Abstract
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 (200mg 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 200mg 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
