Endogenous nitric oxide mediates alleviation of cadmium toxicity induced by calcium in rice seedlings.

The effect of calcium chloride (CaCl2) on rice seedling growth under cadmium chloride (CdCl2) stress, as well as the possible role of endogenous nitric oxide (NO) in this process, was studied. The growth of rice seedlings was seriously inhibited by CdCl2, and the inhibition was significantly mitigated by CaCl2. However, hemoglobin (Hb) and 2-(4-carboxyphenyl)-4, 4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) weakened the promotion effect of CaCl2. The results of NO fluorescence localization suggest that growth accelerated by CaCl2 might be associated with elevated NO levels. The content of Cd, protein thiols (PBT), and nonprotein thiols (NPT) in cell walls, cell organelles, and soluble fractions, respectively, of rice seedlings decreased considerably in the presence of CaCl2, whereas the content of pectin, hemicellulose 1 (HC1), and hemicellulose 2 (HC2) increased significantly. Elimination of endogenous NO in Cd+Ca treatment could promote the transportation of Cd2+ to cell organelles and soluble fractions and increase the content of NPT and PBT in leaves. In addition, transportation of Cd2+ to cell organelles and soluble fractions was retarded in roots, the content of NPT increased, and the content of PBT decreased. With elimination of endogenous NO in Cd+Ca treatment, the content of pectin, HC1, and HC2 decreased significantly. Thus, Ca may alleviate Cd toxicity via endogenous NO with variation in the levels of NPT, PBT, and matrix polysaccharides.