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Expression of Hsp70-2 in rhesus monkey testis during germ cell apoptosis induced by testosterone undecanoate

Xin-Chang Zhou1, Zhi-Hong Zhang, Zhao-Yuan Hu

  • 1State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.

Contraception
|November 22, 2002
PubMed

Insights

High doses of testosterone undecanoate (TU) induce germ cell apoptosis in monkey testes. Heat shock protein 70-2 (Hsp70-2) levels do not prevent early-stage germ cell apoptosis, suggesting a limited role in mitigating TU-induced effects.

Area of Science:

  • Reproductive biology
  • Molecular biology
  • Cellular stress response

Background:

  • Heat shock protein 70-2 (Hsp70-2) acts as a molecular chaperone involved in protein folding and assembly.
  • Hsp70-2 is implicated in mechanisms that inhibit apoptosis.
  • Testosterone undecanoate (TU) is used to suppress spermatogenesis, but its effects on germ cell apoptosis and Hsp70-2 require investigation.

Purpose of the Study:

  • To investigate the association between the Hsp70-2 gene and germ cell apoptosis induced by high-dose testosterone undecanoate (TU) in monkey testes.
  • To compare DNA fragmentation and Hsp70-2 expression in TU-treated versus normal monkey testes.

Main Methods:

  • In situ analysis of DNA fragmentation using TUNEL assay.
  • Quantitative assessment of Hsp70-2 mRNA and protein expression levels.
  • Comparison between testes from TU-treated monkeys and normal control monkeys at various time points (Day 7, 30, and 60 post-injection).

Main Results:

  • Significant germ cell apoptosis was observed in monkey testes by Day 30 after TU injection.
  • Hsp70-2 mRNA levels showed a slight decrease, while Hsp70-2 protein levels remained largely unchanged during the early stages (Day 7-30) of TU-induced germ cell apoptosis.
  • Both Hsp70-2 mRNA and protein levels decreased dramatically by Day 60, coinciding with extensive germ cell depletion.

Conclusions:

  • High-dose TU induces significant germ cell apoptosis in monkey testes, potentially leading to spermatogenesis failure.
  • Hsp70-2 does not appear to play a protective role against early-stage germ cell apoptosis induced by TU.
  • The observed decrease in Hsp70-2 levels at later stages suggests a potential consequence rather than a preventative mechanism against TU-induced germ cell apoptosis.

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