Effect of ultraviolet irradiation on skin collagen.
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Biomedical subjects
Publications and source records attributed to S Shuster.
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The biological activities of alpha-MSH des-acetyl MSH, gamma-MSH and LPH37-58 were compared using the Anolis rate method of bioassay. Dose-response data showed LPH37-58 to be equipotent with alpha-MSH, but des-acetyl MSH and gamma-MSH were found to be much less active. The effect of LPH37-58 was additive to that of alpha-MSH, indicating that LPH37-58 is a full agonist of alpha-MSH. The lower potency peptides des-acetyl MSH and gamma-MSH reduced the effect of alpha-MSH and are, therefore, partial agonists of alpha-MSH. The action of MSH peptides in vivo may be modulated by interaction with agonists.
Immunoreactive alpha-MSH was found in human skin and the skin of numerous other mammals. After hypophysectomy the concentration of alpha-MSH in rat skin showed little change suggesting that the pituitary is not the source of this MSH. In human skin the highest concentration was found in the epidermis and HPLC revealed four peaks of immunoreactive alpha-MSH. Two of these co-eluted with mono- and des-acetyl alpha-MSH standards. An earlier peak probably represented an oxidized MSH and a later running peak, diacetylated alpha-MSH. Although no differences were found in alpha-MSH content of skin from albino and pigmented rats or between involved and non-involved epidermis of patients with vitiligo, its predominance in human epidermis could suggest a relationship with the melanocyte or its melanin. Whether alpha-MSH in the skin has any pigmentary significance or any other role has yet to be established.
The effect of alpha-MSH on coat color was examined in viable yellow mice (C3H/He-A*vy). These mice normally grow a coat of darkly pigmented hair at puberty. This darkening effect was also evident in hair that grew in a region that had been plucked at 13 days of age. Administration of alpha-MSH increased the darkness of this hair and the hair which grew naturally in an unplucked area. However, the natural coat darkening that occurred at puberty was not associated with an increase in plasma immunoreactive alpha-MSH levels. Moreover, although bromocryptine, a dopamine agonist that inhibits alpha-MSH release from the pituitary reduced the darkness of the coat that grew after plucking the reduction in coat darkening was unrelated to changes in plasma alpha-MSH. Nevertheless, this effect of bromocryptine was reversed when alpha-MSH was administered together with the drug. Apomorphine had no effect on coat darkening and produced only a slight decrease in plasma alpha-MSH. Melatonin reduced coat darkening slightly but, like apomorphine, had little effect on plasma alpha-MSH concentrations. Although alpha-MSH may have a physiological role in coat darkening in the C3H/He-A*vy mouse at puberty the response seems to be unrelated to an increase in circulating alpha-MSH. Thus, other factors, such as changes in melanocyte sensitivity to alpha-MSH or inhibitory mechanisms that prevent coat darkening during prepubertal and adult life may be involved in regulation of coat color in the viable yellow mouse.
We have examined the role of the calcium ion in the response of the melanophores of the lizard, Anolis carolinensis to alpha-melanocyte stimulating hormone (alpha-MSH) by a rate method which allows kinetic analysis of melanosome dispersion. Dose-response curves to alpha-MSH were compared in the presence of different calcium concentrations, and Schild regression plots were constructed. An avidly binding analogue of alpha-MSH, Nle4-D-Phe7-alpha-MSH, was used to demonstrate kinetically the involvement of calcium in the melanophore response both for MSH receptor binding and the subsequent transduction of the MSH signal across the melanophore membrane.
The effect of thalidomide on itch was studied in 11 patients with chronic pruritus from psoriasis, eczema, nodular prurigo, senile pruritus and primary biliary cirrhosis. Itch, assessed subjectively by the patients on a 10 cm line and measured objectively as nocturnal scratch movement, was decreased by thalidomide 200 mg on the 2 nights it was given. There was no improvement in the underlying disorders and it is concluded that thalidomide is a primary antipruritic agent. The patients all became drowsy and it seems likely that, as with most other antipruritic agents, the antipruritic action of thalidomide results from a central depressant effect. The primary antipruritic effect of thalidomide should now be assessed therapeutically.
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