Sulfur dioxide induced programmed cell death in Vicia guard cells

Sulfur dioxide (SO2) induced nuclear condensation and nuclear fragmentation and rapid loss of guard cell viability in detached epidermis of Vicia leaves at concentrations of 1 mM and higher (3 h exposure). Caspase inhibitors Z–Asp–CH2–DCB (0.1 mM) and TLCK (0.1 mM) markedly suppressed SO2-induced cell death. The typical nuclear morphological changes and the inhibition effects of caspase inhibitors suggest the activation of a programmed cell death (PCD) pathway. SO2-induced cell death can be blocked by either antioxidants (0.1 mM AsA or 200 U/mL CAT) or Ca2+ antagonists (0.1 mM EGTA or LaCl3). AsA and CAT also blocked SO2-induced ROS production and [Ca2+]cyt increase. However, EGTA and LaCl3 can inhibit SO2-induced [Ca2+]cyt increase, but cannot suppress SO2-induced ROS production. Our results indicate that high concentrations of SO2 induce guard cell death via a PCD pathway through ROS mediating [Ca2+]cyt elevation, which causes harmful effects to plants.

► Sulfur dioxide (SO2) induced programmed cell death (PCD) in Vicia guard cells. ► ROS production in SO2-stimulated guard cells triggered SO2-induced cell death. ► ROS activation of Ca2+ channels and [Ca2+]cyt increase mediated SO2-induced cell death. ► Caspase-like proteases involved in the implementation of SO2-induced cell death. ► High concentrations of SO2 are harmful to plants by triggering guard cell death.