Lipid peroxidation (LPO) is initiated by the attack of free radicals (eg OH ·, O2- and H2O2) on cellular or organelle membranes phospholipids or polyunsaturated fatty acids (PUFA), and with the formation of various types of aldehydes, ketones, alkanes, carboxylic acids and polymerization products. It is an autoxidation process that results. These products are highly reactive with other cellular components and serve as biological markers of LPO. Malondialdehyde (MDA), a toxic aldehyde end product of LPO, causes structural changes that mediate its oxidation, such as fragmentation, modification, and aggregation, especially in DNA and protein. The excessive binding of these reactive aldehydes to cellular proteins alters membrane permeability and electrolyte balance. Degradation of proteins leads to progressive degradation of the biological system mediated by oxidative stress. The chain reaction (CR) of LPO is initiated by the attack of free radicals on the PUFA of the cell membrane to form a carbon centered radical (R*). The O2 · - radical attacks the other lipid molecule to form lipid hydroperoxide (ROOH), thereby spreading the CR and forming the lipid peroxyl radical (ROO). These lipid hydroperoxides severely inhibit membrane functionality by allowing ions such as increased hardness and calcium to leak through the membrane. Damage to the lipid membrane and macromolecule oxidation can result in activation of necrotic or apoptotic tissue death pathways if severe enough.