Changes in skin and hair pigmentation in successful skin grafts in mice.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Carotenoid pigments were extracted chemically from both epidermis and dermis obtained from non-carotenemic individuals at autopsy. Absorption maxima characteristic of beta-carotene were found in the extracts of specimens of epidermis following cantharidin application in volunteers made carotenemic by the ingestion of beta-carotene (180 mg/day for 10 weeks). These maxima were absent in the extracts of epidermis obtained from the volunteers before beta-carotene ingestion.
This study investigates whether supplementation with topical RRR-alpha-tocopherol (Eol), topical RRR-alpha-tocopheryl succinate, and oral RRR-alpha-tocopheryl acetate can reduce the incidence of acute and chronic damage to the skin (i.e., sunburn and pigmentation and skin cancer, respectively) induced by ultraviolet (UV) irradiation to mice. Groups of twenty Skh:2 female hairless pigmented mice were treated with 1) lotion vehicle, 2) 5% Eol lotion, 3) 5% topical RRR-alpha-tocopheryl succinate lotion, or 4) lotion vehicle and oral RRR-alpha-tocopheryl acetate. Within each group, 15 mice were exposed to 0.24 J/cm2 of UV-B radiation three times per week. The animals' weights and food intakes were monitored, and the vitamin E concentrations of skin, liver, and adipose tissue were measured to determine whether the topical Eol resulted in significant tissue levels. Skin pigmentation was scored, and the total number of clinically detectable skin tumors per animal was counted weekly. Results showed that the skin concentrations of Eol, as well as levels in the adipose tissue, were increased after topical application. Mice treated with each form of vitamin E showed no signs of toxicity and had significantly less acute and chronic skin damage induced by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer.
Detection of autofluorescence at the skin surface is highly influenced by melanin and hemoglobin. Epidermal absorption and scattering may also be an influencing factor and is represented in this article as a quantitative parameter, epidermal thickness. To examine this parameter we measured the 370 nm fluorescence in vivo after excitation with 330 nm and the 455 nm fluorescence after excitation with 330 and 370 nm. Measurements were performed on sun-exposed skin at the dorsal aspect of the forearm and shoulder and on nonexposed buttock skin. Skin pigmentation and redness of the same body sites were measured by reflectance spectroscopy. The thickness of the stratum corneum and the cellular part of epidermis was quantified by light microscopy of skin biopsies. Multiple regression analysis was used to find correlations between autofluorescence and the potential influencing factors. We found a highly significant correlation of skin autofluorescence with pigmentation and redness for both emission wavelengths (Em). A small but significant correlation to epidermal thickness was found only for excitation wavelength (Ex) 370 nm and Em455 nm if body site was included in the analysis. No correlation between Ex330:Em370 and Ex330:Em455 and thickness of epidermis was found. For practical use, correction of skin autofluorescence for pigmentation is essential, correction for redness is of less importance and correction for epidermal thickness is unnecessary.
This study was conducted to determine whether oral and/or topical selenium (Se) supplementation can reduce the incidence of acute and/or chronic damage to the skin (i.e., sunburn and pigmentation and/or skin cancer, respectively) induced by ultraviolet (UV) irradiation in mice. Groups of 38 BALB:c female mice or 16 Skh:2 hairless pigmented mice were treated with 1) lotion vehicle, 2) 0.02% L-selenomethionine (SeMet) lotion, or 3) vehicle and 1.5 ppm SeMet in the drinking water. Within each group, 30 BALB:c mice or 12 Skh:2 mice were given UV irradiation (Westinghouse FS 40 bulbs) three times per week in doses of 0.575 and 0.24 J/cm2, respectively. The animals' weights and food intakes and the Se concentrations of skin and liver were measured. Skin biopsies were taken from the backs and abdomens of all animals to evaluate the relative amounts of Se and the damage by UV irradiation. Skin pigmentation was scored, and the total number of clinically detectable skin tumors per animal was counted weekly. Results showed that the skin Se concentrations in areas of application of the lotion containing SeMet were greater than those of animals given comparable oral doses, while the Se concentrations of untreated skin and liver were similar to those of animals receiving oral Se. Mice treated with Se showed no signs of toxicity and had significantly less skin damage by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer.
The skin pigmentation of chronic venous insufficiency is associated both with increased melanin production and also with deposition of haemosiderin. Following treatment by compression sclerotherapy this pigmentation usually decreases. Seven patients with varicose pigmentation were assessed prior to treatment by colour photographs and skin biopsies. About one year after sclerotherapy further photographs and biopsies were taken. Six of the patients showed a definite decrease of pigmentation on the photographs. In all seven the amount of melanin had decreased. The results for haemosiderin were less uniform and showed a variable rise or fall. It therefore seems likely that the discoloured legs of chronic venous insufficiency result from stimulation of melanocytes perhaps similar to a sunburn response or to the mechanism in haemosiderosis. In the same way this may be reversible when the stimulus of venous hypertension or ultraviolet radiation is removed. The haemosiderin discolouration may also result from extravasation of red cells through capillaries if blood leaks out of the tissues during injections without adequate pressure bandaging.
Pigment spread is the natural or experimentally procured (through grafting) progressive encroachment of pigmentation from black or red skin areas into juxtaposed white skin areas, or from black skin areas into red skin areas in spotted guinea pigs and other mammals. So far as spread from black into white skin is concerned, it had previously been shown that migration of epidermal melanocytes into skin lacking homologues of these cells was responsible. However, since red skin already has its own complement of phenotypically "red" melanocytes, the intriguing possibility remained that when black pigment encroaches upon red, rather than melanocyte migration being responsible, phaeomelanin (red)-producing melanocytes are transformed into eumelanin (black)-producing cells by some kind of serially transmissible factor derived from contiguous eumelanotic melanocytes. By utilizing two isogenic strains (Nos. 2 and 13) of spotted guinea pigs and their F(1) hybrids, the mechanism underlying the spread of pigment from black into red skin has been analyzed, employing cellular transplantation antigens as melanocyte "markers." The findings demonstrate unequivocally that a physical migration of pigment cells is responsible. By comparing the extents of pigment spread from black ear skin grafts, or from epidermal cell suspensions prepared therefrom, from parental strain or from F(1) hybrid donors in white host skin areas of F(1) hybrid guinea pigs, it has been possible to evaluate the influence of the intimate contact of melanocytes with alien transplantation antigens on their survival and migratory behavior. No evidence was forthcoming that pigment spread takes place less readily when the cells responsible are confronted by epidermal cells bearing foreign antigens than when they are confronted by cells of their own antigenic constitution. These findings are contrary to expectation if the phenomena of allogeneic inhibition or contact-induced cytotoxicity apply to normal cells in in vivo situations.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The pharmacokinetic characteristics of amiodarone suggest extensive tissue deposition. We confirmed this by measuring tissue concentrations of the drug and of its major metabolite, desethylamiodarone, in human tissues. These were obtained at autopsy (n = 9), surgery (n = 7), or biopsy (n = 2) from 18 patients who had been treated with amiodarone for varying periods of time. High concentrations of amiodarone were found in fat (316 mg/kg wet weight in autopsy specimens, 344 mg/kg wet weight in biopsy specimens). Amiodarone and desethylamiodarone concentrations (mg/kg wet weight, autopsy samples) were also high in liver (391 and 2354), lung (198 and 952), adrenal gland (137 and 437), testis (89 and 470), and lymph node (83 and 316). We also found high concentrations of amiodarone (306 mg/kg wet weight) and desethylamiodarone (943 mg/kg wet weight) in abnormally pigmented ("blue") skin from patients with amiodarone-induced skin pigmentation. These values were 10-fold higher than those in unpigmented skin from the same patients. These high concentrations were associated with lysosomal inclusion bodies in dermal macrophages in the pigmented skin. The inclusion bodies were intrinsically electron dense and were shown to contain iodine by energy dispersive x-ray microanalysis. Lysosomal inclusion bodies shown by electron microscopy to be multilamellar were seen in other tissues. These tissues included terminal nerve fibers in pigmented skin, pulmonary macrophages, blood neutrophils, and hepatocytes and Kupffer cells. These characteristic ultrastructural findings occur in both genetic lipidoses and lipidoses induced by other drugs, e.g., perhexiline. We conclude that during therapy with amiodarone, widespread deposition of amiodarone and desethylamiodarone occurs. This leads to ultrastructural changes typical of a lipidosis. These changes are seen clearly in tissues associated with the unwanted effects of amiodarone, e.g., skin, liver and lung.
Pigmentation, stratum corneum and viable epidermis are considered to be the main factors protecting against ultraviolet radiation. We quantitatively investigated the degree of photoprotection provided by these structures in vitiligo and adjacent normally pigmented skin. In 14 patients 61 MED tests were performed in vitiligo and adjacent normally pigmented skin using a solar simulator. The thickness of stratum corneum and viable epidermis was determined from frozen skin sections, and pigmentation was calculated by measuring skin reflectance at 555 nm and 660 nm. To analyse photoprotection, the UV dose necessary to evoke erythema was regressed against the thickness of stratum corneum and viable epidermis, pigmentation and the erythema grade in the MED test. By analysing regression coefficients we found that stratum corneum was the main photoprotective factor not only in vitiligo but also in normally pigmented skin. The effect of pigmentation in normal skin was slightly less prominent. Stratum corneum was thicker in vitiligo than in normally pigmented skin. However, the photoprotection due to stratum corneum was similar in both groups because significantly less photoprotection was achieved per thickness unit of stratum corneum in vitiligo than in normal skin. Neither in vitiligo nor in normally pigmented skin did the photoprotection depend on viable epidermis. Our data quantitatively document the importance of stratum corneum and pigmentation. Hyperkeratosis in vitiligo offers just as efficient photoprotection as does the normal stratum corneum in pigmented skin.
Skin pigmentation is a physiological feature of great value and usefulness from both an anthropological point of view and a clinical point of view. This article is a first approach to the study of the skin pigmentation of 126 full-term newborn infants (37-42 weeks gestational age) at the Maternity Hospital "La Paz" (Madrid, Spain) using the reflectance method. We provide the normal patterns, which have to be taken into account when applying this method to detect transcutaneous bilirubin and some physiopathological conditions, such as hyperbilirubinemia, anemia, plethora, and hormonal disturbances. Measurements of the reflectance were taken at the forehead, the internal and external aspects of the arm, the thorax, and the gluteus with blue, green, and amber tristimulus filters. With all filters the least pigmented zone was the thorax, and the most pigmented zone was the forehead; the internal aspect of the arm, the gluteus, and the external aspect of the arm were intermediate in increasing order. Our data confirm a higher pigmentation at birth than during the first year. We think that the idea of cephalocaudal progression of hyperbilirubinemia must be rejected. Our results also indicate that the thickening of the skin with gestational age is one of the most important factors in the skin color changes of newborn infants with an apparently different rhythm in males than in females.
BACKGROUND: The antioxidants selenium and vitamin E can be effective in reducing acute and chronic ultraviolet (UV)-induced skin damage. OBJECTIVE: This study investigated whether topical L-selenomethionine with topical RRR-alpha-tocopherol (Eol) or oral RRR-alpha-tocopheryl acetate (Eac) can reduce the incidence of UV-induced skin damage more than treatment with each alone. METHODS: Skh:2 hairless pigmented mice were treated with lotion vehicle, L-selenomethionine lotion, Eol lotion, oral Eac, L-selenomethionine plus Eol lotion, or L-selenomethionine lotion plus oral Eac and exposed to UVB. Skin pigmentation was scored, and the number of skin tumors per animal was counted weekly. RESULTS: Mice treated with selenium and vitamin E had significantly less acute and chronic UV-induced skin damage. CONCLUSION: Topical L-selenomethionine alone and combined with vitamin E gave the best protection against UV-induced blistering and pigmentation. In protecting against skin cancer, topical Eol and topical L-selenomethionine plus oral Eac were best. Significant synergy of L-selenomethionine with vitamin E was not observed.
The two paracrine melanogenic cytokines, stem cell factor (SCF) and endothelin-1 (ET-1), have been demonstrated to play pivotal roles in skin pigmentation including UVB-induced pigmentation and senile lentigo. However, little is known regarding their interactive effect on skin pigmentation. In order to investigate their roles in vivo, facultative pigmentation of human skin xenografts on severe combined immunodeficient (SCID) mice was assessed. After 1 week of acclimation in a pathogen-free barrier, dermatomed fresh cadaveric skin was surgically grafted onto the back of the mice and allowed to heal for 5-6 weeks prior to cytokine administration. Intradermal injections of SCF at 0.7 or 2.0 microg significantly increased skin pigmentation when compared to vehicle control. Despite the lack of a dose-dependent pigmentation response following ET-1 administration, the combination of 0.2 microg SCF and 0.1 microg ET-1 demonstrated a statistically significant increase in tyrosinase gene expression substantiated by the enhancement of melanin content and skin pigmentation compared to treatment with SCF alone or ET-1 alone. These findings establish an in vivo interaction between SCF and ET-1 with regard to their capacity to effect an increase in skin pigmentation.
Ultraviolet light has been implicated as a dominant factor in skin cancer development. Skin pigmentation is traditionally regarded as an important protection against skin cancer. Yet, little is known about how skin pigmentation is modulating induction of DNA damage, which is the primary event in carcinogenesis. We applied a recently developed 32P-postlabeling technique to measure the effect of constitutional pigmentation on the formation of major ultraviolet-induced DNA damage in human skin in vivo. The induction of photoproducts showed a statistically significant negative correlation with erythemal response and skin pigmentation. Our results demonstrated that the constitutional pigmentation is efficiently guarding DNA against the formation of photoproducts. The difference in melanin content is likely to be one of the reasons for the observed interindividual variation in levels of DNA damage after the uniform exposure to ultraviolet B.