Testosterone Depletion Following Leydig Cell Destruction by EDS Induces Testicular Germ Cell Apoptosis and May Involve Granzyme Variants.

Dutta, Dibyendu; Guililat, Hiwot; Park, In; Sang, Samuel; Mills, Nathaniel

doi:10.1093/biolreprod/83.s1.533

Biology of Reproduction

2010

DOI: 10.1093/biolreprod/83.s1.533

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Testosterone Depletion Following Leydig Cell Destruction by EDS Induces Testicular Germ Cell Apoptosis and May Involve Granzyme Variants.

Dibyendu Dutta

Hiwot Guililat

In Park

et al.

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“…Ethylene dimethane sulfonate (EDS) is a nonvolatile mild alkylating agent that selectively eliminates the mature Leydig cells (Dutta et al 2010;Zhang et al 2015) and depletes testosterone within 2 days post-EDS treatment (Woolveridge et al 2001). Testosterone depletion due to EDS treatment results in increased germ cell apoptosis and testosterone replacement can reverse the Leydig cell elimination effects by maintaining the germ cell viability (Henriksen et al 1995).…”

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Testosterone regulates granzyme K expression in rat testes

Dutta

Park

Guililat

et al. 2017

Endocrine Regulations

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Objective. Testosterone depletion induces increased germ cell apoptosis in testes. However, limited studies exist on genes that regulate the germ cell apoptosis. Granzymes (GZM) are serine proteases that induce apoptosis in various tissues. Multiple granzymes, including GZMA, GZMB and GZMN, are present in testes. Th us, we investigated which granzyme may be testosterone responsive and possibly may have a role in germ cell apoptosis aft er testosterone depletion.Methods. Ethylene dimethane sulfonate (EDS), a toxicant that selectively ablates the Leydig cells, was injected into rats to withdraw the testosterone. Th e testosterone depletion eff ects aft er 7 days post-EDS were verifi ed by replacing the testosterone exogenously into EDS-treated rats. Serum or testicular testosterone was measured by radioimmunoassay. Using qPCR, mRNAs of granzyme variants in testes were quantifi ed. Th e germ cell apoptosis was identifi ed by TUNEL assay and the localization of GZMK was by immunohistochemistry.Results. EDS treatment eliminated the Leydig cells and depleted serum and testicular testosterone. At 7 days post-EDS, testis weights were reduced 18% with increased germ cell apoptosis plus elevation GZMK expression. GZMK was not associated with TUNEL-positive cells, but was localized to stripped cytoplasm of spermatids. In addition, apoptotic round spermatids were observed in the caput epididymis.Conclusions. GZMK expression in testes is testosterone dependent. GZMK is located adjacent to germ cells in seminiferous tubules and the presence of apoptotic round spermatids in the epididymis suggest its role in the degradation of microtubules in ectoplasmic specializations. Th us, overexpression of GZMK may indirectly regulate germ cell apoptosis by premature release of round spermatids from seminiferous tubule lumen.

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confidence: 99%

Testosterone regulates granzyme K expression in rat testes

Dutta

Park

Guililat

et al. 2017

Endocrine Regulations

Self Cite

View full text Add to dashboard Cite

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Testosterone Depletion Following Leydig Cell Destruction by EDS Induces Testicular Germ Cell Apoptosis and May Involve Granzyme Variants.

Cited by 1 publication

References 0 publications

Testosterone regulates granzyme K expression in rat testes

Testosterone regulates granzyme K expression in rat testes

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