The moderate oxidative stress induced by glyphosate is not detected in Amaranthus palmeri plants overexpressing EPSPS.

The present study aimed to determine whether glyphosate-induced oxidative stress is directly related to the action mechanism of this herbicide (5-enolpyruvylshikimate-3-phosphate synthase or EPSPS inhibition) and analyse the role of oxidative stress in glyphosate toxicity of the weed Amaranthus palmeri S. Wats. Two kinds of populations were studied using EPSPS amplification: glyphosate-sensitive and glyphosate-resistant (by gene amplification). Plants were grown hydroponically and treated with different glyphosate doses, after which several oxidative stress markers were measured in the leaves. Untreated, sensitive and resistant plants showed similar values for the analysed parameters. Treated glyphosate-sensitive plants showed an increase in shikimate, superoxide and H2O2 contents and dose-dependent lipid peroxidation and antioxidant responses; however, none of these effects were observed in resistant plants, indicating that glyphosate-induced oxidative stress is related to EPSPS inhibition. Oxidative stress is associated with an increase in the activity of peroxidases due to EPSPS inhibition, although the link between both processes remains elusive. The fact that some glyphosate doses were lethal but did not induce major oxidative damage provides evidence that glyphosate toxicity is independent of oxidative stress.

Role of oxidative stress in the physiology of sensitive and resistant Amaranthus palmeri populations treated with herbicides inhibiting acetolactate synthase.

The aim of the present study was to elucidate the role of oxidative stress in the mode of action of acetolactate synthase (ALS) inhibiting herbicides. Two populations of Amaranthus palmeri S. Watson from Spain (sensitive and resistant to nicosulfuron, due to mutated ALS) were grown hydroponically and treated with different rates of the ALS inhibitor nicosulfuron (one time and three times the field recommended rate). Seven days later, various oxidative stress markers were measured in the leaves: H2O2, MDA, ascorbate and glutathione contents, antioxidant enzyme activities and gene expression levels. Under control conditions, most of the analysed parameters were very similar between sensitive and resistant plants, meaning that resistance is not accompanied by a different basal oxidative metabolism. Nicosulfuron-treated sensitive plants died after a few weeks, while the resistant ones survived, independently of the rate. Seven days after herbicide application, the sensitive plants that had received the highest nicosulfuron rate showed an increase in H2O2 content, lipid peroxidation and antioxidant enzymatic activities, while resistant plants did not show these responses, meaning that oxidative stress is linked to ALS inhibition. A supralethal nicosulfuron rate was needed to induce a significant oxidative stress response in the sensitive population, providing evidence that the lethality elicited by ALS inhibitors is not entirely dependent on oxidative stress.