J Skin Stem Cell. 2019 December; 6(4):e103492. Published online 2020 May 13. doi: 10.5812/jssc.103492. Research Article 8-OHdG and hOGG1 as Oxidative DNA Damage Markers in Acne Vulgaris Patients Under Isotretinoin Treatment Muzeyyen Izmirli 1, * , Hasret Ecevit 1 , Hamza Malik Okuyan 1 and Eminenur Rifaioglu 1 1 Mustafa Kemal University, Antakya, Turkey * Corresponding author: Mustafa Kemal University, Antakya, Turkey. Email: muzeyyenizmirli@gmail.com Received 2020 April 07; Revised 2020 April 15; Accepted 2020 April 17. Abstract Background: Acne vulgaris is the most common inflammatory skin disease. It is primarily observed in adolescents and is char- acterized by comedones, papules, pustules, nodules, and cysts on the face, back, chest, chin, and body skin. Acne vulgaris affects about 80% of teenagers and continues beyond the age of 25 years in 3% of men and 12% of women in the world. Isotretinoin is one of the most common treatment agents for acne vulgaris, which causes oxidative DNA damage in the cell. As an important indicator of oxidative DNA damage, 8-hydroxy-2’-deoxyguanosine is repaired with an enzyme called human 8-oxoguanine DNA glycosylase 1 (hOGG1). Objectives: We aimed to evaluate oxidative DNA damage in acne vulgaris before and after isotretinoin treatment by measuring the 8-OHdG and hOGG1 levels. Methods: The 8-OHdG and hOGG1 levels were evaluated from serum samples using the enzyme-linked immunosorbent assay (ELISA) method. Both the serum 8-OHdG (P < 0.05; P < 0.0001) and hOGG1 (P < 0.05; P = 0.04) levels were found to be statistically higher in the sixth month after isotretinoin treatment. Results: In this first report, the 8-OHdG and hOGG1 levels were found to be statistically significantly high after isotretinoin treat- ment. According to our results, the 8-OHdG level increased under isotretinoin administration in acne vulgaris patients. Conclusions: Consequently, healing via hOGG1 likely continues after dropping isotretinoin for DNA. Keywords: Acne, 8-Hydroxy-2’-Deoxyguanosine, Human 8-Oxoguanine DNA Glycosylase 1, Isotretinoin 1. Background Acne vulgaris is the most common inflammatory skin disease, which is primarily observed in adolescents. It is characterized by comedones, papules, pustules, nodules, and cysts on the face, back, chest, chin, and body skin (1). Acne vulgaris affects about 80 percent of people worldwide (2). Four major factors, including excessive sebum pro- duction, hyper-cornification of the pilosebaceous canal, abnormal colonization of Propionibacterium acnes, and in- flammation, play a role in the pathogenesis of the dis- ease (3). As one of the most common treatment agents, isotretinoin can be used for the acne vulgaris treatment and can resolve major etiologic factors in acne pathogen- esis. However, it leads to oxidative damage (4, 5). The hydroxyl radical (OH ) as the oxygen free radical is the most reactive member that reacts with biological molecules such as DNA, which is an important target for free radicals (6). Herein, 8-hydroxy-2’-deoxyguanosine (8- OHdG) is the most common base damage marker for DNA (7). The human 8-oxoguanine DNA glycosylase 1 (hOGG1) enzyme plays a role in a base excision repair mechanism and can repair 8-OHdG (8). Isotretinoin is known to cause oxidative damage. How- ever, hOGG1, as an enzyme used for the 8-OHdG repair mechanism, has not been evaluated in acne. Moreover, the effects of 8-OHdG and levels of its DNA repair enzyme, hOGG1, are unclear on acne vulgaris before and after the isotretinoin treatment. 2. Objectives We evaluated the effect of 8-OHdG and its repair enzyme, hOGG1, on acne vulgaris before and after the isotretinoin treatment. 3. Methods Study population: In the current study, blood samples were taken from individuals referring to the Department Copyright © 2020, Journal of Skin and Stem Cell. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.