Regulation of arsenate stress by nitric oxide and hydrogen sulfide in Oryza sativa seedlings: Implication of sulfur assimilation, glutathione biosynthesis, and the ascorbate-glutathione cycle and its genes

Seed priming by nitric oxide (NO) and hydrogen sulphide (H2S) in combating against abiotic stress in plants is well documented. However, knowledge of fundamental mechanisms of their crosstalk is scrambled. Therefore, the reported study examined the probable role of NO and H2S in the mitigation of arsenate toxicity (As(V)) in rice seedlings and whether their potential signalling routes crossover. Results report that As(V) toxicity limited shoot and root length growth with more As accumulation in roots. As(V) further caused elevated reactive oxygen species levels, inhibited ascorbate-glutathione cycle enzymes and relative gene expression of its enzymes and thus, causing lipid and protein oxidation. These results correlate with reduced nitric oxide synthase-like and (L)-cysteine desulfhydrase activity along with endogenous NO and H2S. While, L-NAME or PAG augmented As(V) toxicity, and addition of SNP or NaHS effectively reversed their respective effects. Furthermore, SNP under PAG or NaHS under L-NAME were able to pacify As(V) stress, implicating that endogenous NO and H2S efficiently ameliorate As(V) toxicity but without their shared signaling in rice seedlings.