Increased DNA and oxidative damage in PCOS: effect of elevated androgens : Oxidative Damage & Androgens in PCOS
Middle East Fertility Society Journal, cilt.31, sa.1, 2026 (ESCI, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 31 Sayı: 1
- Basım Tarihi: 2026
- Doi Numarası: 10.1186/s43043-025-00283-0
- Dergi Adı: Middle East Fertility Society Journal
- Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, EMBASE, Directory of Open Access Journals, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest)
- Anahtar Kelimeler: DNA damage, Hyperandrogenism, Inflammatory, Oxidative stress, Polycystic ovarian syndrome
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Purpose: Polycystic ovary syndrome (PCOS) is a complex endocrine disorder involving ovulatory dysfunction, hyperandrogenism, and metabolic disturbances. Systemic inflammation, mitochondrial dysfunction, and elevated oxidative stress have all been asscoiated to androgen excess in PCOS. This study aims to evaluate the impact of hyperandrogenemia on oxidative stress and DNA damage in PCOS patients. Methods: A prospective case–control study was conducted with 178 women between April and November 2022. The cohort included 112 PCOS patients diagnosed per Rotterdam criteria and 66 healthy controls. PCOS patients were divided into hyperandrogenic (HA-PCOS) and non-hyperandrogenic (non-HA PCOS) subgroups. Blood samples were used for the analysis of oxidative stress markers, lipid profiles, hormones, and metabolism. Results: The HA-PCOS group had significantly higher BMI than both non-HA PCOS and control groups (p < 0.05). Despite hormonal differences, metabolic syndrome prevalence did not differ significantly. In compared with controls, oxidative stress, inflammatory, and DNA damage markers were higher in both PCOS categories. Moreover, the HA-PCOS group showed significantly higher levels of oxidative stress markers (TOS, OSI), inflammatory cytokines (TNF-α, IL-6, IL-1β), and DNA damage compared to non-HA PCOS (p < 0.05). Conclusion: DNA damage, persistent inflammation, and elevated oxidative stress are all associated with hyperandrogenism in PCOS. These results highlight how excessive androgen may be linked to oxidative and inflammatory processes. Future research should explore therapeutic interventions targeting oxidative stress and inflammation in PCOS.