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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.

Author information

1
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.

Abstract

INTRODUCTION:

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

AIM:

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

METHODS:

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.

MAIN OUTCOME MEASURES:

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.

RESULTS:

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.

CONCLUSIONS:

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.

KEYWORDS:

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

PMID:
24251401
DOI:
10.1111/jsm.12376
[Indexed for MEDLINE]

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