Plants do not always have the genetic capacity to tolerate high levels of arsenic (As), which may not only arrest their growth but pose potential health risks through dietary bioaccumulation. Meanwhile, the interplay between the tomato plants and As-NO-driven molecular cell dynamics is obscure. Accordingly, seedlings were treated with As (10 mg/L) alone or in combination with 100 μM sodium nitroprusside (SNP, NO donor) and 200 μM 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO, NO scavenger). Sodium nitroprusside immobilized As in the roots and reduced the shoot translocation by up-regulating the transcriptional expression of the PCS, GSH1, MT2, and ABC1. SNP further restored the growth retardation through modulating the chlorophyll and proline metabolism, increasing NO accumulation and stomatal conductance along with clear crosstalk between the antioxidant activity as well as glyoxalase I and II leading to endogenous H2O2 and MG reduction. Higher PCs and glutathione accumulation helped protect photosynthetic apparatus; however, cPTIO reversed the protective effects of SNP, confirming the role of NO in the As toxicity alleviation.
Keywords: Arsenic toxicity; Oxidative stress; Phytochelatin; Sodium nitroprusside; Solanum lycopersicum L.; Vacuolar sequestration.
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