Cellular injury is defined as an alteration in cell structure or function resulting in stress that exceeds the compensatory ability of the cell. If the injury is severe enough, the cell suffers irreversible injury and dies. Cells death has historically been subdivided into necrosis and apoptosis. Actually, the simple apoptosis-necrosis classification does not adequately represent the complexity of cell death regulation. 'Autophagic cell death', 'mitoptosis', 'mitotic catastrophe'. 'anoikosis' and 'oncosis' are the other expressions rarely used in order to define different types of cell death. Some mechanisms of apoptosis and necrosis are related to the process mediated by reactive oxygen and nitrogen species (ROS and RNS, respectively). Mitochondria are strong producers of ROS and at the same time, particularly susceptible to the oxidative damage produced by their action on lipids, proteins, and DNA. To protect cells from the damage caused by free radicals and related reactants, organisms have evolved several defense mechanisms to remove ROS from the intracellular environment. When free radical generation exceeds the defense capabilities of the organism, molecular damage is sustained. As this damage accumulates, cellular function gradually declines, eventually leading to death of cells, organs and the organism itself. Oxidative damage has been implicated in the pathogenesis of a range of diseases and ageing. Antioxidant and free radical scavenging agents against the destructive actions of free radicals are of obvious interest. In this paper, cell death concepts, their molecular mechanisms, histopathological aspects of oxidative stress related cell injury and death, and cellular anti-oxidative defense systems were reviewed.