ABSTRACT
Chronic and acute exposure to SO2 is associated with increased risks of various damages to plants. In the present study, epidermal strip experiment was employed to investigate SO2-induced guard cells apoptosis and the signal regulation in Hemerocallis fulva. The results showed that with the increase of treatment concentrate of SO2 derivates (a mixture of sodium sulfite and sodium bisulfite, 3:1, mmol L⻹/mmol L⻹, 1.0-5.0 mmol L⻹), the physiological activity of the guard cells declined and cell death occurred. While the concentration of SO2 derivatives exceeded 2.0 mmol L⻹, the percentage of cell death increased significantly (P<0.05). Typical features of apoptosis including nuclear condensation, nuclear elongation, fragmentation etc. were found. Meanwhile, concomitant presence of nitric oxide (NO), reactive oxygen species (ROS) and Ca²âº level increment appeared. However, SO2-induced cell death can be effectively blocked by either of the following substances with their respective optimal concentrations: antioxidant ascorbic acid (Asc; 0.05 mmol L⻹) or catalase (CAT; 200 U mL⻹), nitric oxide (NO) scavenger 2-(4-carboxyphenyl)-4, 4, 5, 5- tetramethylmidiazoline-1-oxyl-3-oxide (c-PTIO; 0.20 mmol L⻹), nitrate reductase inhibitor NaN3 (0.20 mmol L⻹), Ca²âº chelating agent EGTA (0.05 mmol L⻹) or plasma membrane Ca²âº channel blocker LaCl3 (0.05 mmol L⻹). In addition to a significant decrease in cell death rate, a reduction in the levels of reactive oxygen species (ROS), NO and Ca²âº was observed. Further study showed that compared to treatment with SO2 alone, Asc treatment led to a decrease in NO and Ca²âº levels and NaN3 treatment led to a decrease in ROS and Ca²âº levels, but the NO and ROS levels of the LaCl3 treatment changed little. All results suggested that NO, ROS and Ca²âº were involved in the apoptosis induced by SO2 in H. fulva. The process might be related to the burst of NO or ROS, which would activate the plasma Ca²âº channel and result in the increase of intercellular Ca²âº.
