Abstract
Melatonin, being an endogenous signaling molecule plays important role in plant growth and stress alleviation. The present study was conducted to evaluate the ameliorative role of melatonin against Cr toxicity in maize seedlings. The Cr toxicity (50, 100 and 200 mu M) severely affected hydroponically grown seedlings growth in a dose-dependent manner; however, the melatonin (0.5 and 1.0 mu M) application markedly restored toxicity-induced growth retardation. Higher dose of melatonin (1.0 mu M) was more effective in case of lower Cr toxicity (50 and 100 mu M). Exposure of 200 mu M Cr caused 45% and 43% reduction in shoot and root lengths and more than 80% reduction in biomass. In case of 200 mu M Cr toxicity, application of 1.0 mu M MT effectively restored shoot and root lengths reduction (from 45 to 30%) and biomass decline (from 80 to around 60%). Biomass restoration by 1.0 mu M melatonin under 50 and 100 mu M Cr was even more pronounced bringing it near to control plants having no Cr exposure. Further, both melatonin levels also improved root tips, root diameter, root volume and root surface area that had been damaged by Cr exposure. The melatonin also alleviated Cr-induced chlorophyll and carotenoids inhibition, improved relative water content, and markedly lowered proline and MDA content in shoots. Lower accumulation of MDA and proline, and greater membrane stability indices indicate that the melatonin conferred better plant growth by playing the role of antioxidant and detoxifying oxidative stress creating substances. Although antioxidant enzymes viz. SOD, POD, CAT and APX activities were also elevated by MT, this increase was not significantly different in the most of cases. No significant difference in NPK contents of shoot was observed by Cr and melatonin application indicating the growth retardation being caused directly by Cr intrinsic toxicity and not by nutrients deficiency. The melatonin-based amelioration of Cr toxicity in maize seedlings seems as the result of its nature as antioxidant, and not by activation/elevation of antioxidative enzymatic system.