PubMed Health⌕ Search

Biomedical subjects

R M Sayre

Publications and source records attributed to R M Sayre.

At least 19 recordsLinked to original sources
PubMed1992

Beta-carotene does not act as an optical filter in skin.

Beta-carotene, when orally administered, only slightly increases the sunburn threshold in normal humans but effectively diminishes sunlight risk in patients suffering from erythropoietic protoporphyria. In addition, beta-carotene has been shown to inhibit UV-induced carcinogenesis in mice when administered either orally or intraperitoneally. To examine the photoprotective properties of beta-carotene, SKH-HR1 albino hairless mice received beta-carotene supplemented diets for either two or four weeks. At the end of each treatment period the skins were visibly yellow. Whole skin and epidermis from each animal were studied by forward scattering transmission spectroscopy and compared with age-matched controls. While no major optical differences were seen in the whole skin or in the epidermis, the presence of beta-carotene was optically demonstrated by weak but typical beta-carotene absorption peaks in the epidermis following the two week feeding period. The peaks were also apparent in the four week group. However, the beta-carotene peaks could not be resolved through full thickness skin. Despite the yellow appearance of the skin, the absorbance due to the carotene was insufficient to impart significant photoprotection. These results confirm previous theoretical arguments that oral beta-carotene treatment does not attain a sufficient concentration in the skin to produce a typical sunscreen effect by absorption of radiation. When beta-carotene is effective in the treatment of photosensitivity, it must produce its protectiveness through an alternative mechanism.

Animals↗
PubMed1992

In vitro and in vivo ultraviolet-induced alterations of oxy- and deoxyhemoglobin.

Ultraviolet (UV) radiation was found to convert oxyhemoglobin and deoxyhemoglobin stoichiometrically into methemoglobin and a met-like product, respectively. The peak conversion efficiency for oxyhemoglobin occurred at 285 nm and decreased by a factor of 100 by 315 nm. The peak conversion efficiency for deoxyhemoglobin occurred at 290 nm and decreased by a factor of 30 by 320 nm. The transformation of oxyhemoglobin to methemoglobin was also documented in intact erythrocytes using UV-B radiation. Finally, similar transformations were found to occur in human skin with UV-B exposure but not on all volunteers tested. These results imply that methemoglobin will be formed in vivo on solar exposure and provide evidence that UV-B photons reach the blood vessels.

Hemoglobins↗
PubMed1992

Discrepancies in the measurement of spectral sources.

Comparison of spectroradiometric and meter measurements of a series of ultraviolet radiation sources indicates that a wide divergence between readings can occur. We found that with a xenon arc filtered as a solar simulator producing UV-A (320-400 nm) and UV-B (290-320 nm) radiation, the meter can either over- or underestimate the emission of the source when different cut-off filters are used. The most severe the UV-B meter reading, although the UV-A reading can also reading can reading can also be problematic. Meters should be calibrated used to measure.

Spectrum Analysis↗
PubMed1992

Dose-response of chronic ultraviolet exposure on epidermal forward scattering-absorption in SK-1 hairless mouse skin.

This work provides a dose-response model of UV-induced epidermal-stratum corneum thickening induced by irradiation at wavelength lambda. This model assumes that photobiochemical reaction(s) can give rise to hyperplasia in a manner which is predictable from a simple photochemical kinetic scheme. In this work, we derive an equation which predicts an approximately linear relationship between the logarithm of the increase in optical skin thickening measured at 320 nm (delta OD320) and total cumulative dose (DT) seen by the target cells in or near the basal layer. For each excitation wavelength lambda, the slope R(lambda) of the log delta OD320 vs DT plot is proportional to epsilon(lambda) phi rx, where epsilon(lambda) is the extinction coefficient for the target chromophore at excitation wavelength, and phi rx is the quantum yield for the photochemical reaction(s) leading to hyperplasia. Our data previously obtained from irradiation of SK-1 hairless mice with "monochromatic" UV wavebands at 280, 290, 300, 307 and 313 nm (Menter et al., 1988, Photochem. Photobiol. 47, 225-260.) and data from Sterenborg and van der Leun at 254 and 313 nm (1988, Photodermatology 5, 71-82) are in good agreement with this model, except for 254 and 280 nm excitation, which are greatly attenuated by epidermis-stratum corneum. For excitation at the latter wavelengths, "dark" regressive processes successfully compete with the "light" reaction(s) which lead to (pre)cancerous lesion. This difficulty notwithstanding, the "intrinsic" action spectrum for hyperplasia derived from these measurements indicates that the target chromophore preferentially absorbs in the UV-C region.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Pasteuria nishizawae sp. nov., a mycelial and endospore-forming bacterium parasitic on cyst nematodes of genera Heterodera and Globodera.

This study describes Pasteuria nishizawae sp. nov., a fourth species of the genus Pasteuria. This mycelial and endospore-forming bacterium parasitizes the adult females of cyst-forming nematodes in the genera Heterodera and Globodera. The distinct ultrastructural features and unique host range found for this bacterium separate it from two closely related species, Pasteuria penetrans, which parasitizes several species of root-knot nematodes of the genus Meloidogyne, and Pasteuria thornei, which appears to parasitize only one species of the root-lesion nematode, Pratylenchus brachyurus. Because these obligate bacterial parasites of nematodes have not been cultured axenically, the taxonomic relationships described here for each species are based mainly on developmental morphology, fine structure of the respective sporangia and endospores, and their pathogenicity on nematode species.

Animals↗
PubMed1991

Photoprotection by melanin.

This paper is an attempt to summarize the current state of information on melanin and epidermal melanin pigmentation (EMP) as photoprotective agents. The chemistry and biochemistry of melanin (the particle) and its interaction, in its various forms, with UV radiation are considered. Methods of attenuation of UV radiation are discussed in terms of structure and chemical constituents. Photoprotection by constitutive and facultative pigmentation is reviewed with minimum erythema dose (MED) as the end point. The issue of acclimatization to UV radiation is discussed in terms of UVB phototherapy for psoriasis. Finally, skin cancer is considered as an end point and the reduction of its incidence with pigment level is discussed. It is concluded that whilst EMP provides protection, its extent depends on the end point chosen for evaluation. MED is a convenient photobiological end point but is rather insensitive, whereas skin cancer is sensitive but impractical for laboratory studies. Our current state of knowledge of melanin lacks information on its absorption and scattering coefficients and its refractive index. Methods for the quantitative measurement of EMP are also urgently required.

Humans↗
PubMed1991

An action spectrum for ultraviolet induced elastosis in hairless mice: quantification of elastosis by image analysis.

To determine an action spectrum for ultraviolet (UV)-induced elastosis, four groups of 24 albino hairless mice each were exposed to four different spectra emitted by a xenon arc solar simulator fitted with cut-off filters (Schott WG 320, 335, 345, and 360). These filters progressively removed more of the shorter wavelengths until, in the final spectrum, only long wavelength UVA (greater than 335 nm) remained. Exposures continued up to 62 weeks. A fifth group of mice served as controls. Skin biopsies were taken at pre-determined dose points and were processed for light microscopy. Elastosis was quantified by computerized image analysis, yielding dose-response curves for each spectrum. The total energy required for a 50% increase in elastic tissue compared to controls was determined graphically for each spectrum. These were: WG 320, 65 J/cm2; WG 335, 865 J/cm2; WG 345, 1230 J/cm2; and WG 360, 2000 J/cm2. Our results were tested against published action spectra for erythema, photocarcinogenesis and elastosis. The erythema spectrum was the most predictive for elastosis except that the longer UVA wavelengths were less effective for elastosis than for erythema. Solar simulating radiation (WG 320 filter) with its UVB component was the most effective in inducing elastosis. Full spectrum UVA (WG 345) required 20 times more energy while long wavelength UVA (WG 360) required 30 times more energy to induce equivalent elastosis.

Animals↗
PubMed1991

Product application technique alters the sun protection factor.

A number of factors may alter the efficacy of a sunscreen product being tested. Notably among these are (1) the source of ultraviolet (UV) radiation, (2) the filtration of the UV radiation source, (3) such environmental factors as swimming or sweating (4) and/or the amount of product applied. This is the first report in which the technique of product application itself is examined. We find that the act of rubbing the product into the skin appears also to remove product from the skin. In our study, different techniques of product application produced a 25% deviation in product sun protection factor. The variables associated with the application of sunscreening products are discussed.

Humans↗
PubMed1990

A method for the determination of UVA protection for normal skin.

Although the UVB portion of the electromagnetic spectrum (290 to 320 nm) is responsible for most of the harmful effects of sunlight on the skin, wavelengths in the UVA region also contribute to photodamage. A simple and rapid clinical test, the sun protection factor determination, is available to assess the sunburn protective effect of a sunscreen, primarily a UVB effect. However, no practical test has been proposed to measure a sunscreen's UVA protection. We described a method for the calculation of UVA protection in normal subjects. The determination of UVA protection involves three steps: (1) the UV absorbance spectrum of the sunscreen on skin is determined spectrophotometrically; (2) a convolution spectrum is calculated by multiplying the solar spectrum with the Commission Internationale de l'Eclairage UV Hazard Spectrum; and (3) the sunscreen transmission spectrum is then incorporated into the convolution spectrum to obtain the UVA effectiveness ratio, which can be expressed as the UVA protection percentage. Because the UVA protection percentage value is based both on normal erythemic risk and on standard sunlight, the protection for any product can be easily measured. The procedure is simple, and values generated can be reproduced in other laboratories.

Erythema↗
PubMed1990

Spectral comparison of solar simulators and sunlight.

In evaluating sunscreen efficacy, spectral distribution of the irradiation sources can influence the sun protection factor (SPF). The purpose of this investigation was to examine the uniformity of ultraviolet (UV) spectral irradiance of solar simulators used in various SPF testing laboratories, compare them with natural sunlight UV radiation (UVR), and recommend performance limits to ensure that the variability of radiation sources in the UVB region minimally affects SPF estimates. The critical portion of the solar erythemogenic spectrum was identified as the UVB portion, defined as the region between 280 and 320 nm. The spectral irradiance of 26 solar simulators and other UV sources was measured and compared with a summer noon solar spectrum measured in Albuquerque, NM. Proposed spectral limits were developed as a 6-nm "acceptance band" centered on this standard spectrum normalized at 320 nm. The results indicated that the xenon-arc solar simulators currently used in the United States in testing sunscreens either meet the proposed standard solar spectrum or can be readily modified with available UV filters to meet this standard. The devices that have spectral characteristics not resembling sunlight fail to meet the proposed standard and should not be used for sunscreen SPF testing.

Filtration↗
PubMed1990

Reciprocity for solar simulators used in sunscreen testing.

Reciprocity for sunscreen solar protection factors (SPFs) and for delayed erythema was examined using a solar simulator equipped with neutral density filters to vary the beam intensity. Similar SPFs were obtained over a 15-fold intensity difference, using a sunscreen with a low (SPF-4) and a high (SPF-15) protection factor. Reciprocity was also observed for delayed erythema in unprotected skin.

Adolescent↗
PubMed1987

Phosphorylated mixed isomers of L-dopa increase melanin content in skins of Skh-2 pigmented hairless mice.

Dopa phosphates, a new class of compounds, contain phosphate-ester linkages at the 3- and/or 4- positions of the phenylalanine ring of L-dopa. Dopa phosphates have been shown to increase pigment production in the epidermis of hairless mice. Groups of Skh-2 pigmented hairless mice were treated topically with various concentrations of dopa phosphates daily for five weeks. Half of each group received suberythemal UVB radiation three times weekly for four weeks from a bank of filtered FS20 lamps. UVB and dopa phosphates alone each caused a modest increase in epidermal pigmentation. However, treatment of mice with dopa phosphates plus UVB radiation resulted in a marked increase in pigmentation, greater than with either treatment alone. The optimal concentration of dopa phosphates was 0.01% (100 micrograms/ml Tris-glycerol buffer) whether or not they were applied in conjunction with UVB radiation. Histological analyses revealed that dopa phosphates and UVB radiation each caused an increase in the number of pigmented melanocytes in the epidermis. Control groups treated with Tris-glycerol buffer alone, or buffer containing L-phenylalanine or L-dopa showed no significant changes in pigmentation. Our results indicate that dopa phosphates stimulate the production of melanin and affect the development and distribution of melanocytes in the skin of Skh-2 mice. By these criteria, dopa phosphates and UVB act in a similar manner to increase melanin content in the skin. The processes may be related to those recently observed in cultured mouse melanoma cells where dopa phosphates are incorporated into melanin, presumably following enzymatic hydrolysis by cellular phosphatases with the resultant production of L-dopa and inorganic phosphate.

Animals↗
PubMed1987

A novel model for testing enhancers of pigmentation.

Mouse skin, unlike human skin, does not contain active epidermal melanocytes, with the exception of the ear and tail skin in some pigmented strains. We have investigated enhancement of pigmentation in inbred C3H- mice using tail skin as a model for testing the effects of phosphorylated DOPA (DP) and ultraviolet radiation. Mice were restrained by cage dividers and treated with various doses of DP in dimethylsulphoxide (DMSO) or DMSO alone with or without the addition of UV radiation. Each tail served as its own control since only the dorsal surface was treated and irradiated. Pigmentation was graded blindly on histologic sections stained with Fontana-Masson. UV radiation caused a marked increase in epidermal and dermal pigmentation and this was enhanced in a dose-dependent manner by DP. However, there was minimal effect from DP alone.

Animals↗