Overview of oxidative metabolism and autophagy under metal stress

Plants are continuously exposed to a variety of abiotic stresses, including imbalances in micronutrient availability and contamination by heavy metals. One of the primary consequences of such metal imbalances is the overproduction of reactive oxygen species (ROS), which can oxidize proteins, lipids, and DNA, ultimately compromising cellular viability. Autophagy plays a crucial role in maintaining cellular homeostasis by recycling damaged or obsolete cellular components, especially under nutrient-limiting conditions. Increasing evidence indicates that autophagy is activated in response to oxidative stress, as autophagy-deficient mutants tend to accumulate hydrogen peroxide (H2O2), lipid peroxides, and oxidized proteins. Despite extensive research on autophagy in response to various abiotic stresses, its specific role in coping with metals excess or deficiency, and NaCl, remains relatively underexplored. Autophagy could be a key adaptive mechanism, facilitating the removal of damaged cellular components, mitigating oxidative damage, sequestering toxic metals into the vacuole, and enabling the redistribution of essential metals from internal reserves to support plant survival under both metal-deficiency and -toxicity conditions. This review aims to highlight the role of autophagy in plant responses to micronutrient imbalances, heavy metal and salinity toxicity, with a particular focus on the regulatory interplay between ROS and oxidative stress in these processes.