Marouane Ben Massoud

The present research investigates the protective mechanism of nitric oxide (NO) in regulating tolerance to Cu-induced toxicity in shoots of barley (Hordeum vulgare L.). After 10 days, treatment with 200 µM CuCl₂ caused a significant reduction in growth and photosynthetic efficiency concomitant with a strong increase in the contents of reactive oxygen species (ROS), antioxidant enzymes activities such as catalase (CAT), superoxide dismutase (SOD), guaiacol peroxidase (GPOX) and glutathione peroxidase (GPX). An increase in the lipid peroxidation markers malondialdehyde (MDA) and lipoxygenase activity (LOX) indicated oxidative stress. Furthermore, inhibition of growth in 200 μM Cu-treated plants was associated with a reduction in carotenoids, chlorophyll and maximum photosystem II efficiency. However, copper treatment provoked a strong increase in activity of the glutathione-ascorbate cycle enzymes ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), monodehydroascorbate reductase (MDAR) and glutathione reductase (GR), but a decrease in levels of the non-enzymatic antioxidant compounds glutathione (GSH), ascorbate (AsA). The addition of 500 µM of the nitric oxide (NO) donor, sodium nitroprusside (SNP), to the growth medium alleviated Cu toxicity by reducing Cu uptake and enhancing antioxidant capacity, as indicated by increased contents of GSH and AsA. The current results show that NO addition can alleviate Cu toxicity by affecting the antioxidant defense system, photosynthetic system and maintaining the glutathione-ascorbate cycle status, suggesting that NO treatment protects proteins against oxidation by regulating the cellular redox homeostasis.