Correlation between blood antioxidant levels and lipid peroxidation in rheumatoid arthritis

Gambhir, Jasvinder K.; Lali, Pramod; Jain, Anil K.

doi:10.1016/s0009-9120(96)00007-0

Cited by 156 publications

(128 citation statements)

References 21 publications

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“…Since the main source of these two aldehydes is from lipoperoxidation [37,40], we could conclude that the rates of oxidative stress and lipoperoxidation are relatively higher in rheumatic condition than hyperglycemic one. On the other hand, the concentrations of GO and ACR were found to be significantly higher in serum of diabetic group than in rheumatic one.…”

Section: Analysis Of Serum Samples From Healthy Subjects and Patientsmentioning

confidence: 90%

“…Meanwhile, there was no significance difference in the concentration of GO in the two groups. The elevated levels of MDA and HNE in rheumatoid arthritis patients are probably due to high level of ROS produced by activated polymorphonuclear cells and injury resulting from ischemia and reperfusion in the inflamed joints [37]. Beside oxidative stress and increased lipoperoxidation, the presence of ACR at a significantly higher concentration in rheumatic group might be also attributed to the oxidative deamination of polyamines [38] which were previously detected in high levels in rheumatic patients' urine samples [39].…”

Section: Analysis Of Serum Samples From Healthy Subjects and Patientsmentioning

confidence: 94%

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Analytical method for lipoperoxidation relevant reactive aldehydes in human sera by high-performance liquid chromatography–fluorescence detection

El-Maghrabey

Kishikawa

Ohyama

et al. 2014

Analytical Biochemistry

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A validated, simple and sensitive HPLC method was developed for the simultaneous determination of lipoperoxidation relevant reactive aldehydes; glyoxal (GO), acrolein (ACR), malondialdehyde (MDA) and 4-Hydroxy-2-nonenal (HNE) in human serum. The studied aldehydes were reacted with 2,2'-furil to form fluorescent difurylimidazole derivatives that were separated on respectively, with detection limits ranged from 0.030 to 0.11 nmol/mL. The % RSD of intra-day and inter-day precision didn't exceed 5.0% and 6.2%, respectively, and the accuracy (%found) ranged from 95.5 to 103%. The proposed method was applied for monitoring the four aldehydes in sera of healthy, diabetic and rheumatic human subjects with simple pretreatment steps and without interference from endogenous components. By virtue of its high sensitivity and accuracy, our method enabled detection of differences between analytes concentrations in sera of human subjects at different clinical conditions.

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Section: Analysis Of Serum Samples From Healthy Subjects and Patientsmentioning

confidence: 90%

Section: Analysis Of Serum Samples From Healthy Subjects and Patientsmentioning

confidence: 94%

Analytical method for lipoperoxidation relevant reactive aldehydes in human sera by high-performance liquid chromatography–fluorescence detection

El-Maghrabey

Kishikawa

Ohyama

et al. 2014

Analytical Biochemistry

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“…In fact, global oxidative activity is enhanced in RA, in correlation with positive acute-phase reactants such as ceruloplasmin. 23 By contrast, vitamin A and E concentrations are low in RA in conjunction with negative acute-phase markers. 24 These observations emphasize the potential for feedback loops in RA whereby cytokines lead to a dyslipidemia that promotes oxidation, which in turn leads to further cytokine release at endothelial cells.…”

Section: Oxidative Stressmentioning

confidence: 99%

Explaining How “High-Grade” Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis

et al. 2003

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Abstract-There is intense interest in mechanisms whereby low-grade inflammation could interact with conventional and novel vascular risk factors to promote the atheromatous lesion. Patients with rheumatoid arthritis (RA), who by definition manifest persistent high levels of inflammation, are at greater risk of developing cardiovascular disease. Mechanisms mediating this enhanced risk are ill defined. On the basis of available evidence, we argue here that the systemic inflammatory response in RA is critical to accelerated atherogenesis operating via accentuation of established and novel risk factor pathways. By implication, long-term suppression of the systemic inflammatory response in RA should be effective in reducing risk of coronary heart disease. Key Words: immune system Ⅲ risk factors Ⅲ atherosclerosis C onsiderable evidence indicates that patients with rheumatoid arthritis (RA) are at greater risk of developing coronary heart disease (CHD). 1 Seventeen of 21 relevant observational studies show an increased standardized morality ratio in RA and that life expectancy is shortened by 3 to 18 years. Pooled analysis of these studies suggests a 70% increase in risk of death in RA patients. Life expectancy is especially shortened in RA patients treated in specialist referral centers, where the prognosis is comparable to that of triple-vessel CHD or stage 4 Hodgkin's disease. 1 Cardiovascular disease accounts for 35% to 50% of excess mortality in RA patients, with cerebrovascular disease being the second leading cause of death. Intriguingly, most evidence suggests that classic risk factors do not explain excess vascular disease in RA. In an 8-year follow-up of 236 RA patients, a 3.96-fold (95% CI 1.86 to 8.43) higher incidence of cardiovascular events relative to a community-dwelling cohort was noted. 2 However, this risk ratio was only minimally attenuated (to 3.17 [95% CI 1.33 to 6.36]) by adjustment for conventional risk factors. These clinical epidemiological observations strongly suggest that mechanisms other than classic risk factors promote accelerated atherogenesis in RA, and responsible candidate pathways are explored in this review. Inflammation as a Candidate Pathway for CHDIt is firmly established that systemic markers of inflammation, albeit at considerably lower levels than those apparent in RA, independently predict CHD events in men and women with or without existing heart disease. 3,4 The levels of cytokines and other inflammatory mediators detected in CHD are such that high-sensitivity assays rather than conventional assays are required. This concept of inflammatory-driven atherogenesis is consistent with the plaque composition of unstable coronary lesions, with an abundance of inflammatory molecules and immune cells at the shoulder region that act to erode the collagen cap that separates the atheromatous material of the plaque from blood. 4 This appearance is similar to that of inflammatory synovitis in RA. 5 However, whereas in RA, C-reactive protein (CRP) is a powerful measure of synovial infla...

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“…Both genetic and environmental factors contribute to its etiopathogenesis (Deighton and Walker, 1991). It has been reported that reactive oxygen species (ROS) may play an important role in the pathogenesis of RA (Gambhir et al, 1997;Bauerova and Bezek, 1999). Under normal conditions, ROS are formed in oxidative processes at relatively low concentrations in all cells and tissues, and a variety of antioxidative mechanisms serve to control its production.…”

Section: Introductionmentioning

confidence: 99%

“…Under normal conditions, ROS are formed in oxidative processes at relatively low concentrations in all cells and tissues, and a variety of antioxidative mechanisms serve to control its production. Under pathological conditions, the levels of ROS are altered by increased production and/or inadequate removal, which results in oxidative stress, inducing cell damage and lipid peroxidation (Halliwell, 1994;Gambhir et al, 1997). Lipid peroxidation is a well-known mechanism of cellular damage in humans, and is used as an indicator of oxidative stress in cells and tissues.…”

Section: Introductionmentioning

confidence: 99%

The L55M polymorphism of paraoxonase-1 is a risk factor for rheumatoid arthritis

Hashemi¹,

Moazeni‐Roodi²,

Fazaeli³

et al. 2010

Genet. Mol. Res.

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ABSTRACT. Paraoxonase-1 (PON1) is a high-density lipoproteinassociated enzyme that exhibits antioxidant and antiatherogenic activities. We examined a possible association between T172A (L55M) and T(-107)C polymorphisms and rheumatoid arthritis. These polymorphisms were determined in 88 rheumatoid arthritis patients and 78 healthy subjects, using the tetra-amplification refractory mutation system-PCR method. The prevalence of the PON1 55MM genotype was significantly greater among rheumatoid arthritis patients (17%) when compared to control subjects (5.2%) (odds ratio (OR) = 3.75; 95% confidence interval (CI) = 1.87-11.8, P = 0.025). In addition, the M allele was more frequent in rheumatoid arthritis patients (40%) than in healthy subjects (24.7%) (OR = 1.997; 95%CI = 1.243-3.210, P = 0.005). There were no significant differences in the -107C/T polymorphism in the promoter sequence of PON1 between rheumatoid arthritis and normal subjects (χ 2 = 0.861, P = 0.650). In conclusion, the PON1 55MM genotype is a risk factor for rheumatoid arthritis.

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Correlation between blood antioxidant levels and lipid peroxidation in rheumatoid arthritis

Cited by 156 publications

References 21 publications

Analytical method for lipoperoxidation relevant reactive aldehydes in human sera by high-performance liquid chromatography–fluorescence detection

Analytical method for lipoperoxidation relevant reactive aldehydes in human sera by high-performance liquid chromatography–fluorescence detection

Explaining How “High-Grade” Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis

The L55M polymorphism of paraoxonase-1 is a risk factor for rheumatoid arthritis

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