Effect of Nicotine on Retinal Degeneration in Laboratory Mice – A Route-dependent Study

Nicotine, the major addictive, and psychoactive alkaloid present in tobacco products has been used by a large population. Although the role of tobacco smoke on various disorders in different organs, such as lungs, liver, kidney, gonads, and eyes, has been studied, scanty reports elucidate the action of nicotine on ocular health disorders. The current investigation aimed to evaluate the deteriorative effect of nicotine via intraperitoneal and oral routes on retina of Swiss albino mice. Nicotine ditartrate salt at a dose of 1mg/kg b.wt. was injected intraperitoneally and fed by oral gavage to mice for 30 consecutive days. Ocular tissues were dissected out and subjected to histological observation and oxidative stress (SOD, CAT enzyme activities, MDA and GSH levels) analysis. Histological studies showed that nicotine administration caused loss and displacement of cellular components from the RPE, PRC, INL and GCL layers that led to alterations in the thickness of these layers. Nicotine administration caused an elevation of lipid peroxidation and suppression of SOD and catalase enzyme activities and reduced glutathione levels. Intraperitoneal administration of nicotine caused stronger suppression of antioxidative defense and strongly elevated lipid peroxidation than orally treated experimental mice. Specific grading to determine retinal degeneration suggested that mice receiving nicotine intraperitoneally had marked retinal degeneration and mice receiving nicotine orally had mild retinal degeneration. The data showed stronger deterioration of retinal tissues in intraperitoneally administered nicotine-treated mice than that in orally treated mice. Thus, the present study may suggest a route-dependent effect of nicotine on retinal degeneration in the studied mice.