Lipids are an important component of transacting that maintains structure and control cell function. The main target lipids from ROS attacks such as oxygen free radicals and lipid oxidation are associated with various pathological conditions. Oxidation by free radicals in organic compounds has historically been referred to by organic and physical chemists as autoxidation. Lipids and biologically important compounds (proteins, carbohydrates, nucleic acids) undergo a reaction of oxidation by free radicals called peroxidation. Peroxidation is involved in a number of human diseases such as atherosclerosis, cancer, diabetes, recent diseases, as well as disorders and neurosurgery, Alzheimer's and Parkinson's. Lipid peroxidation is involved as a mediator of various pathologies including inflammation, cancer. In addition, lipid peroxidation acts as a regulator of non apoptotic cell death. [1,5]. MDA is the result of lipid peroxidation, which is produced from damage to polyunsaturated fatty acids. MDA is a good indicator of lipid peroxidation and as a biomarker of oxidative stress [7,8].

Fatty peroxyl radicals are early PUFA autoxidation intermediates, and fatty hydroperoxides are the first primary oxidation products. Fatty hydroperoxides, labile species and easily enter radical reactions that lead to molecular transformation and decomposition. Although MDA is generally recognized as a volatile end product from heat, acid, or metal-catalysts, the composition of the autoxidized PUFA composition underlies the lipid transformation. One of the first mechanisms of MDA formation from PUFA containing three or more double bonds show that fatty peroxylradicals are produced during autoxidation and cyclize to oxybridged radicals. Subsequent decomposition of monocyclic peroxides through the intramolecular process produces MDA (and other fragmentation products). Pryor et al. Formulated an alternative mechanism where lipid peroxyl radicals cyclize via oxybridged radicals, five-membered ring to allylicendoperoxide radicals, which separate into prostaglandin-like endoperoxides. Intra-molecular process in the endoperoxide ring to produce MDA. (and hydroperoxide) [9].

The most important type of enzyme catalyst for hydroperoxide reduction so that hydroxide is formed is glutathione peroxidase (GPx). Lipid hydroperoxides are reduced in reactions involving selenocysteine residues GPx. As a result, lipid hydroxide and oxidized glutathione (9) are produced. Selenium is a micronutrient integral part of the enzyme glutathione peroxiidase (GPX) [10]. GPX, an enzyme that depends on micronutrient selenium (Se), plays an important role in the reduction of hydroxide lipids. Compared to hydroperoxides, hydroxides have a significantly lower chemical reactivity character because they are considered stable and relative oxidation products are non-toxic [11].

Vitamin E is not an agent to reduce peroxides bonds, but as a radical scavenging agent. During the process of lipid peroxides, vitamin E acts as a donor of an intermediate electron peroxyl radical (9). Cell plasma has non enzymatic scavenger free radicals such as ascorbic acid, α-tocopherol (vitamins C and E) [11].

Malondialdehyde (MDA) is a product of lipid peroxidation that appears to be produced in a relatively constant proportion of the breakdown of polyunsaturated fatty acids. The MDA count is a good indicator of lipid peroxidation especially in vitro [11]. The chemical analysis of MDA began by measuring a component called thiobarbituric acid-reactive substances (TBARS) to estimate lipid peroxidation with spectrophotometry. Under acidic conditions (eq glacial acetic acid or sulfuric acid) and increasing temperature (eq 95°C), extended reaction time (eq 60 minutes), one MDA molecule reacts with two TBA molecules forming a red-colored, strongly visible light-absorbing (λmax, 532 nm) and fluorescent (λex, 515 nm); λem, 553 nm) derivate or condensation TBA-MDA adduct [12].