Implication of nitric oxide and hydrogen sulfide signalling in alleviating arsenate stress in rice seedlings

Highlights: • Arsenate caused cell death in rice roots and declined photosynthesis. • Nitric oxide and hydrogen sulfide protect rice seedlings from arsenate. • Sucrose and proline metabolism was positively related with arsenate tolerance. • Nitric oxide and hydrogen sulfide independently alleviate arsenate stress. Nitric oxide (NO) and hydrogen sulfide (H₂S) since their discovery have proven to be game changing molecules in alleviating abiotic stress. They individually play role in plant stress management while the pathways of stress regulation through their crosstalk remain elusive. The current study focuses on investigating the interplay of NO and H₂S signalling in the amelioration of arsenate As(V) toxicity in rice seedlings and managing its growth, photosynthesis, sucrose and proline metabolism. Results show that As(V) exposure declined fresh weight (biomass) due to induced cell death in root tips. Moreover, a diminished RuBisCO activity, decline in starch content with high proline dehydrogenase activity and increased total soluble sugars content was observed which further intensified in the presence of Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME, an inhibitor of nitric oxide synthase-like activity), and DL-propargylglycine (PAG, an inhibitor of cysteine desulfhydrase activity). These results correlate with lower endogenous level of NO and H₂S. Addition of L-NAME increased As(V) toxicity. Interestingly, addition of SNP reverses effect of L-NAME suggesting that endogenous NO has a role in mitigating As(V) toxicity. Similarly, exogenous H₂S also significantly alleviated As(V) stress, while PAG further stimulated As(V) toxicity. Furthermore, application of H₂S in the presence of L – NAME and NO in the presence of PAG could still mitigate As(V) toxicity, suggesting that endogenous NO and H₂S could independently mitigate As(V) stress.