Abstract
S-nitrosoglutathione reductase (GSNOR) is involved in the response to cadmium (Cd) exposure. In this study, the plants of mutant (gsnor1-3) with lossing-function of- and over-expression (GSNOROE5) of GSNOR were used to clear the role of GSNOR in Cd tolerance. GSNOR activity increased through upregulating the expression of the AtGSNOR gene and protein in Arabidopsis thaliana under Cd stress, which attenuated Cd tolerance. Oxidative damage was more serious in GSNOROE5 and was alleviated in gsnor1-3 under Cd stress, compared with Col-0. Induction of GSNOR facilitated H2O2 accumulation but inhibited catalase (CAT) activity in shoots under Cd stress. This phenotype was eliminated by 3-amino-1,2,4-triazole (3-AT), a CAT inhibitor. In addition, the expressions of AtCAT1 and AtCAT2 were down-regulated with increasing GSNOR activity under Cd stress. This suggested that GSNOR was involved in the accumulation of hydrogen peroxide (H2O2) through regulating CAT expression and activity under Cd exposure. Furthermore, Cd tolerance and CAT activity were improved by spraying S-nitrosoglutathione (GSNO) onto the surface of the leaves. The in vitro activity of CAT increased with GSNO concentration until a GSNO/CAT ratio of 2 was reached. Thus, CAT activity was relative to GSNOR through regulating the expression and S-nitrosylation level of proteins. In summary, the Cd-induced promotion of GSNOR activity aggravated Cd toxicity in plants by mediating H2O2 accumulation controlled by CAT.