Objective: Nicotine is an important component of cigarette smoke. Nicotine administration may result in oxidative stress by inducing the generation of reactive oxygen species in the periphery and central nervous system. Numerous epidemiological studies have demonstrated an inverse relationship between cigarette smoking and the risk of developing PD and AD. Nicotine might be responsible for this effect. In this study we evalute the malondialdehyde and nitric oxide levels of hippocampus after subchronic nicotine administration.

Materials and Methods: 3-6 months and 12-24 months aged, 40 rats were used. We arranged 4 groups as; young nicotine, aged nicotine, young control and aged control. Each group include 10 male sprague dawley rats. Young nicotine and aged nicotine groups were treated for 18 days with twice daily subcutaneously injections of nicotine (0.45 mg/kg, as the hydrogen tartrate salt) (Sigma, USA) and at the same time young control and aged control groups were treated with isotonic saline by the same way. 15 hours after the final treatment animals were euthanized with ether inhalation. Following brain removal, the hippocampus were dissected out bilaterally. Malondialdehyde was determined by the double heating method of Draper and Hadley. Nitric oxide was determined by the Griess reaction, in which nitric oxide and nitrate were converted to nitrite.

Results: The malondialdehyde and nitric oxide levels of hippocampi represented no difference between groups.

Conclusion: The dosage of nicotine and the period that we administered, represented no oxidant or antioxidant effect. The antioxidant effect of nicotine may be dose spesific or period of administration may be the other fact.