Nitric oxide -mediated regulation of sub -cellular chromium distribution, ascorbate ?glutathione cycle and glutathione biosynthesis in tomato roots under chromium (VI) toxicity

Unprecedented anthropogenic activities have led to contamination of soil and water with toxic metals that present a great threat to crop yields. This situation has compelled researchers to understand metal toxicity responses in order to develop strategies to curtail toxic metal-mediated losses in crop yields. Past decade has witnessed tremendous developments with regard to the role of nitric oxide (NO) in regulating abiotic stresses including toxic metal in crop plants. However, mechanisms related with NO-mediated mitigation of metal toxicity are still less known, and thus investigation in this domain remains underway. Therefore, in this study potential of NO along with its mechanisms of action in mitigating hexavalent chromium [Cr(VI)] toxicity in tomato roots were investigated. Root length and dry weight were declined by Cr(VI) which coincided with increased accumulation of Cr. Major amount of Cr was in the cell wall fraction followed by soluble (including vacuoles) and cell organelles fraction and thus, leading to the cell death in roots. Further, Cr(VI) also declined endogenous NO by inhibiting nitric oxide synthase like activity, and down-regulated ascorbate-glutathione cycle and glutathione biosynthesis, but stimulated oxidative stress markers. In contrast, exogenous addition of NO (as a sodium nitroprusside) reduced toxic effects of Cr(VI) in tomato roots by decreasing Cr accumulation as well as triggering sequestration of Cr into vacuoles and thus collectively protect root from cell death. Moreover, NO also up-regulated ascorbate-glutathione cycle and glutathione biosynthesis, and stimulated phytochelatins, but greatly declined oxidative stress markers. Interestingly, addition of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO) further worsened Cr(VI) toxicity, and Cr(VI) toxicity alleviatory effect of NO was partly reversed by the addition of c-PTIO, suggesting that NO has a crucial role in rendering Cr(VI) toxicity tolerance in tomato roots. Collectively, results suggest that NO mitigates Cr(VI) toxicity in tomato roots by reducing Cr and oxidative stress markers accumulation, triggering sequestration of Cr into vacuoles, and up-regulating ascorbate-glutathione cycle and glutathione biosynthesis, and phytochelatins. © 2020 Elsevier B.V.