Improved Protection Against Solar-Simulated Radiation-Induced Immunosuppression by a Sunscreen with Enhanced Ultraviolet A Protection

Abstract

Ultraviolet radiation-induced immunosuppression is thought to play a part in skin cancer. Several studies have indicated that sunscreens that are designed to protect against erythema failed to give comparable protection against ultraviolet radiation-induced immunosuppression. One possible reason for this discrepancy is inadequate ultraviolet A protection. This study evaluated the level of immunoprotection in mice afforded by two broad-spectrum sunscreens with the same sun protection factor, but with different ultraviolet A protection factors. Both sunscreens contained the same ultraviolet B and ultraviolet A filters, in the same vehicle, but at different concentrations. Solar simulated radiation dose-response curves for erythema, edema, and systemic suppression of contact hypersensitivity were generated and used to derive protection factors for each end-point. The results of three different techniques for determining immune protection factor were compared. A comparison of the two sunscreens showed that the protection factor for erythema in mice was similar to that determined in humans (sun protection factor) but the protection factor for edema in mice was lower. Both sunscreens protected against suppression of contact hypersensitivity but the product with the higher ultraviolet A-protection factor showed significantly greater protection. The three techniques for determining immunoprotection gave very similar results for a given sunscreen, but immune protection factor was always lower than sun protection factor. These data suggest that sun protection factor may not predict the ability of sunscreens to protect the immune system and that a measure of ultraviolet A protection may also be necessary.

Measurement of protection afforded by ultraviolet-absorbing window film using an in vitro model of photodamage

“…UVA exposure inside a car is high enough to be considered significant when calculating a person's lifetime UV exposure [17]. The driver's side shoulder, arm, and hand receive the highest UV exposure while driving because they are closest to the driver's sidewindow [26], so simply applying window film to the driver's side-window alone could reduce lifetime UVA exposure in a meaningful way for most individuals.…”

“…The sun emits 20-fold more UVA than UVB; and, our relative exposure to UVA is further increased by wearing sunscreens, which allow us to remain outside longer without getting sunburned by UVB. In addition to photoaging, UVA contributes to UV-induced immune suppression [26][27][28], skin cancer formation [29,30], and ocular damage, such as cataracts [31,32]. Applying a high-absorbing UVA filter to window glass in a car, home, and office is an easy way to prevent passive exposure to UVA.…”

Oral administration of Polypodium leucotomos delays skin tumor development and increases epidermal p53 expression and the anti‐oxidant status of UV‐irradiated hairless mice

“…In this setting, the only use of topical sunscreens may not be sufficient to afford a complete protection against UVR damage. Moreover, the efficacy of topical sunscreens has been questioned for long-term exposures (4). A potential improvement is the use of systemic (oral) photoprotection.…”

Polypodium leucotomos decreases UV‐induced epidermal cell proliferation and enhances p53 expression and plasma antioxidant capacity in hairless mice

“…In an in vivo setting, this only occurs in exposed areas of the skin, but a similar oxidative stress response can be observed in other tissues, including blood (3,4), which may have repercussions in the onset of the immune response to UVR (5). Topical sunscreens are the obvious form of protection against UVR, but they work well only against the local effects of UVR and their efficacy in long-term exposure is controversial (6); thus, the use of systemic (oral) photoprotection to complement topical sunscreens is a good strategy. In this regard, the use of botanical systemic antioxidants is a subject of interest in photoprotection (7).…”

“…Several apoptotic regulatory proteins, such as Fas, Ras and TNFa, have been shown to be recruited into lipid rafts upon various stimuli (3,4). Ultraviolet light (UV) is one of the stimuli that alters major components of lipid rafts, which induces the expression of various genes and regulates apoptosis through recruiting and promoting the aggregation of Fas, formation of death-inducing signalling complex and activation of Fas-associated death domain protein-caspase 8 cascade in skin cells (5)(6)(7)(8). However, the functions of other lipid rafts-associated proteins in the regulation of UVB-induced apoptosis are still generally unknown.…”