Shoot tolerance mechanisms to iron toxicity in rice (<i>Oryza sativa</i> L.)

Abstract

Iron toxicity frequently affects lowland rice and leads to oxidative stress via the Fenton reaction. Tolerance mechanisms were investigated in contrasting genotypes: the intolerant IR29 and the tolerant recombinant inbred line FL483. Seedlings were exposed to 1000 mg L^-1 ferrous iron, and the regulation of genes involved in three hypothetical tolerance mechanisms was investigated (I) Iron uptake, partitioning and storage. The iron concentration and speciation in different plant tissues did not differ significantly between genotypes. Sub-cellular iron partitioning genes such as vacuolar iron transporters or ferritin showed no genotypic differences. (II) Antioxidant biosynthesis. Only one gene involved in carotenoid biosynthesis showed genotypic differences, but carotenoids are unlikely to scavenge the reactive oxygen species (ROS) involved in Fe toxicity, i.e. H₂ O₂ and hydroxyl radicals. (III) Enzymatic activities for ROS scavenging and antioxidants turnover. In shoots, glutathione-S-transferase and ascorbate oxidase genes showed genotypic differences, and consistently, the tolerant FL483 had lower dehydroascorbate reductase and higher ascorbate oxidase activity, suggesting that high rates ascorbate reduction confer sensitivity. This hypothesis was confirmed by application of exogenous reduced ascorbate or L-galactono-1,4-lactone, which increased lipid peroxidation under iron toxic conditions. Our results demonstrate in planta pro-oxidant activity of reduced ascorbate in the presence of iron.