Biology of Reproduction, Vol 57, 1275-1284, Copyright © 1997 by Society for the Study of Reproduction

ARTICLES

On the synthesis and secretion of rat seminiferous tubule proteins in vivo after ischemia and germ cell loss

TT Turner and DW Miller
Department of Urology, University of Virginia School of Medicine, Charlottesville 22908, USA.

This study was undertaken to determine whether alterations in Sertoli cell protein synthesis and secretion were important precursors to germ cell loss after ischemic insult to the testis. Ischemia was induced by a 1-h, 720 degrees spermatic cord torsion, and this was shown to cause a loss of germ cells over a 15-day period. Seminiferous tubules were perifused in vivo with [35S]methionine. Lumen fluid (LF) was collected by in vivo micropuncture, and seminiferous tubule extract (TE) was collected after tubule homogenization and centrifugation. Electrophoresis of proteins in these fluids followed by autoradiography of radiolabeled proteins allowed examination of synthesized, i.e., TE, and secreted, i.e., LF proteins. No consistent changes were detected in synthesized or secreted proteins prior to the major loss of germ cells; thus, major changes in the capacity of Sertoli cells for protein assembly and transport are not a preliminary feature of post-ischemia germ cell loss. Changes in specific protein synthesis and secretion were also modest in this in vivo environment after germ cell loss. Overall protein synthesis appeared reduced as loss of germ cells progressed, but one protein whose amino acid sequence confirmed identity with a testis-specific stress protein (hst70) was up-regulated after ischemia and germ cell loss.

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