Nitric oxide signaling is involved in arsenic-induced guard cell death in Vicia faba L. (Fabaceae)

Abstract

Nitric oxide (NO) is a key endogenous signaling molecule in the plant response to environmental stresses. Here, we show that NO is involved in arsenic (As) cytotoxicity in Vicia faba L. guard cells. The results showed that NaAsO2 (0.1–10 mg L−1) decreased cell viability and caused cell death in a concentration-dependent manner, accompanied by significant increases in intracellular NO, reactive oxygen species (ROS), and Ca2+ levels as well as nitrate reductase (NR) activity. Arsenic-induced cell death was blocked by NO antagonists (NO scavenger c-PTIO; nitrate reductase inhibitor NaN3), ROS scavengers (AsA or CAT), and Ca2+ antagonists (Ca2+ chelator EGTA; Ca2+ channel blocker LaCl3). In addition, NaN3 and CAT led to a significant decrease in the intracellular Ca2+ level, whereas LaCl3 and EGTA barely affected the intracellular NO and ROS levels. Our results demonstrated that increased levels of NO and ROS activate Ca2+ signaling to control responses to As cytotoxicity and that NR-dependent NO generation contributes to As toxicity in V. faba guard cells.