NOW Foods Header Test
Superoxide Dismutase: A Supplement for Eye Health?
By Greg Arnold, DC, CSCS, November 20, 2006, abstracted from “SOD2 Protects against Oxidation-Induced Apoptosis in Mouse Retinal Pigment Epithelium: Implications for Age-Related Macular Degeneration” in the September 2005 issue of Investigative Ophthalmology & Visual Science
 
Age-related Macular Degeneration (AMD) causes vision loss in more than 200,000 people every year1 and is the leading cause of irreversible visual impairment in the world.2  With research showing that AMD is caused in large part by oxidative stress,(3, 4, 5) it’s not surprising that antioxidant intake has been found to help maintain eye health,6 even though antioxidants are not cures for AMD.
 
These antioxidants have been found to include lutein,7 found in green leafy vegetables,  resveratrol,8 found in walnuts, and blueberries.  Now a new study9 has found that superoxide dismutase (SOD), an antioxidant enzyme found in every cell of our body,10 may also be an antioxidant that helps maintain eye health.
 
In the study, researchers took eye cells from three different groups of mice (regular mice, mice bred to lack the SOD enzyme, and mice bred to have an overabundance of SOD).  They exposed the cells to hydrogen peroxide for one hour, after which the researchers measured eye cell death as well as cell function for 0, 4, 8, 16, and 24 hours after exposure to the hydrogen peroxide.
 
The researchers found that cells with an overabundance of the SOD enzyme had no cell death due to oxidative damage until 16 hours after exposure.  Even at 24 hours after exposure, cells bred to have no SOD still had cell death levels that were 30% higher than the cells with the overabundance of SOD.
 
For the researchers, “a decrease of [SOD]…during the aging process may be a significant contributory factor in AMD.”
 
Greg Arnold is a Chiropractic Physician practicing in Danville, CA.  You can contact Dr. Arnold directly by emailing him at mailto:ChiroDocPSUalum@msn.com or visiting his web site www.CompleteChiropracticHealthcare.com
 
Reference:

1  National Institutes of Health National Eye Institute and Prevent Blindness America. Vision Problems in the US: Prevalence of Adult Vision Impairment and Age-Related Eye Disease in America. Schaumburg, Ill: Prevent Blindness America; 2002

2  National Advisory Eye Council. Vision Research—A National Plan: 1999-2003, Vol. 1. A Report of the National Advisory Eye Council. Bethesda, Md: National Institutes of Health; 1999. NIH publication 98-4120

3  Cai J, Nelson KC, Wu M, et al. Oxidative damage and protection of the RPE. Prog Retin Eye Res. 2000;19:205–221

4  Reddy VN, Giblin FJ, Lin LR, et al. Glutathione peroxidase-1 deficiency leads to increased nuclear light scattering, membrane damage, and cataract formation in gene-knockout mice. Invest Ophthalmol Vis Sci. 2001;42:3247–3255

5  Liang FQ, Godley BF. Oxidative stress-induced mitochondrial DNA damage in human retinal pigment epithelial cells: a possible mechanism for RPE aging and age-related macular degeneration. Exp Eye Res. 2003;76:397–403

6  Van Leeuwen.  Dietary intake of antioxidants and risk of age-related macular degeneration.  JAMA. 2005 Dec 28;294(24):3101-7

7  Seddon JM, Ajani UA, Sperduto RD, et al. Dietary carotenoids, vitamins A, C, and E, and advanced age-related macular degeneration. JAMA. 1994;272:1413-1420

8  Progression of age-related macular degeneration: association with dietary fat, transunsaturated fat, nuts, and fish intake.  Arch Ophthalmol. 2003 Dec;121(12):1728-37

9  Reddy VN.  SOD2 Protects against Oxidation-Induced Apoptosis in Mouse Retinal Pigment Epithelium: Implications for Age-Related Macular Degeneration.  Invest. Ophthalmol. Vis. Sci. 2005 46: 3426-3434

10  Ho YS, Crapo JD. Isolation and characterization of complementary DNAs encoding human manganese-containing superoxide dismutase. FEBS Lett. 1988;229:256–260