Hydroperoxides linoleate

In contrast to numerous literature data, which indicate that protein oxidation, as a rule, precedes lipid peroxidation, Parinandi et al. [66] found that the modification of proteins in rat myocardial membranes exposed to prooxidants (ferrous ion/ascorbate, cupric ion/tert-butyl-hydroperoxide, linoleic acid hydroperoxide, and soybean lipoxygenase) accompanied lipid peroxidation initiated by these prooxidant systems. 

Figure 2-20 Photooxidation. Singlet-oxygen attack on oleate produces two hydroperoxides linoleate yields four hydroperoxides...

Effects of linoleic acid and linoleic acid hydroperoxides on the myofibrils and the solutions of myofibrillar proteins of cod muscle have been proved using the electron microscopy (80). Linoleic acid hydroperoxides were ten times more effective than linoleic acid in reducing the amount of the protein in KCl-extracts from the myofibrils incubated with the acid or its hydroperoxides. Linoleic acid seemed to prevent the dissolution of the myofibril frame work but appeared not to impair the extraction of myosin while hydroperoxides appeared to cause a retention of A-bands (myosin) in the myofibrils. 

Lipoxygenase-Catalyzed Oxidations. Lipoxygenase-1 catalyzes the incorporation of dioxygen into polyunsaturated fatty acids possessing a l(Z),4(Z)-pentadienyi moiety to yield ( ),(Z)-conjugated hydroperoxides. A highly active preparation of the enzyme from soybean is commercially available in purified form. From a practical standpoint it is important to mention that the substrate does not need to be in solution to undergo the oxidation. Indeed, the treatment of 28 g/L of linoleic acid [60-33-3] with 2 mg of the enzyme results in (135)-hydroperoxide of linoleic acid in 80% yield... 

Lipid hydroperoxides are either formed in an autocatalytic process initiated by hydroxyl radicals or they are formed photochemically. Lipid hydroperoxides, known as the primary lipid oxidation products, are tasteless and odourless, but may be cleaved into the so-called secondary lipid oxidation products by heat or by metal ion catalysis. This transformation of hydroperoxides to secondary lipid oxidation products can thus be seen during chill storage of pork (Nielsen et al, 1997). The secondary lipid oxidation products, like hexanal from linoleic acid, are volatile and provide precooked meats, dried milk products and used frying oil with characteristic off-flavours (Shahidi and Pegg, 1994). They may further react with proteins forming fluorescent protein derivatives derived from initially formed Schiff bases (Tappel, 1956). 

Detection of cholesteryl linoleate hydroperoxides and phosphatidylcholine hydroperoxides 63... 

Chan, H.W.S. and Levett, G. (1977). Autoxidation of methyl linoleate. Separation and analysis of isomeric mixtures of methyl linoleate hydroperoxides and methyl hydrox-ylinoleates. Lipids 12, 99. 

Garssen, G.J., Vliegenthart, J.F.G. and Boldingh, J. (1972). The origin and structures of dimeric fetty acids from the anaerobic reaction between soya-bean lipoxygenase, linoleic acid and its hydroperoxide. Biochem. J. 130, 435-442. 

Yagi, K., Ohkawa, H., Oshistii, N., Yamashita, M. and Nakashima, T. (1981). Lesion of aortic intima caused by intravenous administration of linoleic hydroperoxide. J. Appl. Biochem. 3, 58-61. 

Reaction yields depend on the nature of the substrate. Linseed oil contains two polyunsaturated fatty acids 50% linolenic acid and 18% linoleic acid. The corresponding hydroperoxides are obtained with low yields. 

Yeum, K. J., Y. C. Leekim et al. (1995). Similar metabolites formed from beta-carotene by human gastric-mucosal homogenates, lipoxygenase, or linoleic acid hydroperoxide. Arch. Biochem. Biophys. 321(1) 167-174. 

Figure 10.7 Autoxidation of a linoleic acid ester. In step 1 the reaction is initiated by the attack of a radical on one of the hydrogen atoms of the -CH2-group between the two double bonds this hydrogen abstraction produces a radical that is a resonance hybrid. In step 2 this radical reacts with oxygen in the first of two chain-propagating steps to produce an oxygen-containing radical, which in step 3 can abstract a hydrogen from another molecule of the linoleic ester (Lin-H). The result of this second chain-propagating step is the formation of a hydroperoxide and a radical (Lin ) that can bring about a repetition of step 2.

Potato LOX has the potential to be used as an alternative model to the mammalian enzyme because of its great availability(Lopez-Nicolas and others 2000). To date, three isoenzymes of potato LOX have been isolated. Several works have reported linoleic acid as the optimum substrate for potato LOX-1, 9-hydroperoxide being the main product of the reaction. Another LOX substrate, linolenic acid, has been reported as the preferred substrate for both potato LOX-2 and -3, which produce 13-hydroperoxide as the main product. 

Inhibition and stimulation of LOX activity occurs as a rule by a free radical mechanism. Riendeau et al. [8] showed that hydroperoxide activation of 5-LOX is product-specific and can be stimulated by 5-HPETE and hydrogen peroxide. NADPH, FAD, Fe2+ ions, and Fe3+(EDTA) complex markedly increased the formation of oxidized products while NADH and 5-HETE were inhibitory. Jones et al. [9] also demonstrated that another hydroperoxide 13(5)-hydroperoxy-9,ll( , Z)-octadecadienoic acid (13-HPOD) (formed by the oxidation of linoleic acid by soybean LOX) activated the inactive ferrous form of the enzyme. These authors suggested that 13-HPOD attached to LOX and affected its activation through the formation of a protein radical. Werz et al. [10] showed that reactive oxygen species produced by xanthine oxidase, granulocytes, or mitochondria activated 5-LOX in the Epstein Barr virus-transformed B-lymphocytes. 

Schnurr et al. [22] showed that rabbit 15-LOX oxidized beef heart submitochondrial particles to form phospholipid-bound hydroperoxy- and keto-polyenoic fatty acids and induced the oxidative modification of membrane proteins. It was also found that the total oxygen uptake significantly exceeded the formation of oxygenated polyenoic acids supposedly due to the formation of hydroxyl radicals by the reaction of ubiquinone with lipid 15-LOX-derived hydroperoxides. However, it is impossible to agree with this proposal because it is known for a long time [23] that quinones cannot catalyze the formation of hydroxyl radicals by the Fenton reaction. Oxidation of intracellular unsaturated acids (for example, linoleic and arachidonic acids) by lipoxygenases can be suppressed by fatty acid binding proteins [24]. 

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