Elevated Levels of Authentic Plasma Hydroperoxides in NIDDM

Nourooz‐Zadeh, Jaffar; Tajaddini-Sarmadi, Javad; McCarthy, Susan; Betteridge, D. J.; Wolff, Simon P.

doi:10.2337/diab.44.9.1054

Cited by 217 publications

(134 citation statements)

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“…Serum protein thiols were measured by a spectrophotometric method using 5 5' dithiobis nitrobenzoic acid (17). The lipid hydroperoxide content of whole serum was determined with the FOX version II assay for lipid hydroperoxides (FOX 2 ) (18,19). Serum ferritin, FBG and HbA 1c levels were estimated by electrochemiluminescence immunoassay (20) glucose oxidase method (21) and affinity chromatography method (22) respectively.…”

Section: Methodsmentioning

confidence: 99%

Relationship between free iron and glycated hemoglobin in uncontrolled type 2 diabetes patients associated with complications

Shetty

Prakash

Ibrahim

2008

Indian J Clin Biochem

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Free iron in serum has been found in several disease conditions including diabetes. In the present work, we studied the relationship between free iron, fasting blood glucose (FBG) and glycated haemoglobin (HbA 1c ). Study was carried out on 50 type 2 diabetes cases under poor glycemic control associated with complications, 53 type 2 diabetes cases under good glycemic control and 40 healthy controls. We estimated free iron, both ferrous (Fe +2 ) and ferric (Fe +3 ) form, protein thiols, lipid hydroperoxides, FBG, HbA 1c and serum ferritin levels in serum. There was a significant increase in free iron in Fe +3 state (p <0.01), HbA 1c (p<0.01), serum ferritin (p<0.01), lipid hydroperoxides (p<0.01) and significant decrease in protein thiols (<0.01) in diabetes cases under poor glycemic control compared to diabetes cases under good glycemic control and healthy controls. Free iron correlated positively with HbA 1c (p<0.01). Poor glycemic control and increase in glycation of haemoglobin is contributing to the increase in free iron pool which is known to increase oxidant generation.

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Section: Methodsmentioning

confidence: 99%

Relationship between free iron and glycated hemoglobin in uncontrolled type 2 diabetes patients associated with complications

Shetty

Prakash

Ibrahim

2008

Indian J Clin Biochem

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“…The formation of conjugated dienes was measured spectrophotometrically in quartz cuvettes in a Beckman DV 650 spectrophotometer, equipped with a thermostatic control (37 mC) and an automatically exchangeable six-positions cuvette holder, operating at 234 nm. The formation of lipid hydroperoxides was measured at various time-points using the ferrous oxidationXylenol Orange assay [24] or an HPLC procedure for specific quantification of cholesteryl linoleate hydroperoxide and hydroxide [25]. For the first assay, samples (100 µl) were taken and immediately mixed with 1 ml of FOX # reagent, incubated at room temperature for 30 min and the absorbance read at 560 nm [24].…”

Section: Lipoprotein Oxidationmentioning

confidence: 99%

“…The formation of lipid hydroperoxides was measured at various time-points using the ferrous oxidationXylenol Orange assay [24] or an HPLC procedure for specific quantification of cholesteryl linoleate hydroperoxide and hydroxide [25]. For the first assay, samples (100 µl) were taken and immediately mixed with 1 ml of FOX # reagent, incubated at room temperature for 30 min and the absorbance read at 560 nm [24]. Lipid peroxide concentrations were determined, after subtracting the PBS blank at each time point, using a standard curve of known concentrations of t-butyl-hydroperoxide.…”

Section: Lipoprotein Oxidationmentioning

confidence: 99%

When and why a water-soluble antioxidant becomes pro-oxidant during copper-induced low-density lipoprotein oxidation: a study using uric acid

Bagnati

Perugini

Cau

et al. 1999

Biochemical Journal

135

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The inclusion of uric acid in the incubation medium during copper-induced low-density lipoprotein (LDL) oxidation exerted either an antioxidant or pro-oxidant effect. The pro-oxidant effect, as mirrored by an enhanced formation of conjugated dienes, lipid peroxides, thiobarbituric acid-reactive substances and increase in negative charge, occurred when uric acid was added late during the inhibitory or lag phase and during the subsequent extensive propagation phase of copper-stimulated LDL oxidation. The pro-oxidant effect of uric acid was specific for copper-induced LDL oxidation and required the presence of copper as either Cu(I) or Cu(II). In addition, it became much more evident when the copper to LDL molar ratio was below a threshold value of approx. 50. In native LDL, the shift between the antioxidant and the pro-oxidant activities was related to the availability of lipid hydroperoxides formed during the early phases of copper-promoted LDL oxidation. The artificial enrichment of isolated LDL with α-tocopherol delayed the onset of the pro-oxidant activity of uric acid and also decreased the rate of stimulated lipid peroxidation. However, previous depletion of α-tocopherol was not a prerequisite for unmasking the pro-oxidant activity of uric acid, since this became apparent even when α-tocopherol was still present in significant amounts (more than 50% of the original values) in LDL. These results suggest, irrespective of the levels of endogenous α-tocopherol, that uric acid may enhance LDL oxidation by reducing Cu(II) to Cu(I), thus making more Cu(I) available for subsequent radical decomposition of lipid peroxides and propagation reactions.

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“…This non-enzymatic glycation of proteins has been presumed to cause an enhanced oxidative stress, through generation of oxygen free radicals [16][17][18][19]. An enhanced oxidative stress, i. e. increased levels of plasma hydroperoxides, has actually been observed in NIDDM [20][21][22][23][24]. The augmented generation of free radicals could also result in oxidative damage of LDL, the known potentially atherogenic properties of oxidized LDL including monocyte recruitment [25] and modulation of expression of adhesion molecules [26,27].…”

mentioning

confidence: 99%

E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

Cominacini¹,

Pasini²,

Garbin³

et al. 1997

Diabetologia

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Atherosclerosis is the major cause of death in patients with diabetes mellitus, accounting for more than 70 % of mortality in all forms of the disease [1,2]. There is plenty of evidence that monocytes are involved in the pathogenesis of atherosclerosis [3,4], the earliest morphological evidence of the disease being the binding of monocytes to the endothelium [5][6][7]. This adhesion of monocytes, a prerequisite for their recruitment and accumulation in the lesion, is probably due to the appearance of adhesion Diabetologia (1997) Summary Although elevated levels of soluble E-selectin and intercellular cell adhesion molecules-1 (ICAM-1) have been reported in non-insulin-dependent diabetes mellitus (NIDDM), it is not clear by what mechanism this elevation occurs and whether or not it is related to glycaemic control. In this study we analyse: 1) the relation of glycaemic control with the concentrations of E-selectin, vascular cell adhesion molecules-1 (VCAM-1) and ICAM-1 in NIDDM patients; 2) whether metabolic control can affect the oxidative stress (as measured by plasma hydroperoxide concentration and susceptibility of LDL to in vitro oxidation) and hence the adhesion molecule plasma concentrations. Thirty-four (19 males and 15 females) poorly controlled NIDDM patients were studied. All parameters were evaluated at the beginning of the study and after 90 days of dietary and pharmacological treatment. The treatment decreased HbA 1C (p < 0.001), E-selectin (p < 0.001), plasma hydroperoxides (p < 0.003) and the susceptibility of LDL to in vitro oxidation (lag phase) (p < 0.0001). Before treatment HbA 1C , lag phase and lipid hydroperoxides correlated with E-selectin plasma concentration (r = 0.51, -0.57 and 0.54, respectively, p < 0.01). There was also a correlation between HbA 1C and lag phase (p < 0.01) and between HbA 1C and lipid hydroperoxides (p < 0.01). In addition, the variations of HbA 1C , lag phase and lipid hydroperoxide values correlated with those for E-selectin concentration after 90 days' treatment (r = 0.54, -0.64 and 0.61, respectively, p < 0.01). In multiple linear correlation analysis, however, the partial correlation coefficients of HbA 1C (basal and variations) with Eselectin concentration (basal and variations) fell to non-significant values (r = 0.12 and 0.25, respectively) when LDL lag phase and plasma hydroperoxides were kept constant. The results indicate that the improvement of metabolic control in NIDDM patients is associated with a decrease of E-selectin plasma levels; they also suggest that glycaemic control per se is not directly implicated in determining E-selectin plasma concentration; glycaemic control could affect E-selectin concentration through its effect on oxidative stress. [Diabetologia (1997) 40: 584-589]

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Elevated Levels of Authentic Plasma Hydroperoxides in NIDDM

Cited by 217 publications

References 0 publications

Relationship between free iron and glycated hemoglobin in uncontrolled type 2 diabetes patients associated with complications

Relationship between free iron and glycated hemoglobin in uncontrolled type 2 diabetes patients associated with complications

When and why a water-soluble antioxidant becomes pro-oxidant during copper-induced low-density lipoprotein oxidation: a study using uric acid

E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

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