Copyright 2002 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2002
Reactive oxygen species generated in the skin by UV irradiation promote photoaging and photocarcinogenesis. The manganese (Mn) superoxide dismutase (SOD) is a primary antioxidant enzyme that crucially contributes to the homeostasis of oxygen radicals within the mitochondria, and thus critically participates in the control of senescence and tumor generation.
To determine whether repetitive UV-B exposure, as practiced for light hardening during phototherapy for various photodermatoses, can enhance the adaptive antioxidant response by up-regulating MnSOD activity in either the epidermal or the dermal skin compartment.
In vitro experiments to determine MnSOD activity levels in cultured human dermal fibroblasts and epidermal cells (HaCaT cells and primary keratinocytes) at different times after direct UV-B exposure or after incubation of human dermal fibroblasts with supernatants from UV-B–irradiated epidermal cells.
Photobiological research laboratory in a university dermatology department.
Irradiation of cultured human dermal fibroblasts and epidermal cells with UV-B.
Main Outcome Measures
Manganese SOD messenger RNA and activity levels in cultured irradiated or mock-treated skin cells.
No increase in MnSOD activity could be detected in fibroblasts or epidermal cells until 24 hours after UV-B irradiation. However, fibroblasts incubated with supernatants from UV-B–irradiated epidermal cells showed a marked increase in specific MnSOD messenger RNA and activity. Removal of interleukin 1α, interleukin 1β, and tumor necrosis factor α from the supernatants led to a significant reduction of MnSOD mRNA in fibroblasts.
Irradiation of the epidermal cells with UV-B induced a release of soluble factors that amplified MnSOD activity in fibroblasts via a paracrine mechanism.
Naderi-Hachtroudi L, Peters T, Brenneisen P, et al. Induction of Manganese Superoxide Dismutase in Human Dermal FibroblastsA UV-B–Mediated Paracrine Mechanism With the Release of Epidermal
Interleukin 1α, Interleukin 1β, and Tumor Necrosis Factor α. Arch Dermatol. 2002;138(11):1473–1479. doi:10.1001/archderm.138.11.1473
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