Lipid peroxidation radical-induced oxidation

The effect of PJ consumption by patients with CAS on their serum oxidative state was measured also as serum concentration of antibodies against Ox-LDL.31 A significant (p < 0.01) reduction in the concentration of antibodies against Ox-LDL by 24 and 19% was observed after 1 and 3 months of PJ consumption, respectively (from 2070 61 EU/mL before treatment to 1563 69 and 1670 52 F.lI/mL after 1 and 3 months of PJ consumption, respectively). Total antioxidant status (TAS) in serum from these patients was substantially increased by 2.3-fold (from 0.95 0.12 nmol/L at baseline up to 2.20 0.25 nmol/L after 12 months of PJ consumption). These results indicate that PJ administration to patients with CAS substantially reduced their serum oxidative status and could thus inhibit plasma lipid peroxidation. The susceptibility of the patient s plasma to free radical-induced oxidation decreased after 12 months of PJ consumption by 62% (from 209 18 at baseline to 79 6 nmol of peroxides/milliliter). The effect of PJ consumption on serum oxidative state was recently measured also in patients with non-insulin-dependent diabetes mellitus (NIDDM). Consumption of 50 mL of PJ per day for a period of 3 months resulted in a significant reduction in serum lipid peroxides and thiobarbituric acid reactive substance (TBAR) levels by 56 and 28%, respectively.32... 

Hyperglycemia-induced oxidative stress has an important role in the pathogenesis of diabetic complications. Human monocytes exposed to 2-deoxy-D-ribose exhibited loss of cell viability, overproduction of ROS, depletion of glutathione, and apoptosis. Treatment with PLP inhibited these as well as lipid peroxidation and protein oxidation (4). Pyridoxine has a very high level of quenching of hydroxyl radicals (5). Mono- and bicyclic amino pyridinols have been synthesized from pyridoxine hydrochloride and have been shown to have antioxidant properties (6). 

Peroxyl radicals are the species that propagate autoxidation of the unsaturated fatty acid residues of phospholipids (50). In addition, peroxyl radicals are intermediates in the metabolism of certain drugs such as phenylbutazone (51). Epoxidation of BP-7,8-dihydrodiol has been detected during lipid peroxidation induced in rat liver microsomes by ascorbate or NADPH and during the peroxidatic oxidation of phenylbutazone (52,53). These findings suggest that peroxyl radical-mediated epoxidation of BP-7,8-dihydrodiol is general and may serve as the prototype for similar epoxidations of other olefins in a variety of biochemical systems. In addition, peroxyl radical-dependent epoxidation of BP-7,8-dihydrodiol exhibits the same stereochemistry as the arachidonic acid-stimulated epoxidation by ram seminal vesicle microsomes. This not only provides additional... 

As a rule, oxygen radical overproduction in mitochondria is accompanied by peroxidation of mitochondrial lipids, glutathione depletion, and an increase in other parameters of oxidative stress. Thus, the enhancement of superoxide production in bovine heart submitochondrial particles by antimycin resulted in a decrease in the activity of cytochrome c oxidase through the peroxidation of cardiolipin [45]. Iron overload also induced lipid peroxidation and a decrease in mitochondrial membrane potential in rat liver mitochondria [46]. Sensi et al. [47] demonstrated that zinc influx induced mitochondrial superoxide production in postsynaptic neurons. 

Quercetin and rutin suppressed photosensitized hemolysis of human erythrocytes with ho values equal to 40 p.mol l-1 and 150 jjlmt>I I 1, respectively [139]. Suppression of photohemolysis was accompanied by inhibition of lipid peroxidation. Morin inhibited oxygen radical-mediated damage induced by superoxide or peroxyl radicals to the human cells in the cardiovascular system, erythrocytes, ventricular myocytes, and saphenous vein endothelial cells [140]. Rutin protected against hemoglobin oxidation inside erythrocytes stimulated by prooxidant primaquine [141],... 

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. 

Thus, the mechanism of MT antioxidant activity might be connected with the possible antioxidant effect of zinc. Zinc is a nontransition metal and therefore, its participation in redox processes is not really expected. The simplest mechanism of zinc antioxidant activity is the competition with transition metal ions capable of initiating free radical-mediated processes. For example, it has recently been shown [342] that zinc inhibited copper- and iron-initiated liposomal peroxidation but had no effect on peroxidative processes initiated by free radicals and peroxynitrite. These findings contradict the earlier results obtained by Coassin et al. [343] who found no inhibitory effects of zinc on microsomal lipid peroxidation in contrast to the inhibitory effects of manganese and cobalt. Yeomans et al. [344] showed that the zinc-histidine complex is able to inhibit copper-induced LDL oxidation, but the antioxidant effect of this complex obviously depended on histidine and not zinc because zinc sulfate was ineffective. We proposed another mode of possible antioxidant effect of zinc [345], It has been found that Zn and Mg aspartates inhibited oxygen radical production by xanthine oxidase, NADPH oxidase, and human blood leukocytes. The antioxidant effect of these salts supposedly was a consequence of the acceleration of spontaneous superoxide dismutation due to increasing medium acidity. 

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