Abstract
Ferroptosis is one of the forms of programmed cell death. Besides being a necessary micronutrient, iron is the key element that initiates ferroptosis in the cell. Intracellular unstable iron accumulation increases the amount of intracellular ROS, especially by the peroxidation of unsaturated membrane phospholipids. Insufficient antioxidant capacity and decreased glutathione levels play an important role in this process. The research reveals that an imbalance between unoxidized polyunsaturated fatty acids (PUFAs) and oxidized PUFAs, particularly oxidized arachidonic acid, accelerates ferroptosis. These oxidative reactions change the permeability of lysosomal and cellular membranes and cell death occurs. Iron chelators, lipophilic antioxidants, and specific inhibitors prevent ferroptosis. In addition to being accepted as a physiological process, it seems to be associated with tissue reperfusion damage, ischemic, neurodegenerative diseases, hematological and nephrological disorders. Ferroptosis is also being explored as a treatment option where it may offer a treatment option for some types of cancer. In this section, the brief history of ferroptosis, its morphological, molecular, and pathophysiological features are mentioned. Ferroptosis seems to be a rich field of research as a treatment option for many diseases in the future.