UV PROTECTION AND EVALUATION OF EFFICACY OF SUNSCREENS 317 doses of UV radiations lead to a variety of molecular changes, for example, DNA damage in epidermal cells. However, the spectrum of UV radiations accessing viable epidermal cells can be altered by the use of topical sunscreens. Regular use of sunscreens has been shown to reduce actinic keratosis (12), solar elastosis, UV-induced immunosuppression (9,13), and photosensitivity in humans and prevents the formation of squamous cell car- cinomas in animals. This is well established that UV radiations are one of the major ecological causes of skin cancers however, skin cancers can be prevented by the use of physical and chemical sun- protectives. The intervention cost of the use of sunscreen to prevent skin cancers is around AU$ 40,890 per quality-adjusted life year saved and would result in a 76% reduction in melanomas and melanoma-related deaths and 41% reduction in squamous cell carcino- mas (14), whereas, the cost of treating nonmelanoma skin cancer is estimated to be in excess of US$ 650 million a year (15). Furthermore, a thorough understanding of the mechanism of action for sunscreens, the relationship of the spectrum and sun protection factor (SPF), UV index, and different formulations containing UV fi lters can help users in selecting the appropriate sun- screens. MECHANISM OF PHOTOPROTECTION A prophylactic and therapeutic strategy against skin cancers and photoaging is defi ned as photoprotection (16). MECHANISM OF PHOTOAGING Aging is a complex, progressive process that leads to functional and aesthetic changes in the skin. The aging process can be intrinsic (i.e., genetically determined) and extrinsic (due to environmental factors). Exposure of skin to sun enhances the aging of skin, which is a continuous process. Photoaging is different from intrinsic aging. Mechanism of pho- toaging is explained in Figure 2. Aging is a natural phenomenon, which is ahead of any one’s control. It is a multifaceted sequence, in which there is a progressive functional decline due to the amassing of mo- lecular damage. Human skin undergoes chronological or intrinsic aging and photoaging, that is, aging due to extrinsic factors. The skin shows a marked vulnerability to changes due to the structural and physiologic alterations that take place as a result of either intrin- sic or extrinsic aging (Table I). In Figure 3, microscopic structural changes in photoaged (A, B) and intrinsically aged (C, D) skin are clearly visible. Figure 3A reveals the presence of tangled, disorganized elastic material, which consists of damaged elastin, the microfi - brilar component, and fi bronectin. Figure 3B depicts the basophilic degeneration of in- terstitial collagen, which is due to degradation by matrix metalloproteinases. Intact fi bers of interstitial collagen in the Grenz zone “G” (narrow layer of upper dermis just below the epidermis, made of densely packed collagen fi brils, which is not infi ltered in the same way as other layers of the dermis) are present just beneath the epidermis indicating a limited repair process. Figure 3C reveals a slight decrease in elastic fi bers. Figure 3D re- veals decrease in fi ber thickness of interstitial collagen (7).

JOURNAL OF COSMETIC SCIENCE 318 MECHANISM INVOLVED IN ALTERATION OF ELASTIC FIBERS Wrinkling. Wrinkles on the face are prominent characteristics of photoaging. Formation of facial wrinkles is mainly due to loss of natural process of elastic properties of skin. UVB at suberythemal doses leads to reduction of elasticity and fi nally wrinkled skin (8). In photoaged skin, corners of eye are most susceptible and are highly associated with loss of skin elasticity (17). Neutrophil elastase (a serine proteinase) and skin fi broblast elastase (member of metal- loproteinase) are major components that are responsible for the elasticity of skin (18,19). UV exposure to animal skin at less than a suberythemal dose does not cause infi ltration of infl am- matory cell but elicits wrinkles (20). Figure 4 summarizes the mechanism of wrinkling. The main components of elastic fi bers are elastin and fi brillin. Elastin fi bers are formed in such a manner that fi brillin-rich microfi brils surrounds the cross-linked elastin, which is a central core portion (21). Various proteins in dermal or epidermal connective tissues play role in maintaining the integrity and architecture of the skin. Hence, damage to these con- nective tissues can be correlated to structural changes of skin, for example, wrinkling, loss of elasticity, and sagging (22). After UV irradiation, dermal keratinocytes and fi broblasts secrete cytokines, which stimulate gene and protein expression of elastase and collagen. SUN BURN Sun burn cells are the keratinocytes that on receiving a UVB dose (that can irreversibly or severely damage DNA) go through apoptosis. The cancer-prone phenotype can arise if Figure 2. Signaling pathway of photoaging.