Human plasma concentrations of malondialdehyde (MDA) and the F2-isoprostane 15(S)-8-iso-PGF2α may be markedly compromised by hemolysis: Evidence by GC-MS/MS and potential analytical and biological ramifications

Dreißigacker, Ulrike; Suchy, Maria-Theresia; Maassen, Norbert; Tsikas, Dimitrios

doi:10.1016/j.clinbiochem.2009.10.002

Cited by 53 publications

(64 citation statements)

References 13 publications

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“…This result indicates that plasmalogens may be targets and markers of ongoing oxidative stress, and corroborates previous data showing a 20% decrease of plasmalogen phosphatidylethanolamine in erythrocyte membranes from hyperlipidaemic patients [29]. In addition, we found that malondialdehyde, a commonly used overall marker of lipid peroxidation that has been described to correlate with total isoprostanes in plasma and tissues [30,31], was increased to a similar extent in LDL from metabolic syndrome and type 2 diabetic patients, in agreement with the enhanced serum levels of thiobarbituric acid reactive species observed in type 2 diabetic patients [32]. Although isoprostanes are recognised as reliable markers of oxidative stress in vivo, they derive exclusively from the free radical-induced peroxidation of arachidonic acid and their levels were either reported to be increased [7] or unchanged [9] in patients with the metabolic syndrome.…”

Section: Discussionsupporting

confidence: 80%

LDL from obese patients with the metabolic syndrome show increased lipid peroxidation and activate platelets

et al. 2011

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Aims/hypothesis This study assessed oxidative stress in LDL from obese patients with the metabolic syndrome and compared it with that in LDL from type 2 diabetic patients or control volunteers. It also determined the effect on platelets of LDL from the three groups. Methods The profiles of lipids, fatty acids and fatty acid oxidation products were determined in LDL isolated from plasma of patients with the metabolic syndrome, patients with type 2 diabetes and volunteers (n=10 per group). The effects of LDL from the participant groups on the platelet arachidonic acid signalling cascade and aggregation were investigated. Results Compared with LDL from control volunteers, LDL from obese metabolic syndrome and type 2 diabetic patients had lower cholesteryl ester, higher triacylglycerol and lower ethanolamine plasmalogen levels. Proportions of linoleic acid were decreased in phosphatidylcholine and cholesteryl esters in LDL from both patient groups. Among the markers of lipid peroxidation, oxidation products of linoleic acid (hydroxy-octadecadienoic acids) and malondialdehyde were increased by 59% and twofold, respectively in LDL from metabolic syndrome and type 2 diabetic patients. LDL from metabolic syndrome and type 2 diabetic patients were equally potent in activating the platelet arachidonic acid signalling cascade through increased phosphorylation of p38 mitogen-activated protein kinase and cytosolic phospholipase A 2 , and through increased thromboxane B 2 formation. LDL from patients with the metabolic syndrome and type 2 diabetes potentiated platelet aggregation by threefold and 3.5-fold respectively, whereas control LDL had no activating effects on platelets. Conclusions/interpretation The metabolic syndrome in obese patients, without or with diabetes, is associated with increased oxidative stress in LDL, which triggers platelet activation.

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Section: Discussionsupporting

confidence: 80%

LDL from obese patients with the metabolic syndrome show increased lipid peroxidation and activate platelets

et al. 2011

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“…RONS have a transient nature and are difficult to assess in vitro and in vivo (13). Consequently, we measured more stable oxidation products caused by RONS to determine the extent of oxidative damage in I/R injury.…”

Section: Oxidative Damage In Clinical I/r Injurymentioning

confidence: 99%

“…Free 15(S)-8-iso-PGF2a in urine was measured by GC-MS/MS (42). Nitrite and nitrate were measured simultaneously by GC-MS in plasma and urine aliquots as described elsewhere in detail (13,40). The PGE 2 concentration in urine was measured by GC-MS/MS after immunoaffinity column chromatography extraction (42).…”

Section: Laboratory Plasma Measurementsmentioning

confidence: 99%

“…Urinary parameters were corrected for creatinine excretion (43). Study samples were analyzed alongside quality control (QC) samples as described previously (13,40,43). The MDA plasma concentration in the QC samples was determined to be 57.3 -7.8 nM (mean -standard deviation [SD], n = 25) corresponding to an imprecision (relative SD) of 13.7%.…”

Section: Laboratory Plasma Measurementsmentioning

confidence: 99%

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Oxidative Damage in Clinical Ischemia/Reperfusion Injury: A Reappraisal

Vries

Kortekaas

Tsikas

et al. 2013

Antioxidants & Redox Signaling

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Aims: Ischemia/reperfusion (I/R) injury is a common clinical problem. Although the pathophysiological mechanisms underlying I/R injury are unclear, oxidative damage is considered a key factor in the initiation of I/R injury. Findings from preclinical studies consistently show that quenching reactive oxygen and nitrogen species (RONS), thus limiting oxidative damage, alleviates I/R injury. Results from clinical intervention studies on the other hand are largely inconclusive. In this study, we systematically evaluated the release of established biomarkers of oxidative and nitrosative damage during planned I/R of the kidney and heart in a wide range of clinical conditions. Results: Sequential arteriovenous concentration differences allowed specific measurements over the reperfused organ in time. None of the biomarkers of oxidative and nitrosative damage (i.e., malondialdehyde, 15(S)-8-iso-prostaglandin F2a, nitrite, nitrate, and nitrotyrosine) were released upon reperfusion. Cumulative urinary measurements confirmed plasma findings. As of these negative findings, we tested for oxidative stress during I/R and found activation of the nuclear factor erythroid 2-related factor 2 (Nrf2), the master regulator of oxidative stress signaling. Innovation: This comprehensive, clinical study evaluates the role of RONS in I/R injury in two different human organs (kidney and heart). Results show oxidative stress, but do not provide evidence for oxidative damage during early reperfusion, thereby challenging the prevailing paradigm on RONS-mediated I/R injury. Conclusion: Findings from this study suggest that the contribution of oxidative damage to human I/R may be less than commonly thought and propose a re-evaluation of the mechanism of I/R. Antioxid. Redox Signal. 19,[535][536][537][538][539][540][541][542][543][544][545]

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“…Oxidative stress has been associated with aging and multiple age-related diseases, including cancer [26,27], neurodegeneration [28,29], cardiovascular disease [30,31], and diabetes [32]. Commonly assessed markers for oxidative stress are lipid oxidation products such as 8-isoprostane and malondialdehyde, and DNA oxidation products such as 8-hydroxy-2-deoxyguanosine (8-oxo-dG) which can be measured in blood and/or urine [33]. The activity of antioxidant enzymes, e.g., glutathione peroxidase or catalase, can also provide information regarding oxidative stress [34].…”

Section: Resultsmentioning

confidence: 99%

Effects of Intentional Weight Loss on Markers of Oxidative Stress, DNA Repair and Telomere Length - a Systematic Review

2017

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Background: Altered levels of markers of oxidative stress, DNA repair, and telomere integrity have been detected in obese individuals and may underlie the pathogenesis of obesity-related diseases. However, whether or not such effects are reversed by intentional weight loss has not been systematically reviewed. Methods: A literature search in PubMed/Medline identified 2,388 articles of which 21 studies (randomized controlled trial (RCT) (n = 10) and non-randomized intervention studies (n = 11)) were classified as testing the effects of intentional weight loss on i) oxidative stress (n = 15), ii) DNA repair (n = 2), and iii) telomere length (n = 4). Results: Across a broad range of intervention designs, diet-, exercise-, surgery-, balloon-induced weight loss regimens decreased oxidative stress measures. Studies investigating DNA repair capacity or telomere length as endpoints after weight loss were less common in number and yielded null or inconsistent results, respectively. Conclusion: While this systematic review supports a role for intentional weight loss in reducing obesity-associated oxidative stress, it is not clear whether the effects are primary outcomes or secondary to improvement in obesity-associated insulin resistance and/or chronic inflammation. Although the lack of effect of intentional weight loss on DNA repair capacity might be anticipated given that oxidative stress is reduced, additional studies are needed. The inconsistent effects of weight loss on telomere length or DNA repair suggest the need for a re-assessment of intervention designs and assay methodology to definitively address this topic.

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Human plasma concentrations of malondialdehyde (MDA) and the F2-isoprostane 15(S)-8-iso-PGF2α may be markedly compromised by hemolysis: Evidence by GC-MS/MS and potential analytical and biological ramifications

Cited by 53 publications

References 13 publications

LDL from obese patients with the metabolic syndrome show increased lipid peroxidation and activate platelets

LDL from obese patients with the metabolic syndrome show increased lipid peroxidation and activate platelets

Oxidative Damage in Clinical Ischemia/Reperfusion Injury: A Reappraisal

Effects of Intentional Weight Loss on Markers of Oxidative Stress, DNA Repair and Telomere Length - a Systematic Review

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