In recent years it was discovered in animals

In recent years, it was discovered in animals that certain types of non-apoptotic cell death are strictly dependent on iron and ROS. The term ‘ferroptosis’, derived from the Greek word ‘ptosis’ (falling) and the Latin word ‘ferrum’ (iron), is coined to describe such cell death phenomena. Cytoplasmic retraction, shrunken mitochondria, and the formation of lytic vacuoles are the main hallmarks of ferroptosis () . At the molecular level, ferroptotic cell death requires the availability of ROS, such as HO generated through the action of plasma membrane NADPH oxidases, and iron ions (Fe). The availability of suitable lipid substrates, such as polyunsaturated fatty acids (PUFA) that can undergo lipid peroxidation, and the lack of the antioxidant glutathione that suppresses lipid peroxidation are other conditions that are needed for ferroptosis . When ROS react with PUFA in the presence of iron ions, highly toxic hydroxyl (OH) radicals are generated . The reduced ability of the enzyme glutathione peroxidase (GPX4) and/or reduced availability of the amino Apocynin cysteine required for glutathione biosynthesis leads to the depletion of glutathione and consequently the ability of the cell to remove toxic radicals . Although these morphological and biochemical features differentiate ferroptosis from apoptosis or autophagy, like the other two cellular death pathways, ferroptosis appears to be controlled by the host. However, the original role of ferroptosis is unknown in animals. A number of environmental stress factors such as drought, heat, salinity, UV light and ozone, heavy metals, wounding, pest and pathogen attack activate a variety of different cell death pathways in plants. Cell death also occurs during normal plant growth and development such as senescence, tracheary element differentiation, aerenchyma formation, male and female sexual development, organ abscission, and self-incompatibility . While various forms of cell death have long been known to occur in plants, as discussed below, the evidence for ferroptosis-like cell death events has only recently been uncovered. Two recent studies highlighted here suggest that ferroptosis plays essential roles during biotic and abiotic stress adaptation in plants. Firstly, the exposure of root hair cells to heat shock (55°C) triggers cell death with hallmarks of ferroptosis (e.g., shrunken mitochondria, retracted cytoplasm, and lytic vacuoles) described above () . In addition, this cell death was accompanied by elevated iron (Fe) and ROS but reduced glutathione levels, suggesting that this might be a ferroptosis-like cell death phenomenon. Indeed, this cell death was inhibited both by ferrostatins, inhibitors of lipid peroxidation, and also by the iron chelator ciclopiroxolamine (CPX) . Although mostly distinct, heat shock-mediated ferroptotic cell death appears to share certain commonalities with other cell death pathways. For instance, caspases, a group of cysteine-proteases involved in apoptosis, are associated with heat shock-mediated ferroptosis . Interestingly, however, blocking ferroptotic cell death by preincubation with a ferroptosis inhibitor increased plant survival in exposed to heat stress at 43°C . Therefore, in this instance, preventing ferroptotic cell death through chemical or genetic means could be a potential way to improve heat stress tolerance in plants. However, why this disadvantageous cell death has been retained during evolution is not clear. Nevertheless, it is clear that excessive accumulation of toxic radicals under strong stress such as heat shock can no longer be neutralised by the antioxidant machinery and once a certain threshold is exceeded, this might lead to plant cell death. This is consistent with the idea that while low levels of cellular ROS are beneficial, high levels can cause deleterious effects . Therefore, it is possible that ROS need to be accumulated only in specific cells to cause cell death.