A Microassay to Assess the Oxidative Resistance of Low-Density Lipoproteins

Ujhelyi, László; Balla, JÃ3zsef; Muszbek, L.; Kakuk, G.; Belcher, John D.; Jacob, Harry S.; Vercellotti, Gregory M.; Balla, G

doi:10.1093/clinchem/44.8.1762

Cited by 21 publications

(10 citation statements)

References 10 publications

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“…Cord blood HSAA results were under 100%, indicating that the cord blood sera had an enhancing effect on lipid peroxidation. Cord blood serum ferritin, iron, unsaturated transferrin, bilirubin and calculated latent iron-binding capacity results were in the same range as those reported by others (12).…”

Section: Resultssupporting

confidence: 87%

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Acute postnatal increase of extracellular antioxidant defence of neonates: the role of iron metabolism

et al. 2001

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Section: Resultssupporting

confidence: 87%

“…The change of DT at Vmax induced by serum samples represents the antioxidant activity. The prolongation of DT (>100%) indicates an antioxidant effect, while the shortening of DT (<100%) indicates a pro-oxidant effect of the added serum samples (11,12).…”

Section: Methodsmentioning

confidence: 99%

Acute postnatal increase of extracellular antioxidant defence of neonates: the role of iron metabolism

et al. 2001

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“…38 These previous studies prompted us to examine the comprehensive antioxidant capacity of plasma ultrafiltrate from CKD patients on oxidative modification of LDL. Employing the adapted heme-mediated LDL oxidation method, a sensitive marker for assessing the antioxidant potential of water or lipid-soluble compounds, 2,3,39 we found that plasma ultrafiltrate of CKD patients has an enhanced antioxidant effect on oxidative modification of LDL compared to healthy controls, and it exhibits a dramatic drop under the physiological level during HD treatment. Furthermore, we demonstrate that endothelial cell cytotoxicity provoked by LDL oxidation as well as the upregulation of redox-sensitive HO-1 and ferritin genes in response to oxidative stress of LDL are blunted by plasma ultrafiltrate of CKD patients and healthy subjects.…”

Section: Discussionmentioning

confidence: 97%

Hemodialysis reduces inhibitory effect of plasma ultrafiltrate on LDL oxidation and subsequent endothelial reactions

Ujhelyi

Balla

Jeney

et al. 2006

Kidney International

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Oxidative modification of low-density lipoprotein (LDL) and its deleterious effect on endothelium is implicated in the pathogenesis of atherosclerosis. Endothelium responds to such an insult by upregulating the synthesis of heme oxygenase-1 (HO-1) and ferritin. Endothelial cell damage and dysfunction have been observed in patients with chronic kidney disease (CKD) on maintenance hemodialysis (HD). We studied the effect of low-molecular-weight components of uremic plasma on LDL oxidation and LDL-oxidation-provoked endothelial cell reactions, such as the induction of cytotoxicity and the upregulation of cell-protective HO-1 and ferritin. Plasma ultrafiltrate (molecular weight<5000 Da) from CKD patients on HD or when treated conservatively exhibited a pronounced inhibition on heme-mediated oxidative modification of LDL. Endothelial cell cytotoxicity provoked by LDL oxidation was also attenuated by plasma ultrafiltrate from CKD patients. During HD treatment, a dramatic drop occurred in the retardation of oxidative reactions, and a loss of endothelial cytoprotection exerted by plasma ultrafiltrate was noted. The upregulation of HO-1 and ferritin in response to oxidative stress of LDL was blunted by uremic plasma ultrafiltrate that was released by the end of HD. The decreased antioxidant capacity of ultrafiltrate after HD occurred as a consequence of the intradialytic removal of L-ascorbic acid, uric acid, bilirubin, 3-indoxyl sulfate, indoxyl-beta-D-glucuronide, p-cresol, and phenol. Intradialytic removal of L-ascorbic acid, uric acid, bilirubin, 3-indoxyl sulfate, indoxyl-beta-D-glucuronide, p-cresol, and phenol increases the risk of LDL oxidation and subsequent endothelial cell damage, which underlines the importance of activation of cytoprotective HO-1 and ferritin in endothelium.

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“…We found that H 2 S dose dependently delays the accumulation of lipid peroxidation products during hemin-mediated oxidative modification of LDL. Although we have previously shown that hemin at concentrations between 3 and 5 μmol/L does not strictly influence the kinetics of hemin-mediated LDL oxidation [50], to understand the nature of this inhibition we first tested the ability of H 2 S to reduce the availability of hemin in our system. In fact, high concentrations of H 2 S in an aqueous solution can readily reduce hemin content.…”

Section: Discussionmentioning

confidence: 99%

Supression of hemin-mediated oxidation of low-density lipoprotein and subsequent endothelial reactions by hydrogen sulfide (H2S)

Jeney

Komódi

Nagy

et al. 2009

Free Radical Biology and Medicine

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Heme-mediated oxidative modification of low-density lipoprotein (LDL) plays a crucial role in early atherogenesis. It has been shown that hydrogen sulfide (H(2)S) produced by vascular smooth muscle cells is present in plasma at a concentration of about 50 micromol/L. H(2)S is a strong reductant which can react with reactive oxygen species like superoxide anion and hydrogen peroxide. The current study investigated the effect of H(2)S on hemin-mediated oxidation of LDL and oxidized LDL (oxLDL)-induced endothelial reactions. H(2)S dose dependently delayed the accumulation of lipid peroxidation products-conjugated dienes, lipid hydroperoxides (LOOH), and thiobarbituric acid reactive substances-during hemin-mediated oxidation. Moreover, H(2)S decreased the LOOH content of both oxidized LDL and lipid extracts derived from soft atherosclerotic plaque, which was accompanied by reduced cytotoxicity. OxLDL-mediated induction of the oxidative stress responsive gene, heme oxygenase-1, was also abolished by H(2)S. Finally we have shown that H(2)S can directly protect endothelium against hydrogen peroxide and oxLDL-mediated endothelial cytotoxicity. These results demonstrate novel functions of H(2)S in preventing hemin-mediated oxidative modification of LDL, and consequent deleterious effects, suggesting a possible antiatherogenic action of H(2)S.

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A Microassay to Assess the Oxidative Resistance of Low-Density Lipoproteins

Cited by 21 publications

References 10 publications

Acute postnatal increase of extracellular antioxidant defence of neonates: the role of iron metabolism

Acute postnatal increase of extracellular antioxidant defence of neonates: the role of iron metabolism

Hemodialysis reduces inhibitory effect of plasma ultrafiltrate on LDL oxidation and subsequent endothelial reactions

Supression of hemin-mediated oxidation of low-density lipoprotein and subsequent endothelial reactions by hydrogen sulfide (H2S)

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