Overview of Prevention of Photoaging and Pigmentary Changes of the Skin

It is now well established that UV exposure is the basis of photoaging in all skin types. The pigmentary aspect of photoaging as well as all other manifestations may be prevented by limiting exposure to UV light. This may be achieved through sun avoidance and the use of protective clothing, hats, and sunglasses. The judicious use of sunscreen to block both UVA and UVB is an important preventative measure for photoaging. Thus, the selection of a broad spectrum sunscreen with ingredients that block the action spectrum of UVA (oxybenzone, avobenzone) and UVB (paraaminobenzoic acid, octyl methoxycinnamate, and octyl salicylate) or a physical blocker containing titanium dioxide or zinc oxide is essential.

Antioxidants most likely play a role in prevention of photoaging as well. The mechanism by which this occurs has been demonstrated in vivo by Kang [63]. In the first part of the experiment, UV irradiation was demonstrated to increase the levels of the free radical hydrogen peroxide in the skin.Next, the action of antioxidants on free radicals was evaluated. It was demonstrated that the antioxidants genistein (an isoflavone found in soybeans) and N-acetyl cysteine (NAC) (an amino acid derivative that is converted into the antioxidant glutathione) were not able to block UVB and thus did not have sunscreen properties. Instead, genistein and NAC interrupt the UV signaling cascade in human skin that leads to photoaging.Genistein was found to block the activation of epidermal growth factor-receptor (EGF-R) and the MAP kinase pathway, which leads ultimately to the formation of MMPs and the breakdown of extracellular matrix components. NAC did not block activation of EGF-R but, instead, increased the levels of reduced glutathione in human skin. UV also stimulates the ERK pathway, and genistein and NAC both inhibited UV induction of ERK activity. As for the other pathway, UV stimulates JNK phosphorylation. NAC did not effect UV induction of JNK phosphorylation, but genistein did block the phosphorylation of JNK. Genistein and NAC inhibited the induction of cJun protein and inhibited the UV induction of collagenase mRNA. Thus, the UV signaling cascade in human skin that leads to photoaging is interrupted by genistein and NAC.

The antioxidants ascorbic acid and alpha-tocopherol are used in a variety of products that claim to prevent photoaging. The effects of three forms of topically applied tocopherol were studied on UV-radiation-induced free radical formation in a mouse model [64]. Tocopherol sorbate was shown to significantly decrease the UV-radiation-induced radical flux in skin. It was also found to be significantly more protective against skin photoaging than alphatocopherol and tocopherol acetate. Translation from an animal model to human skin is inferred. Ascorbic acid is also a popular ingredient in anti-aging medications. Topical vitamin C was studied in a porcine skin model [65].Animals treated with topical ascorbic acid exhibited fewer sunburn cells than did those animals treated with vehicle after exposure to UVA and UVB, and there were decreases in erythema in vitamin-treated areas. It must be noted that an in vitro model does not prove similar results in human skin. In currently available products, there is uncertainty as to the actual amount of antioxidant contained therein and in the stability of the antioxidant. Furthermore, the percutaneous absorption through human skin of the antioxidant is often unknown. Remembering that the theoretical role of the antioxidants is a preventative one,Traikovich determine the efficacy of topical ascorbic acid in the treatment of mild-to-moderate photodamage in the facial skin of 19 subjects over a 3-month period [66]. He demonstrated a significant improvement in skin surface textural changes after the use of ascorbic acid versus the control group. The problem with this study is that the mechanism of action of the antioxidant, ascorbate, is in the prevention of photoaging as opposed to the treatment of photoaging. Therefore, it seems unlikely that an antioxidant will treat existing photodamage.