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Cadmium accumulation and binding characteristics in intact Sertoli/germ cell units, and associated effects on stage-specific functions in vitro: insights from a shark testis model

✍ Scribed by Leon M. McClusky


Book ID
102293856
Publisher
John Wiley and Sons
Year
2008
Tongue
English
Weight
225 KB
Volume
28
Category
Article
ISSN
0260-437X

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✦ Synopsis


Abstract

The increased human use of cadmium (Cd) and its increased occurrence in the environment is of concern. The testis is sensitive to Cd because of the steroid‐mediated regulation of spermatogenesis, high levels of DNA synthesis and gene transcription, all of which varies in a stage‐related manner. Validated techniques (acridine orange vital staining to detect apoptosis and dextran‐rhodamine exclusion to assess blood–testis barrier function) were recently developed and the shark testis was proposed as an alternative model for assessing stage‐specific functions in living testicular tissue and to study toxicant actions on spermatogenesis. The present paper shows that ^109^Cd accumulation and binding in vitro was stage‐dependent (premeiotic, PrM > meiotic, M > postmeiotic, PoM), rapid and persisted in spermatocysts (intact germ cell/Sertoli cell units) 49 h after washout. In competitive binding analyses of all three spermatocyst stages, Hg, but not Zn, could replace bound ^109^Cd, suggesting that Cd binding was specific. These findings were associated with a biphasic apoptotic response in the PrM spermatocysts, which was maximal at 10 µm CdCl~2~ and 1 µm CdCl~2~ after 2 and 4 days in culture, respectively. Although Cd uptake in PoM cysts was more than 2‐fold less than uptake in PrM cysts, the percentage dextran‐rhodamine permeant PoM cysts was ∼8‐fold greater than in controls in the presence of both 10 µm CdCl~2~ and 30 µm CdCl~2~ after 4 days culture, indicating that blood–testis barrier function in PoM spermatocysts was compromised. These findings demonstrate that this model has utility for use in screening assays of environmental toxicants. Copyright © 2007 John Wiley & Sons, Ltd.