Erythema induction by ultraviolet radiation points to a possible acquired defense mechanism in chronically sun-exposed human skin.

BACKGROUND: It is generally accepted that a UVA-induced erythema is difficult to detect except in the most sensitive individuals. OBJECTIVE AND METHODS: As UVA effects on human skin and skin cells have been shown to depend strongly on anatomical body sites, UVA I, UVA I + II and solar simulator radiations were compared in their ability to induce erythema and melanin pigmentation responses in individuals with skin types I-IV on both previously sun-exposed (arms, forearms, thighs) and nonexposed body sites (buttocks). RESULTS: Erythema induction by UVA I on previously nonexposed skin sites followed a dose response in all skin types which was contrary to the absence of erythema induction seen on previously sun-exposed sites. Melanin expression followed a dose and skin type response and was shown to be more enhanced in previously exposed skin and in skin types III and IV. In contrast, UVA I + II induced erythema on nonexposed skin areas and to a lesser extent on frequently sun-exposed skin. Melanin production by UVA I + II was similar to that seen with UVA I alone in individuals of skin types II and III. Solar simulator radiation was very efficient in erythema induction regardless of previous sun exposure of skin. CONCLUSIONS: We have found that contrary to the widespread opinion that UVA and in particular UVA I could not induce a significant erythema, this waveband is capable of measurable erythema induction on skin nonexposed to sunlight. The diminished erythema induction by UVA I on chronically sun-exposed skin suggests the possibility of a defense mechanism against UVA-induced damage in this tissue.

Expression of intercellular adhesion molecule-1 in UVA-irradiated human skin cells in vitro and in vivo.

Ultraviolet A (UVA) radiation represents an important oxidative stress to human skin and certain forms of oxidative stress have been shown to modulate intercellular adhesion molecule-1 (ICAM-1) expression. ICAM-1 has been shown to play an important part in many immune reactions and the perturbations of this molecule by ultraviolet radiation could have implications in many inflammatory responses. An enhancement immunohistochemical method with avidin/biotin was used for analysing the early effects of UVA radiation on human cell cultures and human skin (340-400 nm). Both in vitro and in vivo data show that ICAM-1 staining in epidermal keratinocytes, which was expressed constitutively, decreased in a UVA dose-dependent manner. The decrease was most noted at 3-6 h following UVA radiation with some ICAM-1 staining returning by 48 h post-UVA. ICAM-1 positive staining in the dermis was specific for vascular structures and was increased 24 h after UVA radiation. Cultured dermal fibroblasts exhibited ICAM-1 staining which increased slightly within 6-48 h post-UVA radiation. As epidermal ICAM-1 expression is depleted following UVA radiation and dermal expression increases due to an increase in the vascular structures, ICAM-1 provides a valuable marker following UVA radiation in human skin that can be readily measured in situ.