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Antioxidant effects of dexmedetomidine against hydrogen peroxide-induced DNA damage in vitro by alkaline Comet assay

BACKGROUND/AIM: Dexmedetomidine (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 eff...

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Detalles Bibliográficos
Autores principales: KOTANOĞLU, Mustafa S., KADIOĞLU, Ela, EMERCE, Esra, KAYMAK, etin, ZCAN, Ayşe, BAŞAR, Hlya
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Scientific and Technological Research Council of Turkey 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7491270/
https://www.ncbi.nlm.nih.gov/pubmed/31905495
http://dx.doi.org/10.3906/sag-1910-76
Descripción
Sumario:BACKGROUND/AIM: Dexmedetomidine (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 H(2)O(2)-induced DNA damage in human lymphocyte cell cultures in vitro by alkaline Comet assay. MATERIALS AND METHODS: Lymphocyte cell cultures were divided into 5 groups, as the negative control, solvent control, positive control, hydrogen peroxide (H(2)O(2); 150 μM) + DEX (1 μM; 2.5 μM; 5 μM), and H(2)O(2) (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. RESULTS: It was observed that H(2)O(2) 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. CONCLUSION: There 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 H(2)O(2)-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.