in non-Hispanic Black young adults relative to non-Hispanic White young adults. Twenty-four participants who self-identified as non-Hispanic Black (n = 12) or non-Hispanic White (n = 12) were recruited. All participants underwent three bouts of reactive hyperaemia. An index of skin blood flow was measured continuously using laser-Doppler flowmetry at a control site and at a site treated with topical 4% lignocaine to inhibit sensory nerve function. Peak reactive hyperaemia was lower in non-Hispanic Black relative to non-Hispanic White participants (P < 0.001). Total reactive hyperaemia was lower in non-Hispanic Black [mean (SD); control, 4085 (955)%CVCmax s; lignocaine, 2127 (639) percent maximal cutaneous vascular conductance * seconds, %CVCmax s] relative to non-Hispanic White [control: 6820 (1179)%CVCmax s; lignocaine, 3573 (712)%CVCmax s] participants (P < 0.001 for both sites). There was no difference between groups for the calculated contribution of sensory nerves to either the peak [non-Hispanic Black, 25 (14)%; non-Hispanic White, 19 (13)%] or total reactive hyperaemic response [non-Hispanic Black, 48 (10)%; non-Hispanic White, 47 (10)%]. These data suggest that cutaneous reactive hyperaemia is lower in non-Hispanic Black young adults, but the sensory nerve contribution is similar in non-Hispanic Black and White young adults.

Project description:People with pale skin, red hair, freckles and an inability to tan--the 'red hair/fair skin' phenotype--are at highest risk of developing melanoma, compared to all other pigmentation types. Genetically, this phenotype is frequently the product of inactivating polymorphisms in the melanocortin 1 receptor (MC1R) gene. MC1R encodes a cyclic AMP-stimulating G-protein-coupled receptor that controls pigment production. Minimal receptor activity, as in red hair/fair skin polymorphisms, produces the red/yellow pheomelanin pigment, whereas increasing MC1R activity stimulates the production of black/brown eumelanin. Pheomelanin has weak shielding capacity against ultraviolet radiation relative to eumelanin, and has been shown to amplify ultraviolet-A-induced reactive oxygen species. Several observations, however, complicate the assumption that melanoma risk is completely ultraviolet-radiation-dependent. For example, unlike non-melanoma skin cancers, melanoma is not restricted to sun-exposed skin and ultraviolet radiation signature mutations are infrequently oncogenic drivers. Although linkage of melanoma risk to ultraviolet radiation exposure is beyond doubt, ultraviolet-radiation-independent events are likely to have a significant role. Here we introduce a conditional, melanocyte-targeted allele of the most common melanoma oncoprotein, BRAF(V600E), into mice carrying an inactivating mutation in the Mc1r gene (these mice have a phenotype analogous to red hair/fair skin humans). We observed a high incidence of invasive melanomas without providing additional gene aberrations or ultraviolet radiation exposure. To investigate the mechanism of ultraviolet-radiation-independent carcinogenesis, we introduced an albino allele, which ablates all pigment production on the Mc1r(e/e) background. Selective absence of pheomelanin synthesis was protective against melanoma development. In addition, normal Mc1r(e/e) mouse skin was found to have significantly greater oxidative DNA and lipid damage than albino-Mc1r(e/e) mouse skin. These data suggest that the pheomelanin pigment pathway produces ultraviolet-radiation-independent carcinogenic contributions to melanomagenesis by a mechanism of oxidative damage. Although protection from ultraviolet radiation remains important, additional strategies may be required for optimal melanoma prevention.

Project description:ObjectiveResearch suggests a difference in sweet taste perception between non-Hispanic black (NHB) and non-Hispanic white (NHW) adults; however, limited research has examined sweet taste perception in relation to the dietary intake of sweet products. The aim of this study was to examine sweet taste perception and the consumption of sweet foods, beverages, and sugar in NHB and NHW adults, and to evaluate whether sweet taste perception is associated with dietary intake.MethodsThis cross-sectional study examined the association between race, sweet taste perception and sweet food, beverages, and sugar consumption in healthy, NHB and NHW adults. Seven day food records were analyzed in Nutrition Data System for Research software. Intensity of sweet taste perception was tested and the general labeled magnitude scale method was used to facilitate group comparisons. Independent t tests, Mann-Whitney tests, and Pearson correlations were used to assess associations.ResultsParticipants were NHB (n = 98) and NHW (n = 90) adults, 41 ± 1 y of age (mean ± SEM) with energy intake of 2271 ± 53 kcal. Body mass index was higher in NHBs than in NHWs (36 ± 1 versus 32 ± 1 kg/m2, P = 0.048), but no differences were observed in age, energy consumption, or total sugar intake. Sweet taste perception rating (median [interquartile range] NHB: 73.5 [63.9-83], NHW: 52.1 [46.4-57.7]; P = 0.001) and added sugar intake (NHB: 39.4 g/1000 kcal [36.3-42.4], NHW: 30 g/1000 kcal [26.7-33.4]; P < 0.001) were greater in NHB. Perceived sweet taste intensity was positively associated with consumption of servings of sweet products among NHBs (R2 = 0.057, P = 0.018) but not NHWs (R2 = -0.012, P = 0.314).ConclusionsNHBs have a higher intensity of sweet taste perception than NHWs. The positive association of sweet taste perception and sweet product consumption in NHBs suggests that a higher intensity of sweet taste perception may be associated with an increased proportion of energy consumption from added sugars.

Dataset Information

Ultraviolet Radiation-Induced Cytogenetic Damage in White, Hispanic and Black Skin Melanocytes: A Risk for Cutaneous Melanoma.

Publications

Ultraviolet Radiation-Induced Cytogenetic Damage in White, Hispanic and Black Skin Melanocytes: A Risk for Cutaneous Melanoma.

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