Ascorbate Supplement Reduces Oxidative Stress in Dyslipidemic Patients Undergoing Apheresis

Chien, Chiang Ting; Chang, Wei; Chen, Heui Wen; Wang, Tzung‐Dau; Liou, Shaw Yih; Chen, Tzay Jinn; Chang, Ya‐Ling; Lee, Yuan Teh; Hsu, Su Ming

doi:10.1161/01.atv.0000127620.12310.89

Cited by 41 publications

(47 citation statements)

References 49 publications

(50 reference statements)

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“…The increase in HDL levels observed in our study might be due to the stimulation of pre-HDL and reverse cholesterol transport as shown by previous findings (Gupta et al, 1993). The observed hypocholesterolaemic effect of the vitamin C and the antioxidant minerals in our study could be the basis for suggesting therapeutic potential of ascorbate in reducing atherosclerotic risk via inhibition of H 2 O 2 -induced oxidative stress in patients with Uremia or dyslipidaemia (Chiang et al, 2004).…”

Section: Discussionsupporting

confidence: 86%

Effect of antioxidants supplementations in salt-induced dyslipidaemia in albino rats

Bilbis¹,

Saidu²,

Ahmad³

et al. 2012

Int. J. Bio. Chem. Sci

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Cardiovascular disease (CVD) is associated with many risk factors including oxidative stress and dyslipidaemia. The current work evaluated the effects of antioxidants supplementation on salt-induced dyslipidaemia in albino rats. Rats were divided into 10 groups of 7 rats each. Groups 2-10 were fed 8% salt diets for 5 weeks while group 1 served as control and were fed normal rat feed. Water was provided to all the groups ad libitum. The animals in groups 3-10 were then supplemented with vitamin A; vitamin C; vitamin E; Cu; Mn; Zn; vitamins A, C and E combined and Cu, Mn and Zn combined respectively for additional 4 weeks simultaneously with salt loading. Group 2 was not supplemented and served as the negative control. Serum levels of total cholesterol, triacylglyceride, low density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, high density lipoprotein (HDL) cholesterol and glucose were estimated. The results indicated that the vitamins reduced significantly serum lipid profiles and the atherogenic index by up to 80%. The serum glucose levels of the rats supplemented with antioxidant vitamins and minerals were also significantly (P<0.05) lowered compared with the negative control group. These results suggest that the reduction of serum lipid profile and glucose level may be due to regulation of cholesterol and lipoprotein metabolism and increased insulin sensitivity as a result of the supplementations. It may thus suggest that the antioxidants may provide protection against CVDs and metabolic syndrome in salt-induced dyslipidaemia in rats.

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Section: Discussionsupporting

confidence: 86%

Effect of antioxidants supplementations in salt-induced dyslipidaemia in albino rats

Bilbis¹,

Saidu²,

Ahmad³

et al. 2012

Int. J. Bio. Chem. Sci

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“…Once induced, ROS impair neighboring tissues/cells and evoke an inflammatory response, with the expression of various inflammatory cytokines [4,5,6]. By exac-erbating pro-inflammation and causing hemolysis via oxidative damage to the RBC membrane [7,8], ROS may aggravate uremic anemia and contribute to poor responsiveness to recombinant human erythropoietin (rHuEPO) therapy.…”

Section: Introductionmentioning

confidence: 99%

N-Acetylcysteine for the Management of Anemia and Oxidative Stress in Hemodialysis Patients

Hsu¹,

Chiang²,

Yang³

et al. 2010

Nephron Clin Pract

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Background/Aims: To explore the efficacy of oral N-acetylcysteine (NAC) supplementation for anemia and oxidative stress in hemodialysis (HD) patients. Methods: Of the eligible patients (n = 325) in an outpatient HD unit, 49 received NAC 200 mg orally thrice a day during the first 3 months, while the other 276 patients not receiving NAC were observed. Results: During the 4-month study, 11 patients receiving NAC withdrew but had no severe adverse effects, while 49 patients not receiving NAC had negative confounding events. Thus only the data of the remaining patients, 38 taking NAC and 227 not taking NAC, were analyzed for efficacy. The demographic and laboratory data of both groups were similar at baseline. When the erythropoietin dosage was stable throughout, only the NAC group had a significant increase in hematocrit, accompanied with a decrease in plasma levels of 8-isoprostane and oxidized low-density lipoprotein. Analyzed as a nested case-control study, NAC supplementation was also found to be a significant predictor of positive outcomes in uremic anemia. Conclusions: Oral NAC supplementation may be a promising therapy for uremic anemia and oxidative stress in HD patients.

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“…PCOOH was also identified in human atherosclerotic lesions (6,7). Furthermore, PCOOH accumulation in plasma has been shown in human subjects with pathological conditions such as hyperlipidemia (8,9), diabetes (10), uremia (9), and alcoholism (11). Because hyperlipidemia and diabetes are strongly associated with increased incidence of atherosclerosis (12)(13)(14), higher plasma PCOOH conditions in these patients may be involved in atherogenesis.…”

mentioning

confidence: 98%

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1

Asai

Okajima

Nakagawa

et al. 2009

Journal of Lipid Research

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The accumulation of phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), in blood plasma and tissues has been observed in various pathological conditions, including atherosclerosis. However, the biological roles of PCOOH in these conditions remain unknown. To estimate the atherogenicity of PCOOH, we evaluated the effect of PCOOH on THP-1 monocytic cell adherence to immobilized vascular endothelial cell adhesion molecules. THP-1 cell adhesion to intracellular adhesion molecule-1 (ICAM-1) was dosedependently increased by addition of PCOOH. Phosphatidylcholine hydroxide (a hydroxyl analog of PCOOH) also induced THP-1 cell adhesion to ICAM-1, whereas nonoxidized PC, sn-2 truncated PCs, and other hydroperoxide compounds did not affect the adhesion. In the PCOOH-treated cells, obvious protruding F-actin-rich membrane structures were formed, and lymphocyte function-associated antigen-1 (LFA-1) was localized to the protruding structures. Cytochalasin D, an actin polymerization inhibitor, suppressed the PCOOH-induced cell adhesion to ICAM-1 and the membrane protrusions. These results indicate that PCOOH evokes LFA-1-mediated cell adhesion to ICAM-1 via actin cytoskeletal organization, and the mechanism may participate in monocyte adherence to the arterial wall in the initiation of atherosclerosis.-Asai, A., F. Okajima, K. Nakagawa, D. Ibusuki, K. Tanimura, Y. Nakajima, M. Nagao, M. Sudo, T. Harada, T. Miyazawa, and S. Oikawa. Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1. J. Lipid Res. 2009. 50: 957-965. Supplementary key words lipid oxidationOxidative lipid modifications play important roles in the pathogenesis of atherosclerosis (1-4). Among oxidatively modified lipids, phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), was observed to be accumulated in arterial walls and blood plasma in atherosclerotic rabbits (5). PCOOH was also identified in human atherosclerotic lesions (6, 7). Furthermore, PCOOH accumulation in plasma has been shown in human subjects with pathological conditions such as hyperlipidemia (8, 9), diabetes (10), uremia (9), and alcoholism (11). Because hyperlipidemia and diabetes are strongly associated with increased incidence of atherosclerosis (12-14), higher plasma PCOOH conditions in these patients may be involved in atherogenesis.In the course of phospholipid oxidation, PC is primarily oxidized to PCOOH. Further oxidative modification of PCOOH yields various secondary oxidation products. To date, a number of the secondary oxidation products have been reported to mediate several atherogenic processes (15, 16). For instance, a series of oxidized PCs with a truncated sn-2 acyl group (sn-2-truncated PCs), such as 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine, activate aortic endothelial cell binding to monocytes (17-19). The sn-2-truncated PCs with a terminal aldehyde gr...

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Ascorbate Supplement Reduces Oxidative Stress in Dyslipidemic Patients Undergoing Apheresis

Cited by 41 publications

References 49 publications

Effect of antioxidants supplementations in salt-induced dyslipidaemia in albino rats

Effect of antioxidants supplementations in salt-induced dyslipidaemia in albino rats

N-Acetylcysteine for the Management of Anemia and Oxidative Stress in Hemodialysis Patients

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1

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