Priming of tomato seedlings with 2-oxoglutarate induces arsenic toxicity alleviatory responses by involving endogenous nitric oxide.

Metal toxicity in crop plants is a matter of scientific concern. Therefore, in recent years efforts have been made to minimize metal toxicity in crop plants. Out of various strategies, priming of seedlings with certain chemicals, like e.g. donors of signaling molecules, nutrients, metabolites or plant hormones has shown encouraging results. However, mechanisms related with the priming-induced mitigation of metal toxicity are still poorly known. Hence, we have tested the potential of 2-oxoglutarate (2-OG) priming in enhancing the arsenate (As ) toxicity tolerance in tomato seedlings along with deciphering the probable role of nitric oxide (NO) in accomplishing this task. Arsenate decreased growth, endogenous NO and nitric oxide synthase-like activity but enhanced the accumulation of As, which collectively led to root cell death. Arsenate toxicity also decreased some photosynthetic characteristics (i.e. F /F qP, F /F and F /F , and total chlorophyll content) but enhanced NPQ. However, priming with 2-OG alleviated the toxic effect of As on growth, endogenous NO, cell death and photosynthesis. Moreover, arsenate inhibited the activities of enzymes of nitrogen metabolism (i.e. nitrate reductase, nitrite reductase, glutamine synthetase and glutamine 2-oxoglutarate aminotransferase) but increased the activity of glutamate dehydrogenase and NH content. Superoxide radicals, hydrogen peroxide, lipid peroxidation, protein oxidation and membrane damage increased upon As exposure, but the antioxidant enzymes (i.e. superoxide dismutase, catalase and glutathione-S-transferase) showed differential responses. Overall, our results showed that 2-OG is capable of alleviating As toxicity in tomato seedlings but the involvement of endogenous NO is probably required.