IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

(Investigative Ophthalmology and Visual Science. 2006;47:729-737.)
© 2006 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.05-0719
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Espinosa-Heidmann, D. G.
Right arrow Articles by Cousins, S. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Espinosa-Heidmann, D. G.
Right arrow Articles by Cousins, S. W.

Cigarette Smoke–Related Oxidants and the Development of Sub-RPE Deposits in an Experimental Animal Model of Dry AMD

Diego G. Espinosa-Heidmann,1 Ivan J. Suner,1,2,3 Paola Catanuto,1 Eleut P. Hernandez,1 Maria E. Marin-Castano,1 and Scott W. Cousins1,3

1From the Bascom Palmer Eye Institute, Department of Ophthalmology, University of Miami School of Medicine, Miami, Florida; the 2Miami Veteran Affairs Medical Center, Miami, Florida; and 3The Duke Center for Macular Diseases, Duke University Eye Center, Durham, North Carolina.

PURPOSE. Oxidative injury to the retinal pigment epithelium (RPE) has been proposed to be an important injury stimulus relevant to the accumulation of subretinal deposits in age-related macular degeneration (AMD). Cigarette smoking is a major risk factor for AMD, and cigarette smoke-related tar contains high concentrations of a potent oxidant, hydroquinone (HQ). This study was an investigation of the effects of cigarette smoke (CS) and HQ in the development of sub-RPE deposits in an experimental mouse model.

METHODS. Sixteen-month-old C57BL/6 female mice were fed a high-fat diet (HFD) for 4.5 months. Mice were divided into two major experimental groups, one to examine the effects of cigarette smoke and one to study the effects of a defined cigarette smoke component such as HQ. In the first group, mice eyes were exposed to blue-green light (positive controls) or to whole cigarette smoke. A third group with no intervention served as the negative control. In the second experimental group, animals received a purified diet with HQ (0.8%) with low or high fat content for 4.5 months. Mice in both groups were euthanatized at 4.5 months and eyes processed for transmission electron microscopy.

RESULTS. As previously demonstrated by our laboratory and others, most mice fed an HFD without other oxidant exposure demonstrated normal morphology or, in a few cases, small nodular basal laminar deposits. Eyes of mice exposed to whole cigarette smoke or to HQ in the food demonstrated a variable degree of basal laminar deposits and diffusely thickened Bruch’s membrane. The choriocapillaris endothelium was variably hypertrophic.

CONCLUSIONS. Exposure to cigarette smoke or the smoke-related redox molecule, HQ, results in the formation of sub-RPE deposits, thickening of Bruch’s membrane, and accumulation of deposits within Bruch’s membrane. Smoke-related oxidants may be another oxidative injury stimulus to the choriocapillaris and RPE, and may explain the association between cigarette smoking and early AMD.




This article has been cited by other articles:


Home page
 IOVSHome page
A. O. Edwards, D. Chen, B. L. Fridley, K. M. James, Y. Wu, G. Abecasis, A. Swaroop, M. Othman, K. Branham, S. K. Iyengar, et al.
Toll-like Receptor Polymorphisms and Age-Related Macular Degeneration
Invest. Ophthalmol. Vis. Sci., April 1, 2008; 49(4): 1652 - 1659.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
K. Kiuchi, M. Matsuoka, J. C. Wu, R. Lima e Silva, M. Kengatharan, M. Verghese, S. Ueno, K. Yokoi, N. H. Khu, J. P. Cooke, et al.
Mecamylamine Suppresses Basal and Nicotine-Stimulated Choroidal Neovascularization
Invest. Ophthalmol. Vis. Sci., April 1, 2008; 49(4): 1705 - 1711.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
O. Alcazar, S. W. Cousins, and M. E. Marin-Castano
MMP-14 and TIMP-2 Overexpression Protects against Hydroquinone-Induced Oxidant Injury in RPE: Implications for Extracellular Matrix Turnover
Invest. Ophthalmol. Vis. Sci., December 1, 2007; 48(12): 5662 - 5670.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
V. Justilien, J.-J. Pang, K. Renganathan, X. Zhan, J. W. Crabb, S. R. Kim, J. R. Sparrow, W. W. Hauswirth, and A. S. Lewin
SOD2 Knockdown Mouse Model of Early AMD
Invest. Ophthalmol. Vis. Sci., October 1, 2007; 48(10): 4407 - 4420.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Z. Wu, T. W. Lauer, A. Sick, S. F. Hackett, and P. A. Campochiaro
Oxidative Stress Modulates Complement Factor H Expression in Retinal Pigmented Epithelial Cells by Acetylation of FOXO3
J. Biol. Chem., August 3, 2007; 282(31): 22414 - 22425.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
L. Jia, Z. Liu, L. Sun, S. S. Miller, B. N. Ames, C. W. Cotman, and J. Liu
Acrolein, a Toxicant in Cigarette Smoke, Causes Oxidative Damage and Mitochondrial Dysfunction in RPE Cells: Protection by (R)-{alpha}-Lipoic Acid
Invest. Ophthalmol. Vis. Sci., January 1, 2007; 48(1): 339 - 348.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
P. T.V.M. de Jong
Age-Related Macular Degeneration
N. Engl. J. Med., October 5, 2006; 355(14): 1474 - 1485.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the Association for Research in Vision and Ophthalmology