Oxidative Stress in the Pathogenesis of Skin Disease
Open accessAbstract
Skin is the largest body organ that serves as an important environmental interface providing a protective envelope that is crucial for homeostasis. On the other hand, the skin is a major target for toxic insult by a broad spectrum of physical (i.e. UV radiation) and chemical (xenobiotic) agents that are capable of altering its structure and function. Many environmental pollutants are either themselves oxidants or catalyze the production of reactive oxygen species (ROS) directly or indirectly. ROS are believed to activate proliferative and cell survival signaling that can alter apoptotic pathways that may be involved in the pathogenesis of a number of skin disorders including photosensitivity diseases and some types of cutaneous malignancy. ROS act largely by driving several important molecular pathways that play important roles in diverse pathologic processes including ischemia-reperfusion injury, atherosclerosis, and inflammatory responses. The skin possesses an array of defense mechanisms that interact with toxicants to obviate their deleterious effect. These include non-enzymatic and enzymatic molecules that function as potent antioxidants or oxidant-degrading systems. Unfortunately, these homeostatic defenses, although highly effective, have limited capacity and can be overwhelmed thereby leading to increased ROS in the skin that can foster the development of dermatological diseases. One approach to preventing or treating these ROS-mediated disorders is based on the administration of various antioxidants in an effort to restore homeostasis. Although many antioxidants have shown substantive efficacy in cell culture systems and in animal models of oxidant injury, unequivocal confirmation of their beneficial effects in human populations has proven elusive.
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UVR exposure causes direct damage to DNA, proteins or lipids, and indirect damage via reactive oxygen species (ROS).
“The molecular effects of this exposure are well defined, causing either direct damage to DNA, proteins or lipids, such as in the formation of DNA photoproducts [1], and indirect damage via the generation of reactive oxygen species (ROS) [2, 3] that attack a range of molecular and cellular targets.”
From Mycosporine-Like Amino Acids for Skin Photoprotection (2019) · cites this paper as [2]
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- Authors
- Bickers, D. R., & Athar, M.
- Affiliations
- Columbia University Irving Medical Center (US)
- Corresponding author
- Bickers, David R.
- Athar, Mohammad
- ORCID
- Athar, Mohammad
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 126
- Issue
- 12
- Pages
- 2565-2575
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2128705246
- Cited by
- 1,092
- References
- 84
- Citations by year
- 2026: 30 · 2025: 52 · 2024: 48 · 2023: 46 · 2022: 57 · 2021: 84 · 2020: 84 · 2019: 65 · 2018: 57 · 2017: 71 · 2016: 75 · 2015: 65 · 2014: 63 · 2013: 64 · 2012: 64
- FWCI
- 3.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (n01cn43300-6-0-1)
- National Cancer Institute (N01 CN15109, U19CA81888, N01-CN-35006-72, N01-CN-43300, CA-10106-01, R01 CA-97249, R03CA101061, U19CA081888, N01-CN-15011-72, R01CA097249, N01-CN-35105)
- 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
- oxidative stress, reactive oxygen species, skin disease pathogenesis, antioxidants, ultraviolet radiation, xenobiotic toxicity, skin cancer, apoptosis, ischemia-reperfusion injury, atherosclerosis, inflammation, antioxidant therapy
- MeSH terms
- Antioxidants, Humans, Photosensitivity Disorders, Skin Diseases, Skin Neoplasms, Signal Transduction, Apoptosis, Reactive Oxygen Species, Oxidative Stress
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