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DOI 10.1159/000068765

Медицинская библиотека · Urologia internationalis · 2003

Total calcium content of sacs associated with inguinal hernia, hydrocele or undescended testis reflects differences dictated by programmed cell death.

Tanyel F Cahit, Ulusu N Nuray, Tezcan E Ferhan, Büyükpamukçu Nebil

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Аннотация

INTRODUCTION

Inguinal hernia and hydrocele are suggested to result from the persistence of smooth muscle (SM) which should undergo programmed cell death (PCD) after presenting transiently to propel the testis. Since Ca(2+) is involved in PCD, the Ca(2+) contents of the peritoneum and sacs associated with undescended testis, inguinal hernia and hydrocele were determined and compared.

MATERIALS AND

METHODS

Sacs were obtained from boys with undescended testis (n = 11), inguinal hernia (n = 22) and hydrocele (n = 10), and girls with inguinal hernia (n = 7). The calcium content of the sacs and peritoneal samples (n = 6) was determined through atomic absorption spectrophotometry. Calcium contents were compared according to their sources using the Mann-Whitney U test and p values of <0.05 were considered significant.

RESULTS

While revealing similar Ca(2+) contents as the peritoneum, sacs associated with undescended testis and hydrocele contained more Ca(2+) contents than the sacs of boys and girls with inguinal hernia (p < 0.05).

CONCLUSIONS

Sacs associated with inguinal hernia, which are known to contain SM all around the mesothelial layer, contain the least Ca(2+). Despite the decrease in SM, sacs associated with hydrocele contain more Ca(2+). Since PCD is associated with Ca(2+) overload and inhibition of Ca(2+) load inhibits PCD, differences in Ca(2+) content may reflect the inhibition of PCD at different stages and for different reasons in inguinal hernia or hydrocele of childhood.

Для цитирования: Tanyel F Cahit, Ulusu N Nuray, Tezcan E Ferhan, Büyükpamukçu Nebil. Total calcium content of sacs associated with inguinal hernia, hydrocele or undescended testis reflects differences dictated by programmed cell death.. Urologia internationalis. 2003. DOI: 10.1159/000068765.

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