Fig. 1: A conceptual model of the plant antioxidant defense network activated in response to stress-induced reactive oxygen species (ROS) production.

Abiotic and biotic stressors trigger the overaccumulation of ROS, such as superoxide (O₂⁻) and hydrogen peroxide (H₂O₂), primarily in organelles like chloroplasts, mitochondria, and peroxisomes. While low levels of ROS function as critical signaling molecules, excessive accumulation leads to oxidative stress, causing damage to vital cellular components, including lipids, proteins, and nucleic acids^183,207. To maintain redox homeostasis, plants employ a sophisticated defense system comprising both non-enzymatic antioxidants (e.g., ascorbate, AsA; glutathione, GSH) and enzymatic scavengers. This network’s primary enzymes include superoxide dismutase (SOD), which converts O₂⁻ to H₂O₂, alongside catalase (CAT) and various peroxidases that detoxify H₂O₂^12,14,15. Among these, ascorbate peroxidase (APX; EC 1.11.1.11) is a central component of the ascorbate-glutathione cycle and a critical regulator of H₂O₂ concentrations, and was therefore selected as a key biomarker for oxidative stress in this study¹¹. The coordinated action of this network enables plants to mitigate oxidative damage while utilizing ROS for stress signaling and physiological adaptation^17,189,208. APX ascorbate peroxidase, AsA ascorbate, CAT catalase, DHA dehydroascorbate, DHAR dehydroascorbate reductase, GPX glutathione peroxidase, GSH reduced glutathione, GST glutathione S-transferase, H₂O₂ hydrogen peroxide, MDHA monodehydroascorbate, MDHAR monodehydroascorbate reductase, NADPH nicotinamide adenine dinucleotide phosphate, O₂•⁻ superoxide anion, POX peroxidases, PRX peroxiredoxins, SOD superoxide dismutase, TRX thioredoxin. Key: Red dotted arrows represent ROS production, solid red arrows indicate causal relationships, black dotted arrows depict regulation and mitigation pathways of ROS.