Hydrogen sulfide may function downstream of hydrogen peroxide in CdCl2-induced stomatal closure in Vigna radiata L.

Abstract

Pharmacological, spectrophotographic and laser scanning confocal microscopy (LSCM) approaches were used to investigate the roles of hydrogen sulfide (H2S) and hydrogen peroxide (H2O2) played in signaling transduction of stomatal closure induced by CdCl2 in Vigna radiata L. In the present study, CdCl2 could induce stomatal closure in a dose- and time-dependent manner, which was inhibited by H2S modulators hypotaurine (HT), aminooxy acetic acid (AOA), hydroxylamine (NH2OH), potassium pyruvate (C3H3KO3), ammonia (NH3), H2O2 modulators ascorbic acid (ASA), catalase (CAT), diphenylene iodonium (DPI) and salicylhydroxamic acid (SHAM). In addition, both the content of H2S, activity of L-/D-cysteine desulfhydrase (L-/D-CDes and pyridoxalphosphate-dependent enzyme) in leaves of V. radiata, and the level of H2O2 in guard cells significantly increased under CdCl2 stress, which were inhibited by H2S and H2O2 modulators, respectively. H2O2 modulators could suppress CdCl2-induced increase of H2S levels, L-/D-CDes activity and stomatal closure in the leaves of V. radiata. However, H2S modulators had no effect on the accumulation of CdCl2-induced H2O2 in guard cells of V. radiata. From these data, it can be deduced that both H2S and H2O2 can mediate CdCl2-induced stomatal closure in V. radiata L., and H2S acts downstream than H2O2 in such process.