Abstract
The testis is known as an immunologically privileged organ. In particular, blood-testis barrier (BTB) formed by blood capillary endothelia in the interstitium and myoid cell layer, basement membrane and epithelial cells of the germ cell ducts preserves autoimmunogeneic germ cells from attack by the self immune system. However, the BTB at the rete testis (RT) and the tubuli recti (TR) is physiologically more weak than that at the seminiferous tubules (ST) in that the former is paritially permeable to anti-sperm antibodies and administered horseradish peroxidase (HRP). Cadmium chrolide (CdCl2), one of various environmental toxicants, is known to injure testicular capillary endothelia primarily with resultant necrosis of the both ST and interstitial tissues in rats and mice when treated with significant doses of CdCl2. In the present study, we investigated histopathological changes of testes in A/J mice treated with low doses of CdCl2 (1 mg/kg bw and 3 mg/kg bw) by examination of changes of the distribution of administered HRP and inherent IgG into the testes. The results showed that light microscopic appearance of the testicular sections looked intact and exhinbited normal spermatogenesis even in 3 mg/kg CdCl2-treatment. In control mice, many HRP-endocytosing macrophages were histochemically found through the interstitial tissues. In contrast, the endocytosis of HRP by testicular macrophages was apparently weakened and HRP stains were preferentially accumulated at the interstitial space around the TR and RT in CdCl2-treated mice. Furthermore, HRP stains were found to infiltrate into some intra- and inter-spaces of epithelial cells lining the ST, the TR and the RT of CdCl2-treated mice. However, it was noted that no HRP stain could be found in lumen of these tubules. On the other hand, the inherent IgG were homogenously distributed through the interstium and IgG-endocytosing macrophages were not observed in both control and CdCl2-treated mice. However, it was found that a few ST had been infiltrated by the inherent IgG in CdCl2-treated mice. Collectively, our results suggest that the low doses of CdCl2 do not evoke the spermatogenic disturbance however cause dysfunction of the testicular macrophages and injure the basement membrane of the ST, the TR and the RT. However, the breakdown of BTB by CdCl2 seemed to be not specific to the TR and the RT where the BTB is known to be incomplete.
