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ORIGINAL RESEARCH article

Front. Endocrinol.
Sec. Reproduction
Volume 15 - 2024 | doi: 10.3389/fendo.2024.1501306
This article is part of the Research Topic A Lifecourse Perspective on Polycystic Ovary Syndrome (PCOS): Bridging Gaps in Research and Practice View all 9 articles

"Mitochondrial DNA oxidation and content in different metabolic phenotypes of women with Polycystic Ovary Syndrome."

Provisionally accepted
Mailén Rojo Mailén Rojo 1*Hernán Pérez Hernán Pérez 1Andrea Millan Andrea Millan 1Alejandra Duarte Alejandra Duarte 2María Constanza Pautasso María Constanza Pautasso 2Giselle Adriana Abruzzese Giselle Adriana Abruzzese 3ALICIA Motta ALICIA Motta 3Gustavo Daniel Frechtel Gustavo Daniel Frechtel 1Gloria Cerrone Gloria Cerrone 1*
  • 1 University of Buenos Aires, Buenos Aires, Argentina
  • 2 CONICET Institute of Immunology, Genetics and Metabolism (INIGEM), Buenos Aires, Buenos Aires, Argentina
  • 3 CONICET Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Buenos Aires, Buenos Aires, Argentina

The final, formatted version of the article will be published soon.

    Polycystic Ovary Syndrome (PCOS) affects 5-20% of reproductive-aged women. Insulin resistance (IR) is common in PCOS with consequent elevated risks of metabolic disorders and cardiovascular mortality. PCOS and obesity are complex conditions associated with Metabolic Syndrome (MS), contributing to cardiovascular disease and type 2 diabetes mellitus (T2D). Obesity and PCOS exacerbate each other, with central obesity driving metabolic changes. Mitochondrial dysfunction, characterized by oxidative stress and reduced antioxidant capacity, plays a key role in PCOS pathology.In our study, we investigated 81 women with PCOS, and 57 control women aged 16 to 46 years old. Relative mitochondrial DNA (mtDNA) content and its oxidation level (8-oxoguanine, 8-OxoG) were determined in peripheral blood leukocytes by the SYBR Green method real-time PCR. Our findings showed that patients with PCOS had decreased mtDNA content and increased oxidation damage. Stratifying these patients by metabolic profile, revealed a progressive decline in mtDNA content from the normal-weight control group to the MHO-PCOS and MUO-PCOS groups, suggesting that lower mtDNA content is linked to obesity and worse metabolic profile. However, mtDNA oxidation levels did not differ significantly among these groups. Additionally, the decline in mtDNA content and the increase in oxidation levels between controls and patients with PCOS lost significance when these relationships were adjusted for the HOMA index. This finding suggests that IR could be the main factor contributing to mitochondrial dysfunction in PCOS. Maintaining optimal mtDNA copies are crucial for mitochondrial and cell function, suggesting potential therapeutic targets for PCOSassociated metabolic disturbances.

    Keywords: Obesity, Oxidative damage, metabolic syndrome, Polycystyc ovary syndrome, mitochondrial DNA

    Received: 24 Sep 2024; Accepted: 17 Dec 2024.

    Copyright: © 2024 Rojo, Pérez, Millan, Duarte, Pautasso, Abruzzese, Motta, Frechtel and Cerrone. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Mailén Rojo, University of Buenos Aires, Buenos Aires, Argentina
    Gloria Cerrone, University of Buenos Aires, Buenos Aires, Argentina

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