The technique of affinity labelling was used to investigate the mechanism of Cd-induced testicular injury in rats. Thirty minutes after injecting a minimum threshold damaging dose of 109CdCl2 (0·012 mmol/kg), 109Cd distribution was determined in subcellular fractions of testicular homogenates and in proteins of the soluble phase separated by Sephadex G-75 chromatography. The effect on Cd distribution of three different pretreatments that prevent Cd damage was also studied for comparison. The principal Cd-binding fractions were the crude nuclear fraction, and two peaks (II and III) in the soluble fraction corresponding to proteins having molecular weights of 30,000 and 10,000, respectively. Pretreatments with (1) Se (0·012 mmol Na275SeO3/kg 30 min before Cd), (2) Zn (0·60 mmol 65Zn acetate/kg 24 hr before Cd), or (3) a half-threshold dose of CdCl2 (0·006 mmol/kg 2 days before Cd) prevented Cd damage and decreased, in all three cases, the uptake of Cd in the crude nuclear fraction and Peak II of the soluble fraction. In the case of Zn, these effects were the results of decreased uptake of Cd by the testes. The other two treatments altered the distribution of Cd between or within the various subcellular fractions. Selenium increased Cd uptake in the testes and the soluble fraction but caused a marked diversion of the Cd in the soluble fraction to the higher molecular weight proteins, the fraction also containing most of the selenium. Pretreatment with Cd increased the relative Cd uptake into the 10,000 mol. wt protein fraction, possibly by inducing the formation of a metallothionein-like protein. These observations suggest that the most plausible target of Cd in Cd-induced testicular injury is the unidentified 30,000 mol. wt Cd-binding protein, although the possibility of the crude nuclear fraction as a target could not be excluded.
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