• cadmium;
  • ovary;
  • δ-ALA-D;
  • seleno-furanoside;
  • mice


Cadmium (Cd) toxicity is a concern to the tobacco-smoking sub-population which includes millions of people worldwide. Although this metal may cause severe damage to embryos and the reproductive organs, the precise mechanisms underlying its toxicity remain unclear. In the present study, the Cd effect on ovary δ-aminolevulinate dehydratase (δ-ALA-D) activity was investigated in vitro and ex vivo. We observed that low concentrations of Cd inhibited cow ovary δ-ALA-D activity in vitro and the IC50 value obtained was 19.17 μM. Furthermore, the protective effect of a novel organic selenium compound (seleno-furanoside) in restoring enzyme activity was evaluated. Seleno-furanoside (10, 50, 100, 200, 400 and 1000 μM) did not reverse the Cd toxicity in bovine ovarian tissue in vitro. According to the in vitro reults, acute Cd exposure (2.5 and 5 mg kg–1) caused a significant inhibition in ovary δ-ALA-D activity in mice (around 27% and 34%, respectively). Therapy with seleno-furanoside (100 µmol kg–1) was able to restore enzyme activity. Thus, we demonstrated for the first time that δ-ALA-D activity from ovary is inhibited by Cd both in vitro and ex vivo. Additionally, seleno-furanoside therapy was effective in restoring ovarian enzyme activity inhibited by Cd exposure in mice, but it did not reverse the in vitro metal effect. This study detected a new toxicity marker of Cd toxicity on ovarian tissue as well as the beneficial effect of a new compound to manage the metal effect after acute exposure. Copyright © 2012 John Wiley & Sons, Ltd.