In order to verify the effects of exposure to Cd and Zn on testicular DAAM1 gene and protein expression and also to ascertain their involvement in the protective role of Zn in prevent the testicular toxicity Cd‐induced in male offspring rats at adult age after gestational and lactational exposure, male offspring rats, from mothers receiving either tap water, Cd, Zn, or Cd + Zn during gestation and lactation periods, were scarified on postnatal days (PND) 70. The reproductive organ (testis, epididymis, and vesicle seminal) were collected, weighed, and analyzed. The results showed that exposure to Cd in utero and through lactation decreased the relative reproductive organ weight, altered the testicular histology at the interstitial and tubular levels, and causing a significant reduction in the daily sperm production (DSP) per testis and per gram of testis, and other then altering the epididymal sperm quality. Furthermore, both mRNA and protein expression of rat testicular DAAM1 were also inhibited in Cd‐treated group. Zn supply has completely corrected the most of these toxic effects. Our results imply that Zn could prevent Cd‐induced testicular toxicity and sperm quality alteration in adult male rat after gestational and lactational exposure, probably via the restoration of the testicular DAAM1 expression inhibited by Cd. The effects of exposure to Cd and Zn on testicular DAAM1 gene and protein expression and heir involvement in the protective role of Zn in prevent the testicular toxicity Cd‐induced in male offspring rats have been studied. The reproductive organ were collected, weighed and analyzed. The results showed that Cd exposure decreased the relative reproductive organ weight, altered the testicular histology, and causing a significant reduction in the daily sperm production other then altering the epididymal sperm quality. In addition, both mRNA and protein expression of rat testicular DAAM1 were also inhibited. Zn supply has completely corrected the most of these toxic effects. Our results imply that Zn could prevent Cd‐induced testicular toxicity probably via the restoration of the testicular DAAM1 expression inhibited by Cd.