Leydig Cells Undergoing Apoptosis in the Perinatal Rat Testis.

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  • Yokoi Hiromichi
    Department of Anatomy and Cell Biology, The University of Tokushima School of Medicine
  • Yamama Yoshihiro
    Department of Anatomy and Cell Biology, The University of Tokushima School of Medicine
  • Tsuruo Yoshihiro
    Department of Anatomy and Cell Biology, The University of Tokushima School of Medicine
  • Kawarada Yoshihiko
    Department of Biochemistry, Akita University School of Medicine
  • Miura Naoyuki
    Department of Biochemistry, Akita University School of Medicine
  • Sugiyama Toshihiro
    Department of Biochemistry, Akita University School of Medicine
  • Ishimura Kazunori
    Department of Anatomy and Cell Biology, The University of Tokushima School of Medicine

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Abstract

It has been suggested that fetal Leydig cells in rat testes decrease in number just before or soon after birth. However, recent studies have indicated that during the perinatal period, the total number of the Leydig cells does not significantly change. The present study examined apoptotic cell death in the rat testis from embryonic day 18 to postnatal day 49. Apoptotic cells were examined by immunohistochemistry with an antibody against single-stranded DNA (ssDNA), and in situ terminal deoxynucleotidyl transferase staining (in situ TdT). During the perinatal period, ssDNA-immunopositive cells and in situ TdT-positive cells were scattered in the interstitium but were barely present in the seminiferous tubules. After postnatal day 7, the positive cells were abundant in the seminiferous tubules but scarce in the interstitium. Double-immunostaining for ssDNA and a steroidogenic enzyme, P450c17, demonstrated that parts of P450c17-positive Leydig cells were ssDNA-positive. Electron microscopic observations revealed that in situ TdT-positive cells had characteristic features of Leydig cells. These results suggest that fetal Leydig cells undergo apoptosis during the perinatal period, and that the number of Leydig cells is regulated by both the rate of cell proliferation and apoptotic cell death.

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