Lipid oxidation polyunsaturated fatty acids, related

The main action of vitamin E in human tissue is to prevent oxidation of polyunsaturated fatty acids (PUFA), thereby protecting lipid and phospholipids in membranes. Vitamin E interacts syn-ergically with other nutrients, such as vitamin C, selenium, and zinc, which are also involved in the oxidation pathway. The recommended intake is strongly related to the quantity of PUFA consumption. Some studies [454-456] on animal models and epidemiological trials in human suggest... 

Lipoxygenases, of which the enzyme from soy beans has been studied the most, also catalyze oxidation of polyunsaturated fatty acids in lipids as indicated in Eq. 21-17. Formation of the hydroperoxide product is accompanied by a shift of the double bond and conversion from cis to trans configuration. Soybean lipoxygenase is a member of a family of related lipoxygenases that are found in all eukaryotes. All... 

Aldehydes The oxidative breakdown of polyunsaturated fatty acids generates a number of aldehydes, which are highly bioactive and well characterized molecules. Aldehydes are longer-lived than free radicals, and are able to attack targets extra or intracellularly (for review see Esterbauer et al., 1991). Among the different aldehydes formed during lipid and LDL oxidation, malondialdehyde and 4-hydroxyl alkenals, in particular 4-hydroxynonenal (4-HNE), have been intensively studied. 4-HNE results from the oxidation of arachidonic acid and, to a lesser extent, linoleic acid (Esterbauer et al., 1991). 4-HNE and related hydroxyalkenals react rapidly... 

Direct Measurements—UVNIS Techniques. The conjugated diene (CD) formed among the polyene hydroperoxide products that are formed as a result of oxidation of polyunsaturated fatty acids (PUFAs) have a UV absorbance that can be monitored to follow the progress of the oxidation. The effect of antioxidants on the suppressed rate of product formation can be followed with time. For example, conjugated dienes from oxidation of linoleate lipid molecules absorb at 234 nm and can be monitored directly , or else after HPLC separation (via normal phase or reverse phase j of the individual isomers. In order to use these findings to calculate the antioxidant activity of phenols and relate it to oxygen uptake studies (equations 7 and 14), one also has to make a correction to account for loss of absorbance due to loss (from decomposition) of hydroperoxides (equation 22) . 

Central among the toxic responses to oxidative stress is the induction of apop-totic death (Curtin et al, 2002 Fleury et al, 2002 Polster and Fkskum, 2004 Ryter et al, 2007). While it is clear that it can be an initiator as well as a signaling event within the apoptotic process, the specific mechanisms underlying these remain uncertain. Likely, these responses could be related to the damage of cellular components e.g. DNA, lipids, and polysaccharides. One potential pathway by which ethanol-mediated oxidative stress may elicit apoptosis of neurons is associated with the oxidation of polyunsaturated fatty acids within mitochondria (Ramachandran et al, 2001, 2003). Among the variety of oxidation products of these fatty acids are toxic/pro-apoptotic aldehydes, the most potent being 4-hydrox-ynonenal (Esterbauer et al, 1990 Uchida et al., 1993). This compound readily induces apoptotic death of neurons (Lovell and Markesbery, 2006 Dwivedi et al., 2007) and is produced in neurons secondary to ethanol-related oxidative stress (Ramachandran et al, 2001, 2003)... 

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