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Protective role of HSF1 and HSP70 in rat testis apoptotic cells exposed to chronic hypobaric hypoxia
Author(s) -
Farias Jorge G.,
Oyarzun Daniela,
Zepeda Andrea
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1110.13
Subject(s) - hsp70 , apoptosis , hsf1 , hypoxia (environmental) , andrology , spermatogenesis , sertoli cell , oxidative stress , biology , immunohistochemistry , western blot , hyperthermia , medicine , endocrinology , heat shock protein , immunology , chemistry , genetics , gene , oxygen , organic chemistry
High altitude exposure is an unusual situation. However, this phenomenon is frequently found in the north of Chile, thanks to the continuous movement of mining workers at the Cordillera de los Andes. In rat testis, this condition known as chronic hypobaric hypoxia (CHH) induces oxidative stress and hyperthermia, conducing to apoptosis and hypospermatogenesis. The main objective of this work was to evaluate the expression of HSP70 and HSF1 in the spermatogenic stages in front of thermal stress induced by CHH and also to determine the apoptotic level. Teen‐weeks‐old male Wistar rats were exposed to normoxia and CHH, corresponding to 4600 m of simulated altitude for a period of 5, 15 and 30 days. Immunohistochemistry and western blot showed a significative and progressive increase in HSP70 expression in spermatogonias, spermatocytes and Sertoli cells along the exposure time. The transcription factor expression HSF1 in testis was also increased in CHH, but it was decreased after 30 days. Finally, apoptosis was increased in spermatogonias, spermatocytes and spermatids but decreased after 15 days in spermatids and after 30 days in spermatogonias and spermatocytes. In conclusion, testicular hyperthermia induced by the CHH exposure conduces to increase HSF1 and HSP70 expression, protecting cell integrity and attenuating the apoptotic effect induced by this condition. By grant: INNOVA CORFO‐Chile 06FCO11BC‐118