Peroxidation products, lipid, effects

There are contradictory data on the effects of dietary ascorbic acid on free radical-mediated damage in animals. Barja et al. [65] found that the administration of 660mg/kg vitamin C to guinea pigs for 5 weeks significantly decreased the levels of protein carbonyls and lipid peroxidation products. On the other hand, the administration of 500mg/kg vitamin C to... [Pg.855]

Lu C., Chan S. L., Haughey N., Lee W. T., and Mattson M. P. (2001). Selective and biphasic effect of the membrane lipid peroxidation product 4-hydroxy-2,3-nonenal on V-methyl-D-aspartate channels. J. Neurochem. 78 577-589. [Pg.100]

In our attempts to determine the possible role of free radical lipid peroxidation in smoke induced injury, the levels of lipid peroxidation products - thiobarbituric acid reactants, mainly malondialdehyde - wereQmeasured in lung homogenates with or without prior incubation at 37 C for one hour, contrary to our expectation, the levels of thiobarbituric acid reactants were found to be decreased, rather than increased, in the lungs of cigarette-smoke-exposed rats (Table III). Such a depression effect, however, was observed only when animals were exposed to whole smoke, and not to the gaseous phase of smoke. [Pg.236]

The potential consequences of the peroxidation of membrane lipids include loss of polyunsaturated fatty acids, decreased lipid fluidity, altered membrane permeability, effects on membrane-associated enzymes, altered ion transport, release of material from subcellular compartments, and the generation of cytotoxic metabolites of lipid hydroperoxides. The physiological significance of lipid peroxidation products is shown in Table 1. [Pg.136]

The cardioprotective effect of melatonin is demonstrated in several studies in in vivo and ex vivo experimental rat models or cardiomyocytes, as reviewed by Reiter.30 Melatonin administration in perfused rat hearts subjected to ischemia and reperfusion increased postischemic recovery of function, reduced the duration of ventricular tachycardia and ventricular fibrillation and this was associated with decreased lipid peroxidation products and OH radical formation, indicating an antioxidant effect of melatonin.31 Furthermore, in pinealectomized rats, occlusion of the left coronary artery followed by reperfusion resulted in significant increase in infarct size than in intact animals.32 Melatonin acts as scavenger of oxygen or nitrogen based reactants, stimulates antioxidant enzymes, stabilizes cellular membrane, increases the efficiency of oxidative phosphorylation, reduces leukocyte recruitment and adhesion molecule expression and reduces homocysteine induced damage (reviewed by Duncker33). [Pg.81]

Bajijiasu. Chen et al. [248] studied the protective effect ofBajijiasu (P-D-fructofuranosyl (2-2) p-D-fructofuranosyl), a dimeric fructose isolated from the Chinese herb radix Morinda officinalis, on Ap-induced neurotoxicity in pheochromocytoma (PC12) cells. Bajijiasu reversed the reduction in cell viability induced by exposure to Ap25 35, reduced Ap25 35-induced toxicity, decreased the accumulation of intracellular ROS and the lipid peroxidation product malondialdehyde, upregulated expression of glutathione reductase and superoxide dismutase, prevented depolarization of the mitochondrial membrane potential ( Em), and blocked... [Pg.408]

It should not be assumed that hydroxy fatty acids are biologically inactive. Hydroxy fatty acids are chemotactic and vasoactive. Such fatty acids could perturb phospholipids in membranes. For instance, cardiolipin containing hydroxy-linoleic acid does not support the electron transport coupled to ATP production of the mitochondrion. 5-Hydroxy de-canoic acid is a well-known inhibitor of the K -ATP channel. Isoprostanes, trihydroxy oxidation products of arachi-donic acid, are vasoconstrictors (76). 13-Hydroxy linoleic acid (13-HODE) is a lipoxygenase-derived metabolite that influences the thromboresistant properties of endothelial cells in culture (77). However, there is some doubt about the tme nature of these hydroxy-fatty acids generated by the cells, as there are several GSH- and NADPH-dependent pathways that can immediately reduce hydroperoxy- to hydroxy-fatty acids. Furthermore, the reduction step of the analytical method would have converted the hydroperoxy- to a hydroxy-group. Nevertheless, much work remains to be done to determine the relative contribution of hydroperoxy- and hydroxy- to the biological effects of fried fat, and in particular their role in endothelial dysfunction and activation of factor VII. There have been earlier suggestions that a diet rich in lipid peroxidation products may lead to atherosclerosis and CHD (34,78). [Pg.209]

Gomez-Ramos, A., Diaz-Nido, J., Smith, M.A., Perry, G. and Avila, J. 2003. Effect of the lipid peroxidation product acrolein on tau phosphorylation in neural cells. J. Neurosci. Res. 71 863-870... [Pg.515]

Two studies in mice (52) and rats (62) reported an increase in lipid peroxidation products, whereas studies in rabbits (54) and rats (16) reported no change. One study in rabbits and one in rats even reported a decrease in lipid peroxidation products (25, 63). The effects of CIA on lipid peroxidation seem conflicting, but may be tissue-specific. In fact, CLA has been claimed to inhibit tumorigenesis by inducing lipid peroxidation in cancer cells, producing a cytotoxic effect on tumor cells and concomitantly attenuating lipid peroxidation in neutral, hpid rich tissues (38). In humans, Basu et al. and Riserus et al. found a 3-7-fold increase in urinary prostaglandin F2a in subjects supplemented with CIA compared to olive oil supplemented controls (35, 64). [Pg.190]

Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...