Membrane lipids constitute a main target for reactive oxygen species causing peroxidative damage. Polyunsaturated fatty acids are particularly affected. The process of lipidperoxidation can be divided in three main phases:

- an initiation phase consisting of the formation of a radical of fatty acid by removal of a methylene hydrogen *H (CH2) from a polyunsaturated fatty acid (RH) by an oxygen radical (mostly * OH).

- a propagation phase corresponding to an amplifying process originating from the oxygen which initiates the first hydroperoxide radical:

This hydroperoxide radical can in turn react with a nearby fatty acid R'H, generating another hydroperoxide and a radical of fatty acid :

This reaction self-maintains and propagates to nearby molecules; it is considered that a radical R * can be at the origin of hundreds of hydroperoxide molecules before the phase of termination intervenes by the formation of a stable compound from the association of two radicals.

- a phase of termination, resulting from a reaction of radicals established on a probabilistic basis. There are three sorts of termination reactions, two by biradicalar reaction and one by reaction with an antioxidant :

The peroxidation of membrane fatty acids, inducing indirect conformational and structural changes of the lipid bilayer, is representative of the radical toxicity of oxygen for membranes and associate proteins such as enzymes, ion channels and receptors. Even though the superoxide radical O2'- is often cited as the origin of peroxidation, it mainly acts as the precursor of two main initiators of lipid peroxidation: the hydroxyl radical "OH originating from H2O2 and the hydroperoxide radical ROO'. H2O2 results from the dismutation of O2'-, which can be spontaneous but is mainly catalyzed by superoxide dismutases (SODs):

The hydroxyl radical (*OH), is produced by H2O2 and O2" through two reactions dependent on iron:

- the Fenton reaction H2O2 + Fe2+-> Fe3+ + 'OH + 'OH

- The Haber-Weiss reaction O2'-+ H2O2-> O2 + 'OH + -OH

Under physiological conditions, most of these toxic species are eliminated by various systems of defence: cellular and extra-cellular enzymes (superoxide dismutases, catalase, glutathione peroxidase) and non-enzymatic substances (ascorbic acid, tocopherol, beta-carotene). In fact, oxygen toxicity occurs when there is an exaggerated production of reactive oxygen species or when the means of defence are overwhelmed. As an example, hemolysis consecutive to bleeding and hematoma formation can be at the origin of a massive delocalization of ionized iron which constitutes an initiator of oxidative processes.

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