Changes in the Peritubular Tissue of Rat Testis after Cadmium Treatment

Abstract

The present study demonstrates histological and immunohistochemical changes in the peritubular testicular tissue of rat testis after application of cadmium chloride. After 5-day cadmium exposure, advanced deterioration of the boundary testicular tissue, mainly oedema, disarrangement of collagen fibres and peritubular cells, dilatation and thrombosis of blood vessels were observed. Changes in the boundary tissue were accompanied with desquamation of the germinal epithelium. Immunohistochemically, positive reaction for alpha-smooth muscle actin and desmin in tunica media of large testicular blood vessels basically was not affected. No reaction for vimentin was seen in endothelial cells of blood capillaries, whereas positive reaction presented only these cells in large blood vessels. The myofibroblasts positively reacting for desmin and alpha-smooth muscle actin form a single incomplete layer in the lamina propria of seminiferous tubules. Vimentin reactivity in the myofibroblasts and in the supporting Sertoli cells as well as Leydig cells in damaged testicular tissue was not observed. An increase in fibroblasts and free inflammatory cells positive for vimentin in the peritubular space on the peripheric area of the testis was observed.

Toxic effects of cadmium on testis of birds and mammals: A review

“…Cd inhibit the assembly of Sertoli cells TJ-permeability barrier and decreased synthesis and/or expression of proteins by promoting protein redistribution at the Sertoli-Sertoli cell interface. Tight junction proteins occludin, N-cadherin and vimentin were partially or completely disrupted by a cadmium injection (Janecki et al, 1992;Hew et al, 1993a;Bekheet, 2010;Marettová et al, 2010). As the time after Cd exposure increased, the lesion within a stage occured with increasing severity, and later stages of the cycle of the seminiferous epithelium were also affected.…”

“…All testicular germ cell populations can by affected by Cd. This includes a decrease in number of spermatogonia and spermatocytes, aberrant morphology in all developing stages, release of immature cells into the lumen (Aoyagi et al, 2002;Zhou et al, 2004;Marettová et al, 2010) and failure in spermiation (Hew et al, 1993b). Elongated and round spermatids, as well as spermatocytes were found in the tubule lumen in >98% of tubules (Mruk and Cheng, 2011).…”

“…• the proliferati on of VSMC, fibrino lysis (Kaji, 2004) • effec ts on the secreti on of fibrino lytic proteins (Yamamo to et al, 1997) • damage in cells of the middle layer of the arterioles in culture (Yamamo to and Kaji, 2002) mamma ls: • necrosis, degeneration of germinal cells, progressive sloughing of germ cells (Xu and Jiang, 1996;Yan et al,1997;Zhou et al, 1999;Li et al, 2000;Goyer et al, 2004;Obianime and Roberts , 2009 ;Bekhee t, 2011) • apop tos is of the semi niferous epith eliu m (Herr anz et al, 2010) • decrease in number of spermatogonia and spermatocytes • aberran t morpho logy, re lease of imm atu re cell s (Aoyagi et al 2002;Zhou et al 2004;Marettová et al,2010) • fail ure in spermi atio n (Hew et al,19 93b) fowl: • testicular hypoplasia, loss in testicular mass (Richardson et al,1974) • edema, necrosis and degeneration of seminiferous tubules (Bokori et a l., 1996;Ma rett ová et al, 201 3) • apop tos is, cell sh rink age (Li et al, 2010 testes had atrophied and the spermatogenic process ceased (White et al, 1978). Edema, necrosis and degeneration of seminiferous tubules were frequently reported in fowl (Bokori et al, 1996;Marettová et al, 2013).…”

“…The exposure to Cd induces of decreased measures of reproductive performance including fertility, abnormal embryonic development, prenatal death, and sexual dysfunction. Acute Cd-induced damage to testes manifests itself by hemorrhagic inflammation, degeneration and dysfunction of the organ and morphological changes Yan et al, 1997;Zhou et al, 1999;Waalkes 2000;Marettová et al, 2010Marettová et al, , 2013. Non-toxic dose of Cd alters gene expression in mouse testes (Zhou et al, 2004) and has potent estrogen-and androgen-like activities in vivo and in vitro, by directly binding to estrogen and androgen receptors (Takiguchi and Yoshihara, 2006).…”

Environmental contaminants

“…99 It is possible that Cd may be affecting osteoblasts' ability to produce collagen type I, a structural protein whose role it is to assemble a scaffold for bone mineralization. In the testis, Cd was found to disrupt the organization of collagen fibrils residing within the tunica propria (it is not known if type I and/or type IV collagen was affected), 100 indicating that Cd targets a critical understructure on which all cells of the seminiferous epithelium reside. Other studies relating to the skeleton have reported the harmful effects of environmental toxicants to be also mediated by AhR.…”