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The function of the blood-testis barrier has been assessed from the ratio of the Cr-EDTA space in the parenchyma to the measured interstitial volume in the testes of rats at various times after unilateral ligation of the efferent ducts. The barrier remained effective during the phase of fluid accumulation and testicular mass gain, which was linear for at least 24 h, but the testis mass began to decrease between 32 and 40 h after efferent duct ligation, and the Cr-EDTA space at 40 and 48 h after efferent duct ligation exceeded the volume of the interstitial tissue. This finding indicated that, at these times, the barrier to Cr-EDTA, which is normally excluded from the tubules, had broken down and the marker was entering the tubules. Thereafter, the Cr-EDTA space decreased again to be less than the interstitial tissue volume, indicating a restoration of the barrier function, although degeneration of the seminiferous epithelium continued to become more obvious. The present study is the first report of a reversible breakdown of the barrier, but the relevance of the breakdown to the effects on spermatogenesis requires further study.
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The concentration of chromium51–EDTA in blood plasma after an intravenous infusion was found to be about 40 times that present in rete testis fluid and 20 times that in the additional seminiferous tubular fluid resulting from ligation of the efferent ducts. These values indicate the effectiveness of the blood–testis barrier to small water-soluble molecules, like Cr–EDTA. The volume of distribution in microlitres of Cr–EDTA in the parenchyma was about 60% of the volume of the interstitial tissue as determined on frozen sections by morphometry, and was similar, or slightly less, in the ligated testes, compared with the unligated testes. Heating the testes to 43°C for 30 min led to the expected reduction several days later in testis mass, but the volume of distribution of Cr–EDTA was no greater than that in the testes of control rats, and the ratio of Cr–EDTA space to interstitial tissue was not different, while the concentration of Cr–EDTA in the additional seminiferous tubular fluid increased only slightly as testis mass fell. These results indicate that the blood–testis barrier was only slightly less effective, if changed at all, during the period of spermatogenic disruption following local heating of the testis.
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Summary. A moderate reduction in testicular blood flow was observed in both testes 24 h after unilateral efferent duct ligation without any corresponding change in testosterone secretion as indicated in the peripheral blood, in testicular venous blood, or in testicular tissue fluid. At 21 days a pronounced unilateral decrease in blood flow was associated with the extensive degeneration of tubules in the testis on the ligated side. These changes were also associated with decreased testosterone secretion by the testis on the ligated side, although Leydig cell function was not abolished since testosterone in the tissue increased rather than decreased. It is therefore concluded that testicular blood flow may play an important role in the changes of testosterone secretion that follow unilateral efferent duct ligation.
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Summary. Concentrations of (+) and (−) gossypol were measured by high performance liquid chromatography after they were incubated with plasma proteins in vitro. The concentration of (−) gossypol decreased more than the concentration of (+) gossypol. A similar decrease in free gossypol concentrations in the blood plasma of rats was observed after intravenous infusion of gossypol enantiomers. The concentration of (−) gossypol was also found to be lower than the concentration of (+) gossypol at the blood–testis barrier. The biological effect of (−) gossypol probably results from its stereospecific binding to extra- and intracellular proteins in vivo and inhibition of the biological activity of some proteins.
Keywords: gossypol enantiomers; HPLC; protein binding; blood–testis barrier; rat
