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Cadmium is a well recognized carcinogenic, cytotoxic and mutagenic transition metal. Recent evidence suggests that the proteins participating in the DNA repair systems, especially in excision and mismatch repair (MMR), are sensitive targets of cadmium toxicity. Microsatellite instability (MSI) is regarded as one of the phenotypes of defective DNA MMR and, consequently, as a marker of high risk for cancer. The purpose of this work is to determine whether cadmium, in the form of cadmium chloride (CdCl2), may induce microsatellite mutations in murine testes. For this study, 2-month-old male ICR-CD1 mice were treated by a single subcutaneous injection of 1, 2 and 3 mg CdCl2/kg body weight and killed after 35 days. A panel of six microsatellite markers, previously reported as being the most sensitive in detecting MSI in murine tumours, was used in this study. The results show that CdCl2 in the doses of 2 and 3 mg/kg induced a decrease in the testis weight and severe histopathologic changes with complete disorganization of testicular structure and evidences of severe necrosis. In addition, the animals exposed to the lowest CdCl2 dose presented MSI in the testis. The results indicate the existence of MSI in at least two nuclear loci suggesting putative genotoxic effects induced by cadmium. [ABSTRACT FROM AUTHOR]

In order to assess the effect of arsenic on the male reproductive impairment in mice, 7-week-old animals were exposed to 7.5 mg sodium arsenite (NaAsO2)/kg body weight, during 35 days (one spermatogenic cycle). One group of animals was sacrificed after exposure, while another group received distilled water for an additional period of 35 days, in order to study the spermatoxic effect and the recovery of spermatogenesis. In mice sacrificed after NaAsO2 exposure, a decrease in testis/body weight ratio and reduction of tubular diameter were observed. Both groups of NaAsO2-exposed animals showed remarkable histopathological changes, such as sloughing of immature germ cells. Animals sacrificed after NaAsO2 exposure showed decreased sperm motility, increased abnormal sperm morphology and decreased sperm viability. The effects of NaAsO2 on sperm motility recovered to normal values after one spermatogenic cycle, while increased sperm abnormality was maintained. However, at this period, a decrease in acrosome integrity was detected. Concerning oxidative stress parameters, animals sacrificed after NaAsO2 exposure showed a decreased selenium-dependent glutathione peroxidase activity, which was not detected after the recovery. Conversely, at this period, total glutathione peroxidase activity increased in exposed animals. These results demonstrate the toxic effects of NaAsO2 on mice spermatogenesis and show the lack of recovery after one spermatogenic cycle. [ABSTRACT FROM PUBLISHER]

Alloys used as prosthetic devices for bone/joint replacement include some heavy metals such as chromium, iron, nickel, or titanium. Unfortunately, due to the aggressive nature of the physiological environment, corrosion of these alloys promotes the release of metal ions into the surrounding tissues causing systemic toxic effects. Our previous preliminary studies have demonstrated that iron induced several morphological changes within mice seminiferous epithelium. The aim of the present work was to investigate, over a one-month period, the possibility of recovery of mice seminiferous epithelium, previously damaged by iron. Male Charles River mice were dosed subcutaneously with 0.5 mL of an iron suspension of 538 mg/L ± 10[sup 10] mg/L (n=5) every 72 hours during two weeks, followed by a recovery period of 30 days. Fragments of the seminiferous tubules were fixed in glutaraldehyde and prepared for light and transmission electron microscopy. Regeneration of spermatogenesis was noted after a one-month period, as illustrated by the presence of normal germ cells, in the usual position within the seminiferous tubules. These germinal elements and the Sertoli cells have shown normal cytological features. These results strongly suggest that the deleterious effects induced by iron are reversible. The presence of residual bodies within Sertoli cells cytoplasm indicates that they are able to perform a normal functional activity in a recovered spermatogenesis. [ABSTRACT FROM AUTHOR]