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Experimental Diabetes Research
Volume 2012 (2012), Article ID 349320, 7 pages
http://dx.doi.org/10.1155/2012/349320
Research Article

Nicotine Exposure Exacerbates Development of Cataracts in a Type 1 Diabetic Rat Model

1Department of Ophthalmology and Visual Sciences, University of Texas Medical Branch at Galveston, Galveston, TX 77555, USA
2Center for Biomedical Engineering, University of Texas Medical Branch at Galveston, Galveston, TX 77555, USA
3Endocrinology, Department of Internal Medicine, Division of Endocrinology & Metabolism, University of Texas Medical Branch at Galveston, Galveston, TX 77555, USA

Received 6 April 2012; Accepted 6 August 2012

Academic Editor: Åke Lernmark

Copyright © 2012 Nima Tirgan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Diabetes and smoking are known risk factors for cataract development. In this study, we evaluated the effect of nicotine on the progression of cataracts in a type 1 diabetic rat model. Diabetes was induced in Sprague-Dawley rats by a single injection of 65 mg/kg streptozotocin. Daily nicotine injections were administered subcutaneously. Forty-five rats were divided into groups of diabetics with and without nicotine treatment and controls with and without nicotine treatment. Progression of lens opacity was monitored using a slit lamp biomicroscope and scores were assigned. To assess whether systemic inflammation played a role in mediating cataractogenesis, we studied serum levels of eotaxin, IL-6, and IL-4. The levels of the measured cytokines increased significantly in nicotine-treated and untreated diabetic animals versus controls and demonstrated a positive trend in the nicotine-treated diabetic rats. Our data suggest the presence of a synergistic relationship between nicotine and diabetes that accelerated cataract formation via inflammatory mediators.