Aida Abdeen Mahmoud - Department of Medical Biochemistry, Faculty of Medicine, Sohag University, Egypt.
Hekmat Abdel-Aziz - Department of Medical Histology, Sohag University, Egypt and of
Mohamed Elbadr - Department of Medical Pharmacology, Faculty of Medicine, Assiut University, Egypt.
Hala ELBadre - Department of Medical Biochemistry, Faculty of Medicine, Assiut University, Egypt.

Background: Tobacco use is responsible for millions of preventable deaths due to cancer. Nicotine, an alkaloid chemical found in tobacco was proved to cause chronic inflammation and oxidative stress. The transcription factor STAT۱ induces the expression of many proinflammatory genes and has been suggested to be a target for anti-inflammatory therapeutics. The following study investigated the effect of Nicotine on STAT۱ pathway and oxidative stress in rat lung tissue.  Methods: Thirty rats were divided into ۳ groups; group I considered as control, group II; its rats were daily injected with Nicotine at a dose of ۰.۴ mg/۱۰۰ gm body for ۸ successive weeks and group III; its rats were daily injected with Nicotine as group II, but the injection was stopped for another ۴ weeks. STAT۱α protein was assessed by immunohistochemistry, COX-۲ and iNOS genes expression were evaluated by real time PCR and thiobarbituric acid reactive substances (TBARS) and total thiols were measured using spectrophotometric methods in the lung tissues of the rats. Results: The results of the study revealed that group II rats had the highest expression of STAT۱α protein and COX-۲ and iNOS genes and oxidative stress in their lung tissues. Nicotine cessation for ۴ weeks caused a marked reduction in the expression of STAT۱α protein, COX-۲ and iNOS genes and oxidative stress. Conclusions: Induction of STAT۱ pathway and the increase in oxidative stress may be the mechanisms through which Nicotine may induce its harmful effects.

COX-۲, iNOS, Nicotine, Oxidative stress, STAT۱.