Leydig 세포 이식

Abstract

It is ordinarily accepted that the synthetic testosterone administration is the choice of treatment for the primary testicular dysfunction. But recently not a few medical scientists reported that the long-standing testosterone replacement is not without side effects. For that reason, we tried to investigate a possibility of in vivo transplantation of Leydig cells as a new biologic androgen substitution therapy. The Leydig cells procured from 6 week-old male Sprague-Dawley rat were auto- transplanted and the level of testosterone secretion and histostructural changes were observed.The results obtained are summarized as follows :1. For the selection of transplantation sites, compared to subcutaneous or scrotal counterparts, renal subcapsular and intraperitoneal transplant showed higher levels of testosterone and the number of transplanted cells was correlated with the level of measured testosterone. 2. Furthermore, if the Leydig cells were transplanted intraperitoneally after the uptake on synthetic collagen, testosterone levels were higher than the ones simply transplanted, resulting in 2.7 times higher at 3 months. 3. The activity of 125-I-hCG decreased 20 to 40% at each month after transplantation compared to the normal levels, but no statistical significance was noted among different periods. 4. Histologic examination revealed neovascularized capillaries and well demarcated uptake of sheet-like group of eosinophilic Leydig cells were observed at 4 weeks. But the evidence of destructive changes such as a focal inflammation with central dystropic ossification was noted after S month. On electron microscopy, the marked indentation of nucleus and presence of lipochrome pigment were seen and the number and size of smooth endoplasmic reticulum and mitochondria were reduced. In conclusion, testosterone output could be increased to the physiologic range by increasing the number of transplant cells or collagen uptake utilizing, etc. However the decrease of testosterone production after 3 months is believed to be a result of focal inflammation and degeneration which in turn caused the decrease in number of secreting Leydig cells and reduced activity of hCG receptors. Further effort is necessary on delaying or preventing the structural and functional decrement of Leydig cells.