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J Sex Med. 2014 Feb;11(2):454-61. doi: 10.1111/jsm.12376. Epub 2013 Nov 20.

Mitochondrial impairment and oxidative stress in leukocytes after testosterone administration to female-to-male transsexuals.

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Endocrinology Service, Foundation for the Promotion of Healthcare and Biomedical Research in the Valencian Community (FISABIO), University Hospital Doctor Peset, Valencia, Spain; Endocrinology Service, University Hospital Doctor Peset, Valencia, Spain; Institute of Health Research INCLIVA, Valencia, Spain; Department of Pharmacology and CIBER CB06/04/0071 Research Group, CIBER Hepatic and Digestive Diseases, University of Valencia, Valencia, Spain; Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain.



Testosterone undecanoate (T) treatment is common in female-to-male transsexuals (FtMs) but can induce impairment of mitochondrial function and oxidative stress.


The effect of T treatment on the mitochondrial function and redox state of leukocytes of FtMs subjects was evaluated.


This was an observational study conducted in a university hospital. Fifty-seven FtMs were treated with T (1,000 mg) for 12 weeks, after which anthropometric and metabolic parameters and mitochondrial function were evaluated.


Anthropometric and metabolic parameters were evaluated. Mitochondrial function was studied by assessing mitochondrial oxygen (O2) consumption, membrane potential, reactive oxygen species (ROS) production, glutathione levels (GSH), and the reduced glutathione/oxidized glutathione (GSH)/(GSSG) ratio in polymorphonuclear cells.


T treatment led to mitochondrial impairment in FtMs as a result of a decrease in mitochondria O2 consumption, the membrane potential, GSH levels, and the (GSH)/(GSSG) ratio and an increase in ROS production. Mitochondrial O2 consumption and membrane potential negatively correlated with T levels, which was further confirmed that the T treatment had induced mitochondrial dysfunction. T also produced a significant increase in total testosterone, free androgenic index, and atherogenic index of plasma, and a decrease in sex hormone-binding globulin and high-density lipoprotein cholesterol.


Treatment of FtMs with T can induce impairment of mitochondrial function and a state of oxidative stress. This effect should be taken into account in order to modulate possible comorbidities in these patients.


Gender Dysphoria; Hormone Therapy in Female-to-Male Transsexuals; Leukocytes; Mitochondria; Oxidative Stress; Testosterone; Transsexuals

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