Nikotin toksisitesi üzerine seçici siklooksijenaz-2 inhibisyonunun etkisi

Abstract

Nikotinin, COX-2 enzimini indükleyerek, oksidatif stresi artırdıgı bilinmektedir. Bu bilgiye dayanarak seçici bir COX-2 inhibitörünün, siklooksijenaz (COX) yolagında serbest radikal olusumunu baskılayabilecegini ve buna baglı olarak nikotin toksisitesinin önlenebilecegini veya azaltılabilecegini düsündük. Bu amaçla, TBARS, GSH ve T-SH ile doku ve serumda çinko ve bakır dagılımları degerlendirildi. Nikotin toksisitesi ve toksisite üzerine seçici COX-2 inhibisyonunun etkisi incelendi. Tüm gruplar kontrol grubuyla karsılastırıldıgında: Kontrol grubuna göre; nikotin grubunun karaciger, akciger, böbrek, beyin ve kalp TBARS düzeylerinde anlamlı ( p<0.001 ) bir artıs bulundu. Kontrol grubuna göre; nikotin grubunun karaciger, akciger, böbrek, beyin ve kalp GSH düzeylerinde anlamlı (p<0.001) bir artıs bulundu. Kontrol grubuna göre; nikotin grubunun karaciger, akciger, böbrek, beyin ve TSH düzeylerinde anlamlı (p<0.001), kalp dokusunda anlamlı olmayan bir artıs bulundu. Kontrol grubuna göre; nikotin grubunun karaciger (p<0.05), akciger (p<0.001) çinko düzeylerinde anlamlı bir artıs, böbrek, beyin ve kalp çinko düzeylerinde anlamlı olmayan (p>0.05) bir artıs bulundu. Kontrol grubuna göre; nikotin grubunun karaciger, böbrek, beyin bakır düzeylerinde anlamlı olmayan bir artıs (p>0.05), akciger (p<0.01) ve kalp (p<0.05) bakır düzeylerinde anlamlı bir artıs bulundu. Kontrol grubuna göre, nikotin grubunun serum çinko düzeylerinde anlamlı bir artıs (p<0.001) bulundu. Nikotin grubuyla nikotin+selekoksib grubu karsılastırıldıgında: Nikotin grubuna göre nikotin+selekoksib grubunun karaciger, akciger, böbrek, beyin ve kalp TBARS düzeylerinde anlamlı (p<0.001) bir azalma bulundu. Nikotin grubuna göre nikotin+selekoksib grubunun karaciger(p<0.01), akciger, böbrek, beyin ve kalp GSH düzeylerinde anlamlı (p<0.001) bir azalma bulundu. Nikotin grubuna göre nikotin+selekoksib grubunun karaciger, böbrek, beyin ve akciger dokularının T-SH düzeylerinde anlamlı (p<0.001) bir azalma bulundu. Kalp dokusunun T-SH düzeylerinde istatistiksel olarak anlamlı olmayan bir azalma bulundu. Nikotin grubuna göre nikotin+selekoksib grubunun karaciger (p<0.01), akciger (p<0.001), böbrek (p<0.01), beyin (p<0.001), kalp (p<0.001) çinko düzeylerinde anlamlı bir azalma bulundu. Nikotin grubuna göre nikotin+selekoksib grubunun karaciger (p<0.05), akciger (p<0.001), böbrek (p<0.01), kalp (p<0.001) bakır düzeylerinde anlamlı bir azalma bulundu. Beyin (p>0.05) bakır düzeylerinde anlamlı olmayan bir azalma bulundu. Nikotin grubuna göre nikotin+selekoksib grubunun serum çinko düzeylerinde anlamlı olmayan bir azalma (p>0.05) bulundu. Anahtar Kelimeler: Nikotin, Siklooksijenaz-2, Lipit peroksidasyon, Antioksidan etki, Eser elementler.

It is known that nicotine increases the oxidative stress, inducing COX-2 enzyme. With this knowledge, we thought that a selective COX-2 inhibitor could swage the free radical constitution on the way of cycloxygenase and according to this, nicotine toxicity could be prevented or decreased. With this aim, with TBARS-GSH and T-SH in tissue and serum, the distribution of zinc and copper were evaluated. The effect of nicotine toxicity and the effect of selective COX-2 on toxicity were examined. When all groups were compared to control groups; Considering control group, a significant increase( P?0.001) was found on the TBARS levels of liver, lung, kidney, brain nicotine group. Considering control group, a significant increase (p?0.001) was found on the levels of liver, lung, kidney and heart GSH of nicotine group. Considering control group, a significant increase (p?0.001) was found on the levels of liver, lung, kidney, brain, heart T-SH of nicotine group. Considering control group, a significant increase was found on the levels of liver (p?0.05), lung (p?0.001), zinc and a non-significant increase (P?0.05) was found on the levels of kidney, brain, heart, zinc of nicotine group. Considering control group, a non-significant (P?0.05) increase on the levels of liver (P?0.01) and heart (P?0.05), copper was found. Considering control group, a significant increase ( P?0.001) was found on the levels of serum zinc. When nicotine group and celecoxibe groups were compared : Considering nicotine group, a significant decrease (P?0.001) was found on the levels of liver, lung, kidney, brain and heart TBARS of nicotine + celecoxibe group. Considering nicotine group, a significant decrease (P<0.001) was found on the levels of liver (P<0.01), lung, kidney, brain and heart GSH of nicotine + celecoxibe group. Considering nicotine group, a significant (P<0.001) was found on the T-SH levels of liver, kidney, brain tissues. A statistically significant decrease (P<0.001) was found on the T-SH levels of lung and heart tissues. Considering nicotine group, a significant decrease was found on the levels of liver (P<0.01), lung (P<0.001), kidney (P<0.001), heart (P<0.001) zinc of nicotine celecoxibe group. Considering nicotine group, on the levels of liver (P<0.05), lung (P<0.001), kidney (P<0.01), heart (P<0.001), copper, a significant level was found. A non-significant decrease was found on the levels of brain (P>0.05) copper of nicotine + celecoxibe group. Considering nicotine group, a non-significant decrease was found on the serum zinc levels of nicotine + celecoxibe group. Keywords: Nicotine, Cyclooxygenase-2, Lipid peroxidation, Antioxidant effect, Trace elements