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.
Highlights
Cataract development affects over 50 million people worldwide leading to a decrease in visual function and a reduction in overall quality of life
We examined the effects of nicotine on diabetes-induced cataract formation in an animal model
We observed an increase in severity of cataracts among nicotine-treated diabetic rats as compared to the untreated diabetic rats
Summary
Cataract development affects over 50 million people worldwide leading to a decrease in visual function and a reduction in overall quality of life. Risk factors for cataract development include diabetes, glaucoma, smoking, ocular inflammation, trauma, advanced age, excessive sunlight exposure, and genetics. Numerous studies have demonstrated the prominent role of diabetes as a risk factor in the development of cataracts [1,2,3,4,5,6]. Cataract formation can be a secondary complication of uncontrolled hyperglycemia in diabetics. This is due to posttranslational modifications of lens proteins via nonenzymatic glycation reactions causing clouding of the lens. Various studies have investigated the formation of lens opacities in Streptozotocin- (STZ-) induced diabetic rat models. Zhang et al 2008 [13] observed initial stages of cataract formation macroscopically 3 weeks after induction of diabetes and whole lens opacity after 12 weeks. A hyperglycemic environment results in greater susceptibility of ocular tissue to further damage from environmental factors and stress
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