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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 485306, 9 pages
http://dx.doi.org/10.1155/2010/485306
Research Article

Testosterone Depletion by Castration May Protect Mice from Heat-Induced Multiple Organ Damage and Lethality

1The Institute of Basic Medical Sciences, National Cheng Kung University School of Medicine, Tainan, Taiwan
2Department of Pharmacy, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan
3Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan
4Department of Obstetrics and Gynecology, Chi Mei Medical Center, Southern Taiwan University, Tainan, Taiwan
5Department of Biotechnology, Southern Taiwan University, Tainan, Taiwan

Received 1 December 2009; Accepted 3 February 2010

Academic Editor: Rene Anand

Copyright © 2010 Chian-Yuh Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

When the vehicle-treated, sham-operated mice underwent heat stress, the fraction survival and core temperature at +4 h of body heating were found to be 5 of 15 and 3 4 . 4 C ± 0 . 3 C , respectively. Castration 2 weeks before the start of heat stress decreased the plasma levels of testosterone almost to zero, protected the mice from heat-induced death (fraction survival, 13/15) and reduced the hypothermia (core temperature, 3 7 . 3 C ). The beneficial effects of castration in ameliorating lethality and hypothermia can be significantly reduced by testosterone replacement. Heat-induced apoptosis, as indicated by terminal deoxynucleotidyl- transferase- mediated 𝛼 UDP-biotin nick end-labeling staining, were significantly prevented by castration. In addition, heat-induced neuronal damage, as indicated by cell shrinkage and pyknosis of nucleus, to the hypothalamus was also castration-prevented. Again, the beneficial effects of castration in reducing neuronal damage to the hypothalamus as well as apoptosis in multiple organs during heatstroke, were significantly reversed by testosterone replacement. The data indicate that testosterone depletion by castration may protect mice from heatstroke-induced multiple organ damage and lethality.