Modulation of Dimorphandra wilsonii Rizz. seed germination through H2O2 production in response to Zn interference of the mitochondrial electron transport chain

• We studied the responses of Dimorphandra wilsonii seeds to zinc.
• Zn-toxicity was related to Zn-induced reactive oxygen species (ROS) accumulation.
• Antioxidant systems allowed seed germination even under high Zn doses (200 mg l−1).
• Respiration appears to be the main Zn target and it should act upstream of Complex IV.

We examined the germination and biochemical features of seeds of the threatened Brazilian species Dimorphandra wilsonii exposed to Zn. Although seed germination decreased with Zn exposure, the species was able to germinate even under high Zn doses (200 mg Zn l−1). Zn-toxicity was related to Zn-induced hydrogen peroxide (H2O2) accumulation, although increased activities of the H2O2-scavenging enzymes catalase and ascorbate peroxidase allowed seed germination in the presence of Zn. Using electron transport chain (ETC) inhibitors, we located the primary reactive oxygen species (ROS) production sites in seeds exposed to 200 mg Zn l−1. Rotenone (an inhibitor of mitochondrial ETC complex I) reduced H2O2 concentrations in embryos of Zn-treated seeds while KCN (an inhibitor of mitochondrial ETC complex IV) and dicumarol (an inhibitor of the plasma membrane ETC) showed no effects. The activities of enzymes related to mitochondrial ETC (Complexes I–IV) were reduced and the pool of oxidized ubiquinone was greater in Zn-treated seeds. Mitochondrial ETCs therefore appear to be the main sites for Zn-induced ROS formation, and that metal appears to act upstream of Complex IV. These results suggest that Zn does not block electron flow in the mitochondrial ETC but directly modify ubiquinone sites in Complexes I and II, resulting in H2O2 formation.

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