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.

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.

Several broad lines of scientific evidence showing that vitamin E functions as a lipid antioxidant, inhibiting the destructive peroxidation of polyunsaturated lipids, have been presented in recent reviews.'-Q Further, the function of vitamin E is a very broad topic, study of which can be based in part on knowledge of other lipid antioxidant reactions and interrelationships. Also, the reactions of and the damage caused by free radical peroxidation of lipids are complex topics, and in a relative sense the mechanisms of damage are not well understood, although they appear to have counterparts in radiation biochemistry. In view of the breadth of this topic, it is appropriate in the first section of this paper to direct attention to the major review sources in which information on the subject is summarized, and to some recently published papers. TABLE 1 lists some of the major factors in the suppression of lipid peroxidation. On the basis of the chemical properties of a-tocopherol and the mechanisms of antioxidation, a-tocopherol would be expected to react as a chain-breaking antioxidant in the inhibition of the free radical peroxidation of lipids. The propagation reaction in which the polyunsaturated lipid LH is peroxidized, L' + OZ'LOZ' LOZ. + LH+ LOOH + L' 1

Vitamin e and free radical peroxidation of lipids

Homogenates of mouse liver and brain at 37 degrees C spontaneously formed lipid peroxides and simultaneously evolved ethane. alpha-Tocopherol, a lipid antioxidant, blocked ethane formation. When mice were injected with carbon tetrachloride (a liquid prooxidant for liver), the animals produced ethane. Ethane evolution in vivo was stimulated by prior administration of phenobarbital and it was diminished by prior injection of alpha-tocopherol. These data suggest that ethane production may be a useful index of lipid peroxidation in tissue homogenates and in intact animals.

https://science.sciencemag.org/content/sci/183/4121/208.full.pdf

Ethane evolution: a new index of lipid peroxidation.

Colostomy: formation and closure

The thiobarbituric acid reacting material produced during enzymatic microsomal lipid peroxidation has been identified as malonaldehyde. The malonaldehyde was condensed with urea to form 2-hydroxy-pyrimidine, which was identified by its ultraviolet spectrum, chromato-graphic properties, and mass spectrum. Incubations with phosphatidyl choline labelled with tritiated arachidonate yielded 2-hydroxy-pyrimidine with a specific activity nearly equal to that of the phospholipid arachidonate. Incubations with tritiated arachidonic acid yielded 2-hydroxy-pyrimidine with a specific activity nearly 2 orders of magnitude less than that of free arachidonic acid. Therefore, phospholipid arachidonate has been established as the major source of the malonaldehyde produced during microsomal lipid peroxidation.

https://febs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1432-1033.1968.tb00428.x

B. Samuelsson

Papers

Formation of Malonaldehyde from Phospholipid Arachidonate during Microsomal Lipid Peroxidation