Involvement of calcium-mediated effects on ROS metabolism in the regulation of growth improvement under salinity.

Salinity reduces Ca(2+) availability, transport, and mobility to growing regions of the plant and supplemental Ca(2+) is known to reduce salinity damages. This study was undertaken to unravel some of the ameliorative mechanisms of Ca(2+) on salt stress at the cellular and tissue levels. Zea mays L. plants were grown in nutrient solution containing 1 or 80 mM NaCl with various Ca(2+) levels. Measurements of growth and physiological parameters, such as ion imbalance, indicated that the Ca(2+)-induced alleviation mechanisms differed between plant organs. Under salinity, H(2)O(2) levels increased in the leaf-growing tissue with increasing levels of supplemental Ca(2+) and reached the levels of control plants, whereas superoxide levels remained low at all Ca(2+) levels, indicating that Ca(2+) affected growth by increasing H(2)O(2) but not superoxide levels. Salinity completely abolished apoplastic peroxidase activity. Supplemental Ca(2+) increased its activity only slightly. However, under salinity, polyamine oxidase (PAO) activity was shifted toward the leaf base probably as an adaptive mechanism aimed at restoring normal levels of reactive oxygen species (ROS) at the expansion zone where NADPH oxidase could no longer provide the required ROS for growth. Interestingly, addition of Ca(2+) shifted the PAO-activity peak back to its original location in addition to its enhancement. The increase in PAO activity in conjunction with low levels of apoplastic peroxidase is supportive of cellular growth via nonenzymatic wall loosening derived by the increase in H(2)O(2) and less supportive of the peroxidase-mediated cross-linking of wall material. Thus extracellular Ca(2+) can modulate ROS levels at specific tissue localization and developmental stages thereby affecting cellular extension.