Ozone exposure activates oxidative stress responses in murine skin
Abstract
Ozone (O(3)) is among the most reactive environmental oxidant to which skin is exposed. O(3) exposure has previously been shown to induce antioxidant depletion as well as lipid and protein oxidation in the outermost skin layer, the stratum corneum (SC), but little is known regarding the potential effects of O(3) on the skin epidermis and dermis. To evaluate such skin responses to O(3), SKH-1 hairless mice were exposed for 2 h to 8.0 ppm O(3) or to ambient air. O(3) exposure caused a significant increase in skin carbonyls (28%) compared to the skin of air exposed control animals. An evident increase in 4-hydroxynonenal-protein adducts was detected after O(3) exposure. O(3) exposure caused a rapid up-regulation of HSP27 (20-fold), and more delayed induction of HSP70 (2.8-fold) and heme oxygenase-1 (5-fold). O(3) exposure also led to the induction of nitric oxide synthase (iNOS) 6-12 h following O(3) exposure. We conclude that skin exposure to high levels of O(3) not only affects antioxidant levels and oxidation markers in the SC, but also induces stress responses in the active layers of the skin, most likely by indirect mechanisms, since it is unlikely that O(3) itself penetrates the protective SC layers.
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Gaseous pollutants such as NO2, SO2, or O3 may exert more acute effects on skin through oxidative damage, lipid reactions, and barrier damage, whereas PM may need chronic exposure or a longer contact duration to penetrate skin hair follicles and cause secondary inflammation.
“Studies suggest that gaseous pollutants such as NO2, SO2, or O3 may exert a more acute effects on skin through oxidative damage, lipid reactions, and barrier damage, whereas PM may need chronic exposure or a longer contact duration to penetrate skin hair follicles and cause secondary inflammation [91–93].”
From Air Pollution and Skin Diseases: A Systematic Review of Epidemiological Evidence (2026) · cites this paper as [92]
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References 39 · Cited by 120
- Authors
- Valacchi, G., van der Vliet, A., Schock, B. C., Okamoto, T., Obermuller-Jevic, U., Cross, C. E., & Packer, L.
- Affiliations
- University of California, Davis (US)
- University of Southern California (US)
- Corresponding author
- Valacchi, Giuseppe
- Venue
- Toxicology
- Publisher
- Elsevier BV
- Published
- 2002-09
- Volume
- 179
- Issue
- 1-2
- Pages
- 163-170
- ISSN
- 0300-483X (ISSN-L)
- OpenAlex
- W2065319723
- Cited by
- 120
- References
- 39
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 4 · 2023: 5 · 2022: 4 · 2021: 5 · 2020: 10 · 2019: 11 · 2018: 6 · 2017: 10 · 2016: 4 · 2015: 8 · 2014: 1 · 2013: 3 · 2012: 2
- FWCI
- 1.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion)
- Funders
- National Institutes of Health (1r13hl057542-01, 5r01hl047628-06)
- National Heart, Lung, and Blood Institute (HL-57542, HL 47628)
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Keywords
- ozone exposure, oxidative stress, skin, stratum corneum, protein carbonylation, heat shock proteins, HSP27, HSP70, heme oxygenase-1, nitric oxide synthase, antioxidant depletion, lipid peroxidation, SKH-1 mice
- MeSH terms
- Aldehydes, Animals, Enzyme Induction, Heat-Shock Proteins, Immunohistochemistry, Mice, Hairless, Ozone, Proteins, Skin, Protein Biosynthesis, Blotting, Western, Oxidative Stress, Nitric Oxide Synthase, Mice, Nitric Oxide Synthase Type II
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