Ultraviolet Radiation: Cellular Antioxidant Response and the Role of Ocular Aldehyde Dehydrogenase EnzymesMarchitti, Satori A Ph.D.; Chen, Ying Ph.D.; Thompson, David C Ph.D.; Vasiliou, Vasilis Ph.D.Eye & Contact Lens: Science & Clinical Practice: July 2011 - Volume 37 - Issue 4 - pp 206-213 doi: 10.1097/ICL.0b013e3182212642 Review Abstract Author Information Solar ultraviolet radiation (UVR) exposes the human eye to near constant oxidative stress. Evidence suggests that UVR is the most important environmental insult leading to the development of a variety of ophthalmoheliosis disorders. UVR-induced reactive oxygen species (ROS) are highly reactive with DNA, proteins, and cellular membranes, resulting in cellular and tissue damage. Antioxidant defense systems present in ocular tissues function to combat ROS and protect the eye from oxidative damage. Important enzymatic antioxidants are the superoxide dismutases, catalase, glutathione peroxidases, glutathione reductase, and members of the aldehyde dehydrogenase (ALDH) superfamily. Glutathione, ascorbic and uric acids, α-tocopherol, nicotinamide-adenine dinucleotide phosphate, and ferritin serve as small molecule, nonenzymatic antioxidants. Ocular tissues have high levels of these antioxidants, which are essential for the maintenance of reduction-oxidation homeostasis in the eye and protection against oxidative damage. ALDH1A1 and ALDH3A1, present abundantly in the cornea and lens, have been shown to have unique roles in the defense against UVR and the downstream effects of oxidative stress. This review presents the properties and functions of ocular antioxidants that play critical roles in the cellular response to UVR exposure, including a focused discussion of the unique roles that the ALDH1A1 and ALDH3A1 enzymes have as multifunctional ocular antioxidants. From the Department of Pharmaceutical Sciences (S.A.M., Y.C., V.V.); and Department of Clinical Pharmacology (D.C.T.), University of Colorado Denver, Aurora, CO. Supported in part by National Institutes of Health (NIH) grant EY17963. The authors have no other funding or conflicts of interest to disclose. Address correspondence and reprint requests to Vasilis Vasiliou, Ph.D., Department of Pharmaceutical Sciences, University of Colorado Denver, Aurora 80045, CO; e-mail: email@example.com Accepted April 23, 2011. © 2011 Lippincott Williams & Wilkins, Inc.