The Contributions of UVA and UVB to Connective Tissue Damage in Hairless Mice

Abstract

UVA, in high-dose single exposures, can, like UVB, be deleterious to skin. Dermal damage resulting from chronic exposure to UVA has not been studied. To investigate the long-term effects, we irradiated albino hairless mice for 30-34 weeks with UVA radiation, alone, from two sources with differing spectral qualities, and in combination with UVB as solar-simulating radiation. The results were compared to UVB alone. Like UVB, the UVA waveband, especially that with a spectral distribution similar to solar UVA, caused elastic fiber damage, increased glycosaminoglycan levels, and produced hypertrophy of deep dermal tissues. There were, however, striking differences between UVB- and UVA-irradiated skin. A combination of UVA and UVB summated the effects of both wavebands. Substantial protection against these effects was afforded by a broad-spectrum sunscreen.

UVA exposure of human skin reconstructed in vitro induces apoptosis of dermal fibroblasts: subsequent connective tissue repair and implications in photoaging

“…Studies of sun exposed versus sun protected skin revealed dermal alterations (Berstein et al, 1996;Warren et al, 1991), but do not allow determination of the respective roles of UVB and UVA radiations. Induction of dermal actinic damages after chronic UVA exposures has been obtained using hairless mice (Kligman et al, 1985). Studies on fibroblast or keratinocyte cultures revealed that through the generation of oxidative species (Tyrell and Keyse, 1990), UVA induces a decrease in Epidermal Growth Factor (EGF) binding (Djavaheri-Mergny et al, 1994), a modification of phospholipid metabolism (Hanson and deLeo, 1990) and lipid peroxidation (Morlie Á re et al, 1991;Moysan et al, 1995).…”

Epidermaltrans-urocanic acid and the UV-A-induced photoaging of the skin

“…Unlike chronologically aged skin that results from a general atrophy and a gradual decline in the production of the dermal matrix (3), UV-A (320-400 nm) photoaged skin is characterized by a gross increase in the elastic fibers (elastin, fibrillin, and desmosine) of the skin replacing the collagenated dermal matrix (elastosis) (4)(5), an increase in glycosaminoglycans (4)(5), collagen cross-linking, epidermal thickening (4)(5)(6), and an increase in the number of dermal cysts (7). The deep lines, leathered appearance, and the sagging of the skin surface typically associated with ''old age'' are thought to result from UV-induced photodamage to the skin and to occur over the course of a lifetime (3).…”

Oral Administration of KTNG0345 Prepared from Red Ginseng Extracts Reduces UVB-induced Skin Wrinkle Formation in Hairless Mice

“…Any reduction in the synthesis of collagen or increase in the breakdown of collagen by MMPs is likely to result in an overall reduction in collagen and wrinkling 3) . The chronic exposure of hairless mouse dorsal skin to UVB is known to increase skin thickness and wrinkle formation, and to significantly enhance MMP activities in hairless mice 25,26) . The present , before and after the treatment period (five times weekly for 8 weeks) performed concurrently with UVB-irradiation (three times weekly).…”