Regulation of ascorbate-glutathione cycle by exogenous nitric oxide and hydrogen peroxide in soybean roots under arsenate stress.

The role of nitric oxide (NO) and hydrogen peroxide (HO) is well known for regulating plant abiotic stress responses. However, underlying mechanisms are still poorly understood. Therefore, the present study investigated the involvement of NO and HO signalling in the regulation of arsenate toxicity (As) in soybean roots employing a pharmacological approach. Results show that As toxicity declined root length and biomass due to greater As accumulation in the cell wall and cellular organelles. Arsenate induced cell death due to enhanced levels of reactive oxygen species, lipid and protein oxidation and down-regulation in ascorbate-glutathione cycle and redox states of ascorbate and glutathione. These results correlate with lower endogenous level of NO. Interestingly, addition of L-NAME increased As toxicity. However, addition of SNP reverses effect of L-NAME, suggesting that endogenous NO has a role in mitigating As toxicity. Exogenous HO also demonstrated capability of alleviating As stress, while NAC reversed the protective effect of HO. Furthermore, DPI application further increased As toxicity, suggesting that endogenous HO is also implicated in mitigating As stress. SNP was not able to mitigate As toxicity in the presence of DPI, suggesting that HO might have acted downstream of NO in accomplishing amelioration of As toxicity.