A number of studies indicate that matrix metalloproteinase might be involved in photoaging, but little is known about their direct contribution to ultraviolet-induced histologic and morphologic changes in the skin in vivo. This study reports the relationship between changes of matrix metalloproteinase activities and ultraviolet B-induced skin changes in hairless mouse. The role of matrix metalloproteinase in the skin changes was studied by topical application of a specific matrix metalloproteinase inhibitor. The backs of mice were exposed to ultraviolet B three times a week for 10 wk. Histologic studies showed that the basement membrane structure was damaged, with epidermal hyperplasia, in the first 2 wk of ultraviolet B irradiation, followed by the appearance of wrinkles, which gradually extended in the latter half of the ultraviolet B irradiation period. We observed enhancement of type IV collagen degradation activity, but not collagenase or matrix metalloproteinase-3 activity, in extracts of ultraviolet B-irradiated, wrinkle-bearing skin. Gelatin zymographic analysis revealed that gelatinases, matrix metalloproteinase-9 and matrix metalloproteinase-2, were significantly increased in the extract. In situ zymographic study clarified that the activity was specifically localized in whole epidermis of ultraviolet B-irradiated, wrinkled skin in comparison with normal skin. The activity was induced around the basal layer of the epidermis by a single ultraviolet exposure of at least one minimal erythema dose. Furthermore, topical application of a specific matrix metalloproteinase inhibitor, CGS27023A, inhibited ultraviolet B-induced gelatinase activity in the epidermis, and its repeated application prevented ultraviolet B-induced damage to the basement membrane, as well as epidermal hyperplasia and dermal collagen degradation. Ultraviolet B-induced wrinkles were also prevented by administration of the inhibitor. These results, taken together, suggest that ultraviolet B-induced enhancement of gelatinase activity in the skin contributes to wrinkle formation through the destruction of basement membrane structure and dermal collagen in chronically ultraviolet B-exposed hairless mouse, and thus topical application of matrix metalloproteinase inhibitors may be an effective way to prevent ultraviolet B-induced wrinkle formation.

Human body odor consists of various kinds of odor components. Here, we have investigated the changes in body odor associated with aging. The body odor of subjects between the ages of 26 and 75 was analyzed by headspace gas chromatography/mass spectrometry. 2-Nonenal, an unsaturated aldehyde with an unpleasant greasy and grassy odor, was detected only in older subjects (40 y or older). Furthermore, analysis of skin surface lipids revealed that omega7 unsaturated fatty acids and lipid peroxides also increased with aging and that there were positive correlations between the amount of 2-nonenal in body odor and the amount of omega7 unsaturated fatty acids or lipid peroxides in skin surface lipids. 2-Nonenal was generated only when omega7 unsaturated fatty acids were degraded by degradation tests in which some main components of skin surface lipids were oxidatively decomposed using lipid peroxides as initiator of an oxidative chain reaction. The results indicate that 2-nonenal is generated by the oxidative degradation of omega7 unsaturated fatty acids, and suggest that 2-nonenal may be involved in the age-related change of body odor.

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Background: The development of sebocytes and lipogenesis are known to be dependent on androgens. However, it is not fully understood whether growth factors are involved in the regulation of cell proliferation and lipid formation in sebaceous glands. Objective: This study was designed to evaluate the effect of growth factors such as epidermal growth factor (EGF), transforming growth factor α (TGF-α), basic fibroblast growth factor (bFGF) and keratinocyte growth factor (KGF) on cell proliferation and lipogenesis in cultured hamster sebocytes. Methods: Cell proliferation and intracellular lipid accumulation in these hamster sebocytes treated with growth factors were examined. Results: EGF, TGF-α and bFGF augmented the proliferation of hamster sebocytes for 8 days in a time- and dose-dependent manner. However, KGF had no effect on their proliferation. Moreover, the accumulation of intracellular lipids consisting mainly of triglycerides was suppressed in EGF-, TGF-α-, bFGF- and KGF-treated hamster sebocytes. Conclusion: EGF, TGF-α and bFGF, but not KGF, have mitogenic activity on hamster sebocytes, and all these growth factors act as antilipogenic factors. Moreover, it is likely that the formation of intracellular lipid droplets is independent of cell proliferation in hamster sebocytes.

Electrolytic polymerization of thiophene gives a metallic film with a conductivity of ca. 100 S/cm, and which becomes a semiconductive polymer with an optical absorption edge of 2.0 eV when reduced by electrochemical or chemical means.