Abstract
Chromium [Cr(VI)] pollution is a major environmental risk, reducing crop yields. 5-Aminolevunic acid (5-ALA) considerably improves plant abiotic stress tolerance by inducing hydrogen peroxide (H
O
) and nitric oxide (NO) signalling. Our investigation aimed to uncover the mechanism of tomato tolerance to Cr(VI) toxicity through the foliar application of 5-ALA for three days, fifteen days before Cr treatment. Chromium alone decreased plant biomass and photosynthetic pigments, but increased oxidative stress markers, i.e., H
O
and lipid peroxidation (as MDA equivalent). Electrolyte leakage (EL), NO, nitrate reductase (NR), phytochelatins (PCs), glutathione (GSH), and enzymatic and non-enzymatic antioxidants were also increased. Foliar application of 5-ALA before Cr treatment improved plant growth and photosynthetic pigments, diminished H
O
, MDA content, and EL, and resulted in additional enhancements of enzymatic and non-enzymatic antioxidants, NR activity, and NO synthesis. In Cr-treated tomato seedlings, 5-ALA enhanced GSH and PCs, which modulated Cr sequestration to make it nontoxic. 5-ALA-induced Cr tolerance was further enhanced by sodium nitroprusside (SNP), a NO donor. When sodium tungstate (ST), a NR inhibitor, was supplied together with 5-ALA to Cr-treated plants, it eliminated the beneficial effects of 5-ALA by decreasing NR activity and NO synthesis, while the addition of SNP inverted the adverse effects of ST. We conclude that the mechanism by which 5-ALA induced Cr tolerance in tomato seedlings is mediated by NR-generated NO. Thus, NR and NO are twin players, reducing Cr toxicity in tomato plants via antioxidant signalling cascades.