The changes of heavy metal and metallothionein distribution in testis induced by cadmium exposure

Abstract

Cadmium (Cd) is known to cause various disorders in the testis, and metallothionein (MT) is known as a protein, which has a detoxification function for heavy metals. However, the changes of Fe, Cu, and Zn distribution in the testis induced by Cd exposure have not been well examined. Moreover, only a few studies have been reported on the localization of MT after Cd exposure. In this study, we have investigated the changes of Fe, Cu, and Zn distribution in Cd-exposed testis by a newly developed in air micro-Particle Induced X-ray Emission (PIXE) method. Also, we examined the distribution of MT expression in testis. In the testis of Cd-treated rats with significant increases of lipid peroxidation, the sertoli cell tight junction was damaged by Cd exposure, resulting from disintegration of the blood testis barrier (BTB). Evaluation by in air micro-PIXE method revealed that Cd and Fe distribution were increased in the interstitial tissues and seminiferous tubules. The histological findings indicated that the testicular tissue damage was advanced, which may have been caused by Fe flowing into seminiferous tubules followed by disintegration of the BTB. As a result, Fe was considered to enhance the tissue damage caused by Cd exposure. MT was detected in spermatogonia, spermatocytes, and Sertoli's cells in the testis of Cd-treated rats, but was not detected in interstitial tissues. These results suggested that MT was induced by Cd in spermatogonia, spermatocytes, and Sertoli's cells, and was involved in the resistance to tissue damage induced by Cd.

Testicular toxicity induced by dietary cadmium in cocks and ameliorative effect by selenium

“…Histologically, the toxic effects of Cd in the rat testes showed as severely damaged seminiferous tubules with degeneration and disintegration of spermatogenic cells and Leydig cells (Burukoglu and Baycu 2008;Manna et al 2008;Fouad et al 2009). In the testis of Cd-treated rats there were significant increases in lipid peroxidation and the Sertoli cell tight junction was damaged by Cd exposure leading to a breakdown of the blood-testis barrier (Kusakabe et al 2008). The present study demonstrated that dietary Cd induced similar histopathological changes in the testes (edema, necrosis, degeneration of seminiferous tubules and apoptosis in the spermiogenic region of the seminiferous epithelium (Figs 1 and 2) as was observed following Cd administration in rodents (Liu et al 2001;Xu et al 2005;Burukoglu and Baycu 2008;Fouad et al 2009).…”

Human spermatozoal RNAs

“…Cathepsins are a family of cystein proteases that likely prevent atrophy of seminiferous tubules and support spermatogenesis to pachytene spermatocytes (61,62). Metallothioneins, on the other hand, function as detoxicants to prevent tissue damage of testes by heavy metals (63). Furthermore, the ontology analysis found 'embryo development ending in birth or egg hatching' as the topranked gene otology (GO) term for 1,358 exclusivelyexpressed transcripts in group P. The exclusively-expressed genes corresponding to this GO term include adducin 1 (ADD1), activin A receptor type-II like 1 (ACVRL1), androgen receptor (AR), and aryl-hydrocarbon receptor nuclear translocator (ARNT).…”

Long-term effect of diet amended by risk elements contaminated soils on risk element penetration and physiological parameters of rats

“…(Matovic et al 2011). Therefore, the supplementation of the organism with essential elements can lead to improvement of animal health status as described by Kusakabe et al (2008) in the case of Fe, Cu, and Zn. Matovic et al (2011) reported the effects and interactions of magnesium and zinc supplementation in this context.…”