Ünüvar S.Aktay G.2024-08-042024-08-0420101015-3918https://doi.org/10.1501/eczfak_0000000552https://hdl.handle.net/11616/90805We examined the tissue thiobarbituric acid reactive substances (TBARS), non-protein thiol (NP-SH) and total thiol (T-SH) group levels in order to deduce the role of cyclooxygenase-2 (COX-2) pathway on nicotine-induced oxidative tissue damage. Wistar Albino male rats were divided into three groups: Group I; 0.9% saline (ip), Group II; nicotine ditartarate (1.5 mg/kg, ip), Grup III; celecoxib (15 mg/kg, ip)+nicotine ditartarate (1.5 mg/kg ip). At the end of the 7th day, liver, lung, kidney, heart and brain tissues were removed. Nicotine treatment significantly increased TBARS, NP-SH and T-SH levels in all tissues. However, celecoxib treatment prior the nicotine injection, significantly decreased the TBARS levels and T-SH contents in all tissues in addition to NP-SH content in kidney, liver, lung and brain compared to nicotine group. Nicotine treatment caused excessive production of free radicals and evoked the antioxidant molecules. However, inhibition of cyclooxygenase-2 selectively prevented the nicotine-induced oxidative tissue damage dramatically. We concluded that, cyclooxygenase-2 pathway may be a notable mechanism of the nicotine toxicity.eninfo:eu-repo/semantics/openAccessAntioxidant activityCyclooxygenase-2Lipid peroxidationNicotine toxicityOxidative stressArticle391354210.1501/eczfak_00000005522-s2.0-84888124270Q4