Melatonin-mediated nitric oxide improves tolerance to cadmium toxicity by reducing oxidative stress in wheat plants.

Two independent trials were conducted to examine the involvement of nitric oxide (NO) in MT-mediated tolerance to Cd toxicity in wheat plants. Cadmium toxicity considerably led to a decrease in plant growth, total chlorophyll, PSII maximum efficiency (Fv/Fm), leaf water potential, potassium (K) and calcium (Ca). Simultaneously, it caused an increase in levels of leaf malondialdehyde (MDA), hydrogen peroxide (HO), electron leakage (EL), cadmium (Cd) and nitric oxide (NO) compared to those in control plants. Both MT (50 or 100 μM) treatments increased plant growth attributes and leaf Ca and K in the leaves, but reduced MDA, HO as well as leaf Cd content compared to those in Cd-stressed plants. A further experiment was designed to understand whether or not NO played a role in alleviation of Cd stress in wheat seedlings by melotonin using a scavenger of NO, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO) combined with the MT treatments. Melatonin-enhanced tolerance to Cd stress was completely reversed by the supply of cPTIO, which in turn considerably reduced the levels of endogenous NO. The results evidently showed that MT enhanced tolerance of wheat seedlings to Cd toxicity by triggering the endogenous NO. This was reinforced by the rise in the levels of MDA and HO, and decrease in the activities of superoxide dismutase (SOD; EC 1.15.1.1), catalase (CAT; EC. 1.11.1.6) and peroxidase (POD; EC. 1.11.1.7). The cPTO supply along with that of MT caused growth inhibition and a considerable increase in leaf Cd. So, both MT and NO together enhanced Cd tolerance in wheat.