title: Testosterone-induced hypertrophy, fibrosis and apoptosis of cardiac cells--an ultrastructural and immunohistochemical study.
abstract: BACKGROUND
  Androgen abuse is an increasing problem amongst professional and amateur athletes. Moreover, testosterone, apart from its widely accepted indications, is used for a variety of other indications such as aging and ischemia. Its actions are mainly attributed to a specific genomic mechanism through the androgen receptor, but emerging evidence reveals non-genomic effects as well. The use of androgens has been linked with several adverse effects. The purpose of this study was to examine the effects of testosterone on the morphology and the ultrastructure of the myocardium and to investigate the possible role of apoptosis.
  
  
  METHODS
  We used 12 adult male Wistar rats, separated into 2 groups. Group A consisted of 6 rats that were administered high doses of testosterone enanthate, while group B consisted of 6 male Wistar rats that received placebo (normal saline) intramuscularly. After the last day of treatment, all rats were anesthetized and sacrificed, and the hearts were removed and processed for optical and electron microscopy and immunohistochemical detection of caspase-3, an apoptosis marker.
  
  
  RESULTS
  We found significant myocardial hypertrophy along with abundant ultrastructural alterations. The immunohistochemical staining of the myocardial cells for caspase-3 was positive in group A (experimental group), which is interpreted as an activation of apoptosis by testosterone treatment.
  
  
  CONCLUSIONS
  Testosterone abuse has serious adverse effects, including myocardial hypertrophy, myocardial fibrosis and activation of apoptosis. These findings need to be taken into account whenever androgens are prescribed to improve performance or as hormone therapy.
authors.affiliation: Department of Histology-Embryology and Anthropology, Aristotle University of Thessaloniki, Thessaloniki, Greece.
authors.forename: Theodora
authors.initials: T
authors.lastname: Papamitsou
authors.forename: Dimitris
authors.initials: D
authors.lastname: Barlagiannis
authors.forename: Vasileios
authors.initials: V
authors.lastname: Papaliagkas
authors.forename: Eleni
authors.initials: E
authors.lastname: Kotanidou
authors.forename: Maria
authors.initials: M
authors.lastname: Dermentzopoulou-Theodoridou
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D024022:Fibrillar Collagens / Q000378:metabolism; D005355:Fibrosis; D006984:Hypertrophy; D007150:Immunohistochemistry; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000648:ultrastructure; D009206:Myocardium / Q000473:pathology* / Q000648:ultrastructure*; D009210:Myofibrils / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D053140:Organelle Shape / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013194:Staining and Labeling; D013739:Testosterone / Q000494:pharmacology*
chemical_list: D024022:Fibrillar Collagens; D013739:Testosterone