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Abstract

°á·Ð
¼º¼÷ ¼öÄƹ鼭ÀÇ °Å¼¼±º, °Å¼¼ ¡¤ ½Ä¿°±º, °Å¼¼ ¡¤ AD25±º ¹× °Å¼¼ ¡¤
AD50±º¿¡¼­ Ç÷û testosterone, À½°æ, º¹ºÎÀü¸³¼± ¹× Á¤³¶¾ç¿±ÀÇ ¹«°Ô º¯È­
±×¸®°í À̵é Àå±â¿¡¼­ ÀϾ´Â apoptosis Çö»óÀ» Á¶»çÇÑ ¼ºÀûÀº ´ÙÀ½°ú °°´Ù.
1. °Å¼¼±º, °Å¼¼ ¡¤ ½Ä¿°±º, °Å¼¼ ¡¤ AD25±º ¹× °Å¼¼ ¡¤
AD50±ºÀÇ Ç÷û testosteroneÀÇ º¯È­´Â °Å¼¼ÈÄ ½ÃÀÏÀÌ °æ°úÇÒ¼ö·Ï °øÈ÷ °¨¼Ò
ÇÏ´Â °æÇâÀ» ³ªÅ¸³Â´Ù.
2. °Å¼¼±º, °Å¼¼ ¡¤ ½Ä¿°±º, °Å¼¼ ¡¤ AD50±º ¹× °Å¼¼ ¡¤
AD50±ºÀÇ À½°æ, º¹ºÎÀü¸³¼± ¹× Á¤³¶¾ç¿±ÀÇ ¹«°Ô´Â °øÈ÷ ¼­¼­È÷ °¨¼ÒÇÏ´Â °æ
ÇâÀ» ³ªÅ¸³Â´Ù.
3. ApoptosisÀÇ ¾ïÁ¦Çö»óÀº °Å¼¼±º ¹× °Å¼¼ ¡¤ ½Ä¿°±º¿¡ ºñÇÏ¿© °Å¼¼ ¡¤
AD25±º¿¡¼­´Â °üÂûµÇÁö ¾ÊÀ¸³ª °Å¼¼ ¡¤ AD50±º¿¡¼­´Â
apoptosisÀÇ ¾ïÁ¦ È¿°ú¸¦ ³ªÅ¸³Â´Ù.
4. Hemaloxylin-eosin¿°»ö°ú ApopTag in situ¿°»ö¿¡¼­ apoptosis´Â º¹ºÎÀü¸³¼±¿¡¼­ ÇöÀú
ÇÏ°Ô ³ªÅ¸³ª¸ç ±× ´ÙÀ½Àº Á¤³¶°ú À½°æÀÇ ¼øÀ̾ú´Ù.
ÀÌ»ó¼Ò°ßÀ¸·Î ¼º¼÷¹é¼­¿¡¼­ °Å¼¼ÈÄ¿¡ Ç÷û testothroneÀÇ °áÇÌÀ¸·Î º¹ºÎÀü¸³¼±, Á¤³¶¾ç¿±
¹× À½°æ¼øÀ¸·Î ¹«°Ô°¨¼Ò¸¦ ³ªÅ¸³ÂÀ¸¸ç apoptosis´Â Áõ°¡ÇÏ¿´°í °Å¼¼ ¡¤ AD50
±º¿¡¼­ actinomycin D°¡ À½°æ ¹× º¹ºÎÀü¸³¼±¿¡¼­ ÅðÈ­°úÁ¤À» Áö¿¬½ÃÅ°´Â °ÍÀ» °üÂûÇÒ ¼ö
ÀÖ¾ú´Ù.
#ÃÊ·Ï#
Testosterone is required for the development and maintenance of the male accessory
sex organs and their normal function. And it was reported that castration affect cells in
the adult male rat accessory sex glands by induction of programmed cell death
(apoptosis). So, in this study, the authors made an experiment to evaluate the effect of
testosterone in the maure male rat penis and accessory sex glands following castration.
Also, we utilized actinomycin D, a potent inhibitor of messenger and ribosomal RNA
synthesis, in the experiment herein to assess the significance of regression process in
the glands.
Following are the changes in the serum testosterone level, the weight of the penis,
ventral prostate and seminal vesicles and apoptosis occurrence of the control (castration,
castration¡¤normal saline) and experimental (castration AD25, castration ¡¤
AD50) group of mature rats.
1. After castration, the control group and the experimental group showed decreased
level of serum testosterone.
2. In the both groups, the weight of the penis, ventral prostate and seminal vesicles
decreased gradually.
3. Compared to the control group, the castration¡¤AD25 did not show
the inhibition of castration induced regression of penis and ventral prostate. However,
castration ¡¤ AD50 showed the inhibition.
4 In the H-E staining and ApoTag in situ staining, the ventral prostate showed the
most prominent apoptosis occurrence followed by the seminal vesicles and penis.
These results suggest that after castration of the mature rat, due to testosterone
deficiency, the weight of penis, ventral prostate and seminal vesicles decreased with the
occurrence of apoptosis. Also, actinomycin D 50 §¶ seems to delay the regression
process.

Å°¿öµå

Rat penis; Testosterone; Apoptosis;

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