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Mol. Hum. Reprod. Advance Access originally published online on April 4, 2009
Molecular Human Reproduction 2009 15(6):363-371; doi:10.1093/molehr/gap024
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© The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

A molecular evaluation of germ cell death induced by etoposide in pubertal rat testes

Rina J. Ortiz, Carlos Lizama, Verónica A. Codelia and Ricardo D. Moreno1

Departamento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile

1 Correspondence address. Fax: +56-2-222-5515; E-mail: rmoreno{at}bio.puc.cl

Etoposide is widely used in the treatment of patients with testicular cancer. The mechanism underlying apoptosis induction in cancer cells has been studied in different cell types, but it is not known whether the same factors participate in viable germ cells undergoing programmed cell death. Since testicular cancer primarily affects young males, we used pubertal rats (21 days old) as a model to determine different apoptotic parameters after etoposide treatment in healthy testes. We found that one intratesticular injection of etoposide (1.2 µg/testis) induced a significant increase in spermatocytes undergoing apoptosis, along with activation of caspase-9, -8 and -3 after 24 h of treatment. Spermatocyte apoptosis was inhibited when a general caspase inhibitor was added along with etoposide. Etoposide induces a significant stabilization/activation of p53, resulting in an increase level of this protein. The mRNA of Bcl-2 antagonist of cell death (BAD), a pro-apoptotic gene and a transcriptional target of p53, was significantly increased after etoposide treatment. Thus, our results suggest a single injection of etoposide induces apoptosis in healthy pachytene spermatocytes mediated by p53 and caspase activation. These findings will assist the search for new therapies to prevent the deleterious effect of cancer drugs upon normal cells.

Key words: spermatogenesis/spermatocyte/caspase/etoposide/cancer

Submitted on January 9, 2009; resubmitted on March 3, 2009; accepted on March 18, 2009.


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