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Effects of morphine on testosterone levels in rat C6 glioma cells: Modulation by anastrozole
Author(s) -
Ceccarelli Ilaria,
Rossi Antonella,
Maddalena Melinda,
Weber Elisabetta,
Aloisi Anna Maria
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21830
Subject(s) - testosterone (patch) , aromatase , testosterone propionate , anastrozole , medicine , endocrinology , aromatase inhibitor , morphine , leydig cell , radioimmunoassay , hypothalamus , chemistry , androgen , luteinizing hormone , hormone , cancer , breast cancer
Abstract Rat C6 glioma cells are commonly used to investigate the functions of glial cells. To evaluate the presence of testosterone and its metabolism in rat C6 glioma cells, we cultured them in media with or without the addition of testosterone propionate and anastrozole, a blocker of aromatase, the enzyme needed to transform testosterone into estradiol. The same procedure was repeated with morphine (10 and 100 µM), known to decrease testosterone levels in the brain (in rats) and plasma (in rats and humans). Confluent cells were exposed to the test media for 48 h and then collected. Cell pellets were used to determine testosterone by radioimmunoassay. The C6 cells contained detectable levels of testosterone and the levels increased with the addition of testosterone to the medium. Aromatase blockage by anastrozole increased cellular levels of testosterone regardless of the addition of exogenous testosterone. Both concentrations of morphine dose‐dependently decreased testosterone levels in the C6 cells; this effect was also present with the contemporary administration of anastrozole. Our findings show that testosterone is present in rat C6 glioma cells and can be metabolized by aromatase. Moreover, the presence of morphine in the culture medium strongly decreased testosterone, demonstrating that the glia would be a target of the morphine‐induced hypogonadal effect. J. Cell. Physiol. 221: 1–4, 2009. © 2009 Wiley‐Liss, Inc