Testicular dysfunction induced by cadmium and its improvement caused by selenium in the mouse.

Histological observation revealed widespread and severe necrosis at 3 days after the final injection of Cd (0.012 mmol/Kg. daily for 2 consecutive days). Two months later, the changes were further aggravated. In addition, severe atrophy was found, and there was an increase in materials which could be stained by the Kossa method. These changes were prevented by the simultaneous injection of Se (0.024 mmol/Kg, daily for 2 consecutive days). Two months later, the Cd group showed no longer its reproduction. As a result of the Cd injection, at 3 days lipoperoxide concentration, expressed as substances reacting with thiobarbituric acid, was increased significantly, and accompanied by a decrease of glutathione. The levels of lipoperoxide and glutathione values were restored to the control level by the Se injection. At 3 days, testicular Zn and Mg decreased significantly, but Ca and Fe increased markedly in the Cd group. Ca increased mainly in the slow-speed centrifugation fraction, while Mg decreased evenly. In the Cd + Se group, there was no detectable change of metal concentration. However, Se stimulated the Cd uptake into the testis and vice versa. The testicular Cd and Se contents were maintained at a constant level for 2 months. The proportions of Cd existing in the cytosol fraction were 80% and 45% in the Cd group and the Cd + Se group, respectively. Furthermore, the recovery rates for cytosolic Cd in the F2 fractions corresponding to metallothionein were 60% and 75% in the Cd and Cd + Se groups, respectively. Our results suggest that Se has multiple functions against testicular Cd toxicity and that the toxicity once blocked by Se does not occur for a relatively long time.