Excessive Ca(NO3)2 significantly inhibited the Ca2+-ATPase activity
through severe oxidative damage, disordering the enzyme function. Massive
Ca2+ entered the cytoplasmand sub-cellular organelle
from intercellular, disrupting the normal function of organs. Our
study showed that exogenous EBL improved Ca2+-ATPase activity
in shoot and root cells through protecting the enzyme-protein
against oxidative damage (Yuan et al., 2013, Fig. 2), which could be
attributed to exclude excessive Ca2+ out to the intercellular space.
EBL significantly improved ATP synthesis by increased availability
of P, which provided energy to guarantee cell normal function
and resist salinity stress. Thus, the level of Ca2+ in the cytoplasm
was lower and more stable, which guaranteed normal physiological
metabolism and signal transduction in cells. It demonstrated
that EBL could keep Ca2+ homeostasis in shoot and root cells under
Ca(NO3)2 stress through the regulation of Ca2+ location and distribution