Sodium nitroprusside (SNP) improves tolerance to arsenic (As) toxicity in Vicia faba through the modifications of biochemical attributes, antioxidants, ascorbate-glutathione cycle and glyoxalase cycle.

The present study was conducted to evaluate the effect of arsenic (As) toxicity and the mitigating role of nitric oxide (NO) donor sodium nitroprusside (SNP) on Vicia faba. Arsenics stress decreased the growth and biomass yield, and photosynthetic pigments, but it enhanced As accumulation. Supplementation of NO enhanced the afore-mentioned parameters except As accumulation which decreased in both shoot and root. Supplementation of NO enhanced the shoot tolerance index (Shoot TI%), root tolerance index (Root TI%) but it declined the As translocation factor (TF). Application of NO alleviated the As-induced decline in net assimilation rate, stomatal conductance, transpiration and leaf relative water content. The levels of proline and glycine betaine (GB) further increased due to NO application, whereas malondialdehyde (MDA), hydrogen peroxide (H2O2), electrolyte leakage (EL) and methylglyoxal (MG) declined considerably. Activities of enzymatic antioxidants such as superoxide dismutase (SOD) and catalase (CAT) increased under As stress. Supplementation of NO up-regulated the enzymes involved in Asc-Glu cycle and glyoxalase cycle under As toxicity. Another experiment was setup to authenticate whether NO was certainly able to alleviate As toxicity. For this purpose, the NO scavenger [2-(4-carboxy-2 phenyl)-4,4,5,5-tertamethylimidazoline-1-oxyl-3-oxide (cPTIO)] was added to As and NO supplemented plants. Addition of cPTIO to NO supplemented As-treated plants showed the same effect when As alone was supplied to plants. In conclusion, addition of NO to the growth medium maintained the plant performance under As toxicity through modulation of physio-biochemical attributes, antioxidant enzymes, and the Asc-Glu and glyoxalase systems.