Skin Aging Photoaging

The aging of skin is an intrinsic, degenerative process over time, comparable to what occurs in other organs, that results in a thinner but smooth skin with reduced elasticity. This process is superimposed to varying degrees by premature (extrinsic) aging caused by exposure to environmental stress, e.g., ultraviolet (UV) radiation. Photoaged skin occurs at unshielded body sites such as the face and the backside of hands as a consequence of chronic overexposure to natural or artificial sunlight (163). Clinical characteristics of photoaged skin are wrinkle formation, laxity, and a leathery appearance.

Ultraviolet radiation, and mainly long-wavelength ultraviolet A (UVA) light (320-400 nm), is a strong oxidant. In UV-irradiated skin, photosensitizing reactions lead to the formation of reactive oxygen species (ROS) such as singlet oxygen, superoxide anions, hydroxyl radicals, and hydrogen peroxide (164). ROS play a pivotal role in photoaging because they damage proteins directly (e.g., collagen) and activate matrix-degrading enzymes, leading to the destruction of the dermal layer in skin (165-167). Protection against photooxidative stress and consequently photoaging should be accomplished primarily via diminishing exposure to sunlight and by application of topical sunscreens. In addition, the use of antioxidants, whether topical or systemic, is a promising and common strategy to limit or prevent oxidative damage induced by UV light (168-170).

Sunscreen effect of vitamin E. Vitamin E has an absorbance maximum at 292 nm which is in the UVB range of light (290-320 nm). Like other sunscreen compounds, although with lesser activity, vitamin E may provide skin photoprotection via absorption of hazardous UVB radiation (169). In particular, topically applied vitamin E that does not effectively penetrate into the epidermis might act as an external sunscreen. UV irradiation of vitamin E results in formation of dimers and trimers that could contribute to photoprotection through their action as UV-absorbing compounds, could contribute to photoprotection (171).

Antioxidant action of vitamin E. Studies in humans on the antioxidant potential of vitamin E in skin are scarce. In a small clinical trial, vitamin E supplementation for 2 wk before sun exposure protected against TBARS formation in blood (172). Other studies indicate antioxidant activity of vitamin E in skin because vitamin E is readily depleted after a single suberythemal dose of UV light in human skin (173). In experimental studies with mice, repeated daily exposures to UVB light resulted in an increase in skin vitamin E levels and formation of oxidation products of vitamin E (174). Other studies in animals reported prevention of ROS formation in skin as detected by in vivo chemi-luminescence (175), prevention of lipid peroxidation (176), and up-regulation of a network of enzymatic and nonenzymatic antioxidants by vitamin E (177).

Antioxidant action of vitamin E has also been shown in vitro in cultured skin fibroblasts via diminution of ROS generation (178) and prevention of UVA-induced up-regulation of the stress responsive gene for heme oxygenase-1 (179). Vitamin E

also inhibited, to a certain degree, photoinactivation of the iron regulatory protein-1 in UVA-irradiated skin cells, and thus formation of oxidative stress by free intracellular iron (180). In primary keratinocytes, vitamin E (Trolox) diminished the UVB-induced stress signaling response as determined by a modulation of mitogen activated protein kinase (MAPK) activation (181).

In addition to direct antioxidant activity, vitamin E modulates cell signaling and gene expression in skin. Aging of skin, whether intrinsic or due to environmental stress exposure, is associated with increased PKC activity, leading to induction of collagenase (MMP-1, a matrix metalloproteinase) and thus tissue degradation. Vitamin E is able to inhibit collagenase overexpression in aging skin fibroblasts via PKC inhibition (182). Moreover, Trolox inhibited UVA-induced collagenase expression in skin fibroblasts in vitro (183). These findings strongly suggest a beneficial role of vitamin E in the prevention of skin photoaging.

Vitamin E seems to have a major protective role in human skin because it accumulates on the skin outer surface, the stratum corneum (SC) (184). Delivery of vitamin E onto the skin surface appears to be specific via continuous secretion by sebaceous glands (185). In sun-exposed body areas such as the face, vitamin E levels in the SC are 20-fold higher compared with unexposed areas (185). Upon exposure to environmental oxidative stress such as UV light (173) or ozone (186), a destruction of vitamin E occurs in the outer layers of the SC, indicating that vitamin E has an important antioxidant function in skin protection.

Topical application of vitamin E. In an experimental model of photoaging using hairless mice chronically exposed to UV radiation, topical application of vitamin E (5%) reduced visible skin changes and histologic alterations caused by UVB radiation (e.g., collagen damage, epidermal thickening, dermal infiltration) (187). Another study in mice revealed that vitamin E prevents UV-induced immunosuppression (188).

To date, no clinical trials have evaluated the effect of topical administration of vitamin E on parameters of photoaging in humans. One clinical study reported improved hydration of the SC and enhanced water-binding capacity of the skin after topical application of vitamin E (189). No photoprotection against erythema occurred with topical application of vitamin E (190). The efficacy of topical vitamin E depends greatly on the formulation used. In human skin ex vivo, the penetration of vitamin E was best after the use of encapsulated "nanotopes" followed by liposomal encapsulation and aqueous solubilization of vitamin E acetate. When applied in oil, no penetration of vitamin E into deeper layers was observed; it remained at the surface and in the SC (191). In the same study, up to 50% deacetylation of vitamin E acetate occurred by nonspecific esterases, generating the antioxidant active form of vitamin E. This effect did not occur on the skin surface or in the SC but only in the deeper skin layers where metabolically active cells are present.

Systemic application of vitamin E. In several studies vitamin E alone or in combination with other antioxidants (vitamin C, carotenoids) prevented biological end points of photodamage such as erythema in mice (192) and humans (193-196). For example, in a clinical trial using megadoses of Trolox (2 g/d), protection from erythema formation was observed. This effect was more pronounced in combination with vitamin C (3 g/d), suggesting that vitamin E and C act synergistically in an antioxidant network suppressing the sunburn reaction (194). Clinical data are not yet available on the effects of vitamin E supplementation on photoaging.

It may be hypothesized that a systemic application of vitamin E provides an additional benefit to topical application of sun protection products via constant accumulation in skin and, moreover, in tissues affected by UV radiation to which topical products cannot be administered (e.g., buccal mucosa cells in the oral cavity). Studies in this regard would be of interest.

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