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This version published online on June 30, 2009
Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2009-0466
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Submitted on March 4, 2009
Accepted on June 24, 2009

Mitochondrial Complex I Impairment in Leukocytes from Polycystic Ovary Syndrome Patients with Insulin Resistance

Victor M. Victor*, Milagros Rocha, Celia Bañuls, Maria Sanchez-Serrano, Eva Sola, Marcelino Gomez, and Antonio Hernandez-Mijares*

University Hospital Doctor Peset Foundation, Avda Gaspar Aguilar 90, 46017, Valencia, Spain; University Hospital Doctor Peset, Endocrinology Service, Avda Gaspar Aguilar 90, 46017, Valencia, Spain; Department of Physiology, University of Valencia, Valencia, Spain; Department of Medicine, University of Valencia, and Research group CIBER CB/06/02/0045 Actions in Epidemiology and Public Health; University Hospital Doctor Peset Foundation, Avda Gaspar Aguilar 90, 46017, Valencia, Spain; University Hospital Doctor Peset, Endocrinology Service, Avda Gaspar Aguilar 90, 46017, Valencia, Spain; Department of Physiology, University of Valencia, Valencia, Spain; Department of Medicine, University of Valencia; and Research group CIBER CB/06/02/0045 Actions in Epidemiology and Public Health

* To whom correspondence should be addressed. E-mail: vmviktor{at}gmail.com or hernandez_antmij{at}gva.es.

Context: Insulin resistance is a feature of polycystic ovary syndrome (PCOS) and is related to mitochondrial function.

Objective: Our objective was to assess mitochondrial function by evaluating mitochondrial oxygen (O2) consumption, reactive oxygen species (ROS) production, levels of glutathione (GSH), the GSSG/GSH ratio, TNF{alpha} levels and membrane potential. Additionally, we have evaluated mitochondrial complex I as a target of the oxidative stress responsible for PCOS in polymorphonuclear cells (PMNs).

Design and Setting: This was a prospective controlled study conducted in an academic medical center.

Patients: The study population consisted of 20 lean reproductive-age women with PCOS and 20 body composition-matched controls.

Main Outcome Measures: We evaluated mitochondrial O2 consumption using the Clark-type O2 electrode, levels of ROS, GSH and membrane potential by means of fluorescence microscopy, TNF{alpha} levels by ELISA and complex I activity by spectrophotometric assay.

Results: An impairment in mitochondrial function was observed in PCOS patients, evident by a decrease in mitochondrial O2 consumption, an increase in ROS production, GSSG/GSH ratio and TNF{alpha} levels, a drop in GSH levels and an undermining of membrane potential. Furthermore, an impairment of mitochondrial complex I was identified.

Conclusion: This study supports the hypothesis of an association between insulin resistance and an impaired mitochondrial oxidative metabolism. We also propose that the oxidative stress responsible for PCOS takes place at complex I. These abnormalities may contribute to the increased risk of type 2 diabetes among women with PCOS.
Key words: ovary • ovarian syndrome • diabetes • cell biology • testosterone






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