ABSTRACT
E-mail: jsegura@uma.es 3Department of Biología Molecular y Bioquímica, Facultad de Ciencias, Campus
de Teatinos, Universidad de Málaga, 29071 Málaga, Spain E-mail: fcarrion@uma.es
4Department of Biología Molecular y Bioquímica, Facultad de Ciencias, Campus de Teatinos, Universidad de Málaga, 29071 Málaga, Spain
E-mail: marquez@uma.es
Oxidative stress develops when the production of oxidative species exceeds the capacity of the cell to detoxify them. In parallel, apoptosis can occur when cellular damage, including damage to genetic material, has exceeded the capacity for repairing it. Th e generation of mitochondrial reactive oxygen species (ROS) is mainly a consequence of oxidative phosphorylation. Oxidative stress may induce apoptosis through the intrinsic pathway by the release of cytochrome c and other apoptotic factors from the mitochondria. Any imbalance in redox status may relate to pathogenesis including cancers. ROS can also act as a second messenger in cell signalling and are essential for various biological processes in normal cells. ROS levels are regulated by a number of enzymes such as superoxide dismutase, catalase, glutathione peroxidase, thioredoxins, and physiological antioxidants. DNA damage by ROS can cause multiple lesions, including activation of p53-mediated DNA damage response that can induce apoptosis. Lipid peroxidation has been shown to
alter membrane properties, and mitochondrial membrane potential, also aff ecting cell death. Th e direct oxidation of amino acid residues promotes oxidation of the sulfh ydryl groups of proteins or the formation of carbonyls, which can alter protein structure and lead to loss of its normal function and, eventually, to apoptosis.
