Abstract
Tropospheric ozone (O3) is a source of oxidative stress. This study examined the ability of a topical antioxidant (WEL-DS) to inhibit O3-mediated damage in a human epidermal skin model. Four groups of tissues (N = 24) were compared: Group 1 (control) were untreated and unexposed; Group 2 were untreated and exposed to O3 (0.4 ppm, 4 h); Group 3 were pretreated with WEL-DS and unexposed; Group 4 were pretreated with WEL-DS and exposed to O3 (0.4 ppm, 4 h). Pretreated tissues were topically treated with 20 uL of WEL-DS and incubated for up to 20 h at 37 °C [humidified, 5% carbon dioxide (CO2)]. After 24 h, tissues were re-treated with WEL-DS and exposed to O3. Tissues were evaluated for Reactive Oxygen Species (ROS), hydrogen peroxide (H2O2), 4-hydroxynonenal (4-HNE) protein adducts, NF-κB p65 response and histology. In O3-exposed groups, WEL-DS significantly inhibited ROS formation vs. untreated tissues (p < 0.05). Pretreatment with WEL-DS inhibited H2O2 production vs. untreated tissues (p < 0.05), and decreased NF-κB p65 transcription factor signal. Oxidative stress induction in O3-exposed tissues was confirmed by increased levels of 4-HNE protein adducts (marker of lipid peroxidation); WEL-DS application reduced this effect. WEL-DS inhibited damage in tissues exposed to O3 with no significant changes in epidermal structure. A comprehensive topical antioxidant significantly diminished O3-induced oxidative damage in a human epidermal skin model.
Highlights
Skin provides a protective barrier against radiation from ultraviolet (UV) exposure and other external environmental stressors, and has a natural ability to protect itself against the effects of aging, harmful UV radiation, and exposure to other environmental factors such as ozone (O3) through an elaborate antioxidant defense system [1,2,3,4,5,6,7,8,9]
As determined by dichlorofluorescein diacetate (DCF-DA) assay, exposure to 0.4 ppm of O3 induced a significant increase of Reactive Oxygen Species (ROS) production in untreated exposed tissues compared to air-exposed tissues (p < 0.05; Fig. 1)
Research using an in vivo skin model demonstrated an increase of proliferative, adaptive and proinflammatory cutaneous tissue responses to O 3 exposure [28]
Summary
Skin provides a protective barrier against radiation from ultraviolet (UV) exposure and other external environmental stressors, and has a natural ability to protect itself against the effects of aging, harmful UV radiation, and exposure to other environmental factors such as ozone (O3) through an elaborate antioxidant defense system [1,2,3,4,5,6,7,8,9] These external environmental stressors generate free radicals that, coupled with intrinsic aging, can overwhelm the skin’s natural endogenous defenses, causing oxidative damage [1, 2, 8,9,10]. These molecular mechanisms induced by a cumulative exposure to O3 lead to tissue damage and compromise skin barrier integrity
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