• Mustafa Sirri Kotanoğlu, Ela Kadioğlu, Esra Emerce, Çetin Kaymak, Ayşe Özcan, and Hülya Başar.
• Department of Anesthesiology and Reanimation, Ankara Training and Research Hospital, University of Health Sciences, Ankara, Turkey
• Turk J Med Sci. 2020 Aug 26; 50 (5): 1393-1398.

Background/AimDexmedetomidine (DEX) is an alpha-2 adrenergic agonist that is commonly used as a sedative and anesthetic. The protective effects of DEX against oxidative damage under both in vitro and in vivo conditions have been demonstrated. It was aimed to evaluate and compare the protective effects of DEX and vitamin C (Vit C) on DNA against H2O2-induced DNA damage in human lymphocyte cell cultures in vitro by alkaline Comet assay.Materials And MethodsLymphocyte cell cultures were divided into 5 groups, as the negative control, solvent control, positive control, hydrogen peroxide (H2O2; 150 μM) + DEX (1 μM; 2.5 μM; 5 μM), and H2O2 (150 μM) + Vit C (1 μM; 2.5 μM; 5 μM), and incubated at 37 °C for 1 h. Cell viability was measured using the Trypan blue test. DNA damage was measured using the Alkali Comet Technique and the % percent tail intensity was evaluated. Statistical analysis was performed using 1-way ANOVA and the Tukey multiple comparison test.ResultsIt was observed that H2O2 significantly induced DNA damage in the lymphocytes and this damage was decreased significantly with Vit C and DEX. It was observed that Vit C at doses of 1 μM and 2.5 μM had a significantly stronger antioxidant effect, but there was no significant difference between the antioxidant effects of Vit C and DEX with a dose of 5 μM. The dose of 5 μM DEX was found to be the most effective in reducing oxidative DNA damage.ConclusionThere is limited data on the protective effects of DEX against oxidative DNA damage. The primary effect might be cytoprotection. The results herein showed that DEX was protective against H2O2-induced in vitro oxidative DNA damage in lymphocyte cell cultures in a dose-dependent manner. DEX might have a potential therapeutic value in the prevention of oxidative DNA damage in patients.This work is licensed under a Creative Commons Attribution 4.0 International License.

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