Hydrogen sulfide manages hexavalent chromium toxicity in wheat and rice seedlings: The role of sulfur assimilation and ascorbate-glutathione cycle.

The role of hydrogen sulfide (H2S) is well known in the regulation of abiotic stress such as toxic heavy metal. However, mechanism(s) lying behind this amelioration are still poorly known. Consequently, the present study was focused on the regulation/mitigation of hexavalent chromium (Cr(VI) toxicity by the application of H2S in wheat and rice seedlings. Cr(VI) induced accumulation of reactive oxygen species and caused protein oxidation which negatively affect the plant growth in both the cereal crops. We noticed that Cr(VI) toxicity reduced length of wheat and rice seedlings by 21% and 19%, respectively. These reductions in length of both the cereal crops were positively related with the down-regulation in the ascorbate-glutathione cycle, and were recovered by the application NaHS (a donor of H2S). Though exposure of Cr(VI) slightly stimulated sulfur assimilation but addition of H2S further caused enhancement in sulfur assimilation, suggesting its role in the H2S-mediated Cr(VI) stress tolerance in studied cereal crops. Overall, the results revealed that H2S renders Cr(VI) stress tolerance in wheat and rice seedlings by stimulating sulfur assimilation and ascorbate-glutathione which collectively reduce protein oxidation and thus, improved growth was observed.

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 (H2O2) 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 H2O2 signalling in the regulation of arsenate toxicity (AsV) in soybean roots employing a pharmacological approach. Results show that AsV 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 AsV toxicity. However, addition of SNP reverses effect of L-NAME, suggesting that endogenous NO has a role in mitigating AsV toxicity. Exogenous H2O2 also demonstrated capability of alleviating AsV stress, while NAC reversed the protective effect of H2O2. Furthermore, DPI application further increased AsV toxicity, suggesting that endogenous H2O2 is also implicated in mitigating AsV stress. SNP was not able to mitigate AsV toxicity in the presence of DPI, suggesting that H2O2 might have acted downstream of NO in accomplishing amelioration of AsV toxicity.