Free radical-mediated chain oxidation of low density lipoprotein and its synergistic inhibition by vitamin E and vitamin C

Sato, Keizo; Niki, Etsuo; Shimasaki, Hiroyuki

doi:10.1016/0003-9861(90)90508-v

Cited by 307 publications

(144 citation statements)

References 21 publications

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“…Each antioxidant vitamin level in our studied groups correlated with their plasma antioxidant status. b-Carotene prevents oxidation of LDL (Jialal & Norkus, 1991); vitamin C also prevents oxidation of LDL and preserves vitamin E and b-carotene levels during oxidative stress (Sato et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Effect of diet on plasma total antioxidant status in phenylketonuric patients

et al. 2003

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Background: Phenylketonuria (PKU), an inborn error of phenylalanine (Phe) metabolism, is treated with a low Phe lifelong diet, which is a vegetarian and contains many antioxidants. Aim: The aim of this study was to evaluate the effect of diet on plasma total antioxidant status in our PKU patients. Methods, Results: Twenty-two PKU patients on strict diet (group A), 24 PKU patients who did not accurately follow their dietary control (group B) and 40 healthy children (controls) of comparable age took part in this study. Nutrients, as well as blood levels of lipids, vitamin C, b-carotene and a-tocopherol were evaluated in all groups. Vitamin C intake and its blood levels did not differ between the groups. However, the intake of b-carotene, a-tocopherol (2211 AE 116, 14 AE 1.0 mg=24 h) and their blood levels (0.7 AE 0.09, 34 AE 0.9 mmol=l) in group A were statistically significantly higher (P < 0.001) as compared with those of group B (1352 AE 118, 10 AE 1.0 mg=24 h and 0.49 AE 0.08, 22 AE 0.6 mmol=l) and controls (1290 AE 120, 9.0 AE 0.9 mg=24 h and 0.40 AE 0.09, 24 AE 1.6 mmol=l). Lipid intakes and their blood levels were lower in patients on the strict diet. Plasma total antioxidant status was higher in the same group of patients (group A). Additionally, positive correlations were found between the antioxidant vitamin blood levels and the plasma total antioxidant status in the groups, especially in the group A. PKU patients of group A showed significantly higher antioxidant status (1.6 AE 0.2 mmol=l) as compared with those of group B (1.0 AE 0.19 mmol=l; P < 0.001) and controls (1.01 AE 0.2 mmol=l). Conclusions: The high plasma antioxidant status in patients with PKU, especially in those with a good compliance with their diet, is possibly due to the amounts of antioxidants which are present in their special low Phe vegetarian diet.

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Section: Discussionmentioning

confidence: 99%

Effect of diet on plasma total antioxidant status in phenylketonuric patients

et al. 2003

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“…The Effect of ⅐ NO Release Rate on ABAP-mediated LDL Oxidation-ABAP, a peroxyl radical generator, has been shown to oxidize LDL by initiating lipid peroxidation (28). Addition of ABAP (1 mM) to LDL (200 g/ml protein) led to a time-dependent increase in TBARS formation over a period of 10 h after a 2-h lag period (Fig.…”

Section: Verification and Characterization Of ⅐ No Release Frommentioning

confidence: 95%

The Effect of Nitric Oxide Release Rates on the Oxidation of Human Low Density Lipoprotein

Goss

Hogg

Kalyanaraman

1997

Journal of Biological Chemistry

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1-Substituted diazen-1-ium-1,2-diolates, a class of nitric oxide ( ⅐ NO) donor compounds that spontaneously release ⅐ NO at different rates, were used to investigate the effect of ⅐ NO release rate upon the oxidation of low density lipoprotein (LDL). All donor compounds conferred an inhibitory effect upon the oxidation of LDL; however, the effect exhibited a biphasic dependence upon the rate of ⅐ NO release. The ⅐ NO release rate that maximally inhibited oxidation was dependent upon the rate of oxidation. When LDL was rapidly oxidized by copper(II) sulfate, a faster release rate was more effective. In contrast, when LDL was oxidized slowly by 2,2 -azobis-2-amidinopropane hydrochloride, a slower release rate was most effective. This biphasic relationship between ⅐ NO release rate and the duration of inhibition was also demonstrated when LDL oxidation was initiated with 5-amino-3-(4-morpholinyl)-1,2,3-oxadiazolium, a peroxynitrite generator. We conclude that the antioxidant ability of ⅐ NO is dependent not only upon the rate of its release from ⅐ NO donors, but also upon the rate of oxidation. This conclusion is supported by a kinetic model of LDL oxidation in the presence of ⅐ NO.The chronic inhibition of nitric oxide synthase (NOS) 1 accelerates atherosclerosis in cholesterol-fed rabbits (1, 2). Supplementation of L-arginine, the substrate for NOS, has been shown to decrease fatty streak formation in rabbits and correct endothelial dysfunction in hypercholesterolemic humans (3-5). These data suggest that basal production of ⅐ NO from the vascular endothelium can suppress the changes associated with early atherosclerotic lesion formation. Moreover, augmentation of ⅐ NO production can partially counteract the effects of elevated cholesterol levels.The mechanisms by which ⅐ NO affects atherosclerotic lesion formation are unclear; however, there are many possibilities.⅐ NO has been shown to inhibit inflammatory cell adhesion to the endothelium (6) and suppress smooth muscle cell proliferation (7). In later stages of atherosclerosis, the anti-thrombolytic properties of ⅐ NO (8) may also be relevant.It has frequently been proposed that the initiation of the atherosclerotic process is oxidative in nature. Free radicalmediated oxidative damage to both the vascular endothelium and low density lipoprotein (LDL) has been proposed to be a vital component of the atherosclerotic mechanism (9, 10). We have recently shown that ⅐ NO suppresses the oxidative modification of LDL (11-13) and inhibits the toxicity of oxidized LDL to endothelial cells (14). We have proposed that the way in which ⅐ NO inhibits oxidative processes is by scavenging propagatory lipid peroxyl radicals, thus suppressing the lipid peroxidation chain reaction (11)(12)(13)(14). This mechanism will generate lipid/NO adducts that have recently been identified (15,16).Many biological effects of ⅐ NO appear to be related to the rate of ⅐ NO formation (15,17,18). Bolus delivery of high concentrations of ⅐ NO may result in limited LDL oxidation that can be augmente...

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“…15 , 16 Synergistic protective effects of vitamins C and E were reported against lipid peroxidation in a model membrane system 17 and in solution, 1 8 -20 and against oxidation of low density lipoprotein. 21 In the present study, we investigated the effect of vitamin C on experimental compression injury to the spinal cord in rat by using a mutant strain of Wistar rats unable to synthesize ascorbic acid.…”

Section: Introductionmentioning

confidence: 99%

Effect of dietary vitamin C on compression injury of the spinal cord in a rat mutant unable to synthesize ascorbic acid and its correlation with that of vitamin E

et al. 1996

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The roles of vitamin C on secondary pathological changes after spinal cord injury were investigated by evaluating the effects of dietary vitamin C on experimental spinal cord injury in a mutant strain of Wistar rats unable to synthesize ascorbic acid (ODS rats). Two groups of ODS rats were given vitamin C-deficient or vitamin C-supplemented diet for 1 week before injury. Motor disturbance induced by spinal cord injury was found to be greater in the vitamin C-deficient group. Histologically, the area of bleeding in the spinal cord was also greater in the vitamin C-deficient group. The levels of ascorbic acid and a-tocopherol in the spinal cord tissue and serum decreased during and after compression injury of the spinal cord. The decrease of a-tocopherol was similar in the two groups. However, the decrease of ascorbic acid was greater in the vitamin C-supplemented group. These results indicated that their protective effects against spinal cord injury are through scavenging water-soluble free radicals by vitamin C and lipid-soluble by vitamin E, and the effects of these vitamins were suggested to be independent.

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Free radical-mediated chain oxidation of low density lipoprotein and its synergistic inhibition by vitamin E and vitamin C

Cited by 307 publications

References 21 publications

Effect of diet on plasma total antioxidant status in phenylketonuric patients

Effect of diet on plasma total antioxidant status in phenylketonuric patients

The Effect of Nitric Oxide Release Rates on the Oxidation of Human Low Density Lipoprotein

Effect of dietary vitamin C on compression injury of the spinal cord in a rat mutant unable to synthesize ascorbic acid and its correlation with that of vitamin E

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