Endogenous nitric oxide and its potential sources regulate glutathione-induced cadmium stress tolerance in maize plants

It was aimed to assess that up to what extent endogenous nitric oxide (NO) and its sources are involved in glutathione (GSH)-mediated tolerance of maize plants to cadmium (Cd) stress. The Cd-stressed maize plants were sprayed with or without GSH (1.0 mM) once every week for two weeks. Before initiating the stress treatment, the Cd-stressed plants sprayed with GSH were supplied with or without 0.1 mM, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO; a NO scavenger) for two weeks or with 0.1 mM sodium tungstate (ST; a nitrate reductase inhibitor), or 0.1 mM NG-nitro-L-arginine methyl ester hydrochloride (L-NAME). Cadmium stress suppressed the activities of dehydroascorbate reductase, monodehydroascorbate reductase, and glyoxalase II, while increased leaf NO, Cadmium content, proline, oxidative stress, the activities of glutathione reductase, ascorbate peroxidase, the key enzymes of oxidative defense system, glyoxalase I, NR and NOS. GSH reduced oxidative stress and tissue Cd²⁺ content, but it improved growth, altered water relations, and additionally increased proline levels, activities of the AsA-GSH cycle, key enzymatic antioxidants, glyoxalase I and II, NR and NOS as well as NO content. The cPTIO and ST supplementation abolished the beneficial effects of GSH by reducing the activities of NO and NR. However, L-NAME did not retreat the favorable effects of GSH, although it reduced the NOS activity without eliminating NO content, suggesting that NR might be a prospective source of NO generated by GSH in Cd-stressed plants, which in turn accelerated the activities of antioxidant enzymes.