EDTA reduces cadmium toxicity in mustard (Brassica juncea L.) by enhancing metal chelation, antioxidant defense and glyoxalase systems

To investigate the possible role of EDTA in mitigating cadmium (Cd) toxicity, we treated mustard (Brassica juncea L.) seedlings with CdCl2 (0.5 mM and 1.0 mM, 3 days) alone and in combination with 0.5 mM EDTA in a semihydroponic medium. In the absence of EDTA, mustard seedlings accumulated Cd in their roots and shoots in a concentration dependent manner. Overaccumulation of Cd boosted generation of hydrogen peroxide (H2O2) and superoxide anions (O-2(center dot-)), increased lipoxygenase (LOX) activity, lipid peroxidation, and cytotoxic methylglyoxal (MG) content. It also disturbed components of the antioxidant defense and glyoxalase systems. Furthermore, Cd stress decreased growth, leaf relative water content (RWC) and chlorophyll (chl) content but augmented the proline (Pro) content. On the other hand, EDTA supplemented Cd-stressed seedlings improved the constituents of the AsA-GSH cycle with the upregulated activities of ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT). Moreover, addition of EDTA to the Cd-stressed seedlings notably enhanced Gly I activity in contrast to the stress treatment. Ethylenediaminetetraacetic acid decreased Cd accumulation in the both shoots and roots, as well as increased other nonprotein thiols (NPTs) in leaves, including the phytochelatin (PC) content. It also decreased H2O2 and O-2(center dot-) generation, lipid peroxidation and MG content but enhanced RWC, chl and Pro contents in the leaves, which confirmed the improved growth of seedlings. The findings of the study suggest that exogenous application of EDTA to the Cd-treated seedlings reduces Cd-induced oxidative injuries by restricting Cd uptake, increasing NPTs concentration and upregulating most of the components of their antioxidant defense and glyoxalase systems.