Publisher Summary This chapter discusses microsomal lipid peroxidation Lipid peroxidation is a complex process known to occur in both plants and animals It involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and the eventual destruction of membrane lipids, producing a variety of breakdown products, including alcohols, ketones, aldehydes, and ethers Biological membranes are often rich in unsaturated fatty acids and bathed in an oxygen-rich, metal-containing fluid Lipid peroxidation begins with the abstraction of a hydrogen atom from an unsaturated fatty acid, resulting in the formation of a lipid radical The formation of lipid endoperoxides in unsaturated fatty acids containing at least 3 methylene interrupted double bonds can lead to the formation of malondialdehyde as a breakdown product Nonenzymic peroxidation of microsomal membranes also occurs and is probably mediated in part by endogenous hemoproteins and transition metals The direct measurement of lipid hydroperoxides has an advantage over the thiobarbituric acid assay in that it permits a more accurate comparison of lipid peroxide levels in dissimilar lipid membranes

Microsomal lipid peroxidation.

Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes.

Determination of malonaldehyde precursor in tissues by thiobarbituric acid test

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

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Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

Publisher Summary This chapter discusses the methods used for the qualitative and quantitative determination of aldehydes in biological systems. It focuses on 4-hydroxynonenal (HNE) and malondialdehyde (MDA). 4-Hydroxynonenal is produced as a major product of the peroxidative decomposition of polyunsaturated fatty acids (PUFA) and possesses cytotoxic, hepatotoxic, mutagenic, and genoroxic properties. Increased levels of HNE are found in plasma and various organs under conditions of oxidative stress. In addition to HNE, lipid peroxidation generates many other aldehydes that may also be of toxicological significance. Malondialdehyde is in many instances the most abundant individual aldehyde resulting from lipid peroxidation, and its determination by thiobarbituric acid (TBA) is one of the most common assays in lipid peroxidation studies. In vitro MDA can alter proteins, DNA, RNA, and many other biomolecules. Recently, it has been demonstrated with monoclonal antibodies that malonaldehyde-altered protein occurs in atheroma of hyperlipidemic rabbits.

Determination of aldehydic lipid peroxidation products: malonaldehyde and 4-hydroxynonenal

The nature and mechanism of formation of the thiobarbituric acid (TBA)-reactive material produced in the autoxidation of polyunsaturated fatty acids (PUFA) or their esters has been studied. On the basis of chemical studies and

Autoxidation of polyunsaturated fatty acids: II. A suggested mechanism for the formation of TBA-reactive materials from prostaglandin-like endoperoxides.

Letter: A suggested mechanism for the production of malonaldehyde during the autoxidation of polyunsaturated fatty acids. Nonenzymatic production of prostaglandin endoperoxides during autoxidation.

Neat samples of polyunsaturated fatty acids were exposed to ozone in air in a flow system and the formation of peroxides, conjugated dienes and thiobarbituric acid (TBA)-reactive material was followed as a function of time. The effect of ozone is to shorten the induction period normally observed in autoxidation studies, but the ozone, at the concentrations used here (0–1.5 ppm), appears to have no effect on the rates of product formation after the induction period. During the induction period, increasing ozone concentrations give rise to substantially increased rates of peroxide (or materials which titrate like peroxide) formation, a slightly increased rate of conjugated dienes formation, and no significant increase in the rate of production of TBA-reactive material. Vitamin E lengthens the induction period but appears to have no other effect. Some of these data are in conflict with earlier reports of Menzel et al.

Autoxidation of polyunsaturated fatty acids. Part I. Effect of ozone on the autoxidation of neat methyl linoleate and methyl linolenate.

Reactions of the hydrogen atom in solution. VI. Addition of hydrogen atoms to substituted benzenes. Use of the Hammett equation for correlating radical reactions

J. P. Stanley

Papers

Autoxidation of polyunsaturated fatty acids: II. A suggested mechanism for the formation of TBA-reactive materials from prostaglandin-like endoperoxides.

Letter: A suggested mechanism for the production of malonaldehyde during the autoxidation of polyunsaturated fatty acids. Nonenzymatic production of prostaglandin endoperoxides during autoxidation.

Autoxidation of polyunsaturated fatty acids. Part I. Effect of ozone on the autoxidation of neat methyl linoleate and methyl linolenate.

Reactions of the hydrogen atom in solution. VI. Addition of hydrogen atoms to substituted benzenes. Use of the Hammett equation for correlating radical reactions

Reactions of radicals. 41. Reactivity patterns of the methyl radical