Thermodynamic and Kinetic Aspects of the Lipid Peroxidation of Arachidonic Acid

2011 ◽  
Vol 8 (4) ◽  
pp. 390-400
Author(s):  
Claire Claire E. Tornow ◽  
Betsy Lau ◽  
M. C. Milletti
1995 ◽  
Vol 74 (3) ◽  
pp. 369-380 ◽  
Author(s):  
Maeve R. Nolan ◽  
Seamus Kennedy ◽  
W. John Blanchflower ◽  
D. Glenn Kennedy

In a 2×2 balanced factorial experiment the biochemical effects on pigs of two dietary factors were investigated. The first factor was α-tocopherol and Se supplementation and the second factor was supplementation with α-tocopherol-stripped linseed oil. In pigs fed on diets depleted of α-tocopherol and Se, increases in concentrations of markers of lipid peroxidation (4-hydroxynonenal and hexanal) were observed. However, skeletal myopathy was only observed in those pigs fed on diets depleted of α-tocopherol and Se and supplemented with oil. In those pigs, increased lipid peroxidation was observed in heart and supraspinatus muscle. The plasma concentration of thromboxane B2 was increased in pigs fed on diets depleted of α-tocopherol and Se, suggesting an increased tendency towards platelet aggregation. However, this change was reversed in pigs depleted of α-tocopherol and Se, but supplemented with oil. This may have been a consequence of loss of arachidonic acid, the substrate for thromboxane formation, as a result of lipid peroxidation.


1983 ◽  
Vol 212 (1) ◽  
pp. 167-171 ◽  
Author(s):  
Y Fujimoto ◽  
H Tanioka ◽  
I Keshi ◽  
T Fujita

Lipid peroxidation induced by ascorbic acid and Fe2+ was inhibited by mepacrine (phospholipase A2 inhibitor) and aspirin (prostaglandin cyclo-oxygenase inhibitor) in rabbit kidney-medulla slices. Moreover, ascorbic acid and Fe2+ potentiated the inhibitory effect on prostaglandin E2 formation by mepacrine, but they had no influence on prostaglandin E2 production decreased by aspirin. Lipid peroxidation induced by ascorbic acid and Fe2+ appears to be affecting the activity of prostaglandin endoperoxide synthase. These results suggest that lipid peroxidation is connected closely with the prostaglandin-generating system, and it has the potential to modulate the turnover of arachidonic acid and prostaglandin synthesis.


2004 ◽  
Vol 32 (1) ◽  
pp. 139-140 ◽  
Author(s):  
M. Guichardant ◽  
B. Chantegrel ◽  
C. Deshayes ◽  
A. Doutheau ◽  
P. Moliere ◽  
...  

Several markers of lipid peroxidation are available with different degrees of specificity, from malondialdehyde as a global marker, to F2-isoprostane, which is specifically produced from arachidonic acid. Among these, 4-hydroxynonenal is recognized as a breakdown product of fatty acid hydroperoxides, such as 15-hydroperoxy-eicosatetraenoic acid and 13-hydroperoxy-octade cadienoic acid from the n−6 fatty acids. Furthermore, 4-hydroxyhexenal (4-HHE) derives from n−3 fatty acid hydroperoxides. We have recently described the occurrence of 4-hydroxydodecadienal (4-HDDE) from the 12-lipoxygenase product of arachidonic acid 12-hydroperoxy-eicosatetraenoic acid. These three hydroxy-alkenals may be measured in human plasma by GC–MS, but they may partly be generated in the course of sampling, and the relative volatility of 4-HHE makes its measurement quite unreliable. We have successfully characterized and measured the stable oxidized carboxylic acid products from the hydroxy-alkenals 4-HNA, 4-HHA and 4-HDDA in urine. The ratio between 4-HHA and 4-HNA found in the same urinary sample might provide useful information on the location of lipid peroxidation, accounting for the high enrichment of the cerebrovascular system with docosahexaenoic acid, the main n−3 fatty acid in humans.


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