Comparison of Serum Malondialdehyde Levels Determined by Two Different Methods in Patients With COPD: HPLC or TBARS Methods

Tuğ, Tuncer; Karataş, Fikret; Terzi, Selim Murat; Özdemir, Necmi

doi:10.1309/wteet9tj2lumb3c3

Cited by 26 publications

(15 citation statements)

References 19 publications

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“…This assay recorded the highest MDA plasma level and was approximately 2-fold greater than the median MDA level determined by HPLC, suggesting once more an issue of assay bias when colorimetric assays are employed for plasma or serum MDA quantitation. Consequently, a number of research groups ( 18,25,27 ) have recommended HPLC as the preferred MDA assay for human plasma samples; but notwithstanding these previous recommendations, the fi eld continues to support the publication of research articles reporting TBARS values as a specifi c measure of MDA levels/lipid peroxidation ( 12,(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

A specific, accurate, and sensitive measure of total plasma malondialdehyde by HPLC

Moselhy

Reid

Yousef

et al. 2013

Journal of Lipid Research

141

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The process of lipid peroxidation results in a range of intermediates and end products including lipid hydroperoxides, aldyehydes, and malondialdehyde (MDA). These aldehydes and lipid hydroperoxides form DNA adducts and may result in extensive single-strand and doublestrand breaks ( 4 ). Various intermediates and end products generated during the lipid peroxidation cascade have been assayed, but the most-commonly employed approach continues to be the thiobarbituric acid (TBA) test ( 5 ).Although it is widely acknowledged that TBA reacts with a range of oxidized lipids, both saturated and unsaturated aldehydes, ( 6, 7 ) sucrose, and urea ( 8 ), to form various chromogens, referred to as TBA-reactive substances (TBARS), it is the reaction of TBA with MDA to produce a pink pigment ( 9 ) with an absorption maximum at 532 nm ( 10 ) and mass ion at 323 amu ( 11 ) that is a true indicator of lipid peroxidation. Historically, the TBARS test has been assayed by ultraviolet (UV) spectrophotometry or fl uorescence assays, but the specifi city of the TBA test, enabling the selective determination of MDA, may be achieved via chromatographic separation of the pink TBA 2 -MDA adduct ( 12 ). The adoption of HPLC techniques improves assay specifi city and the sensitivity of MDA determination, and we have previously confi rmed the validity of quantifying the TBA 2 -MDA adduct as a specifi c measure of lipid peroxidation in human biological fl uids ( 13 ).Despite the widely acknowledged limitations of the TBARS test ( 14 ), and in particular its lack of specifi city, it continues to be reported as a true measure of MDA in clinical disease ( 1,15,16 ). It is proposed that the poor assay specifi city associated with TBARS assays may lead to an overestimation of the levels of MDA in human plasma and other biological tissues and fl uids, and this, in turn, may Abstract Malondialdehyde (MDA) is one of the most commonly reported biomarkers of lipid peroxidation in clinical studies. The reaction of thiobarbituric acid (TBA) with MDA to yield a pink chromogen attributable to an MDA-TBA 2 adduct is a common assay approach with products being quantified by ultraviolet-Vis assay as nonspecific TBAreactive substances (TBARS) or chromatographically as MDA. The specifi city of the TBARS assay was compared with both chromatographic assays for total plasma MDA. The levels of total plasma MDA were signifi cantly lower than the plasma TBARS in each of the samples examined, and interestingly, the interindividual variation apparent in the level of plasma MDA was not evident in the plasma TBARS assay. Each of the four online chromatographic detectors yielded a precise, sensitive, and accurate determination of total plasma MDA, and selected-ion monitoring was the most-accurate assay (101.3%, n = 4). The online diode array detectors provided good assay specifi city (peak purity index of 999), sensitivity, precision, and accuracy. This research demonstrates the inaccuracy that is inherent in plasma TBARS assays, which claim to quantify MDA, and it is pro...

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Section: Discussionmentioning

confidence: 99%

A specific, accurate, and sensitive measure of total plasma malondialdehyde by HPLC

Moselhy

Reid

Yousef

et al. 2013

Journal of Lipid Research

141

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“…Increases in MDA have been observed in several disease conditions, such as diabetes (Dierckx et al, 2003), breast cancer (Akbulut et al, 2003) or Alzheimer disease (Delibas et al, 2002). In patients with COPD, increases in circulatory MDA were associated with the reductions of total antioxidant capacity in the blood (Tug et al, 2004). In addition, MDA levels were significantly higher in COPD patients compared to healthy controls, and during acute exacerbation compared to stable state of the disease (Calikoglu et al, 2002).…”

Section: Lipid Peroxidationmentioning

confidence: 97%

“…It plays a major role in maintaining cell membrane's integrity by limiting lipid peroxidation by ROS (Canbaz et al, 2003) and so suppresses the oxidative damage of the membranes (Lee et al, 2002). Serum concentrations of vitamin A and vitamin E were significantly lower in patients with COPD compared to healthy subjects, and decreased further during COPD exacerbations (Tug et al, 2004). Vitamin C (ascorbic acid) is a water-soluble, chain-breaking antioxidant, which scavenges aqueous superoxide radicals and has multiple antioxidant properties.…”

Section: Non-enzymatic Antioxidantsmentioning

confidence: 99%

“…Several studies have indicated that the antioxidant capacity of plasma is decreased in smokers and in patients with COPD, in association with increased markers of oxidative stress in the lungs, bronchoalveolar lavage fluid, and plasma (Comhair et al, 2000;Tug et al, 2004,). Products of lipid peroxidation are increased also in plasma of smokers and of patients with COPD (Tkáčová et al, 2005;Kluchová et al, 2006).…”

Section: Smoking-induced Changes In Antioxidant Defence Mechanisms Inmentioning

confidence: 99%

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The role of oxidative stress in lung injury induced by cigarette smoke

Kluchová

Tkáčová

2006

Biologia

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Oxidative stress is a damaging process resulting from an imbalance between excessive generation of oxidant compounds and insufficient antioxidant defence mechanisms. Oxidative stress plays a crucial role in the initiation and progression of cigarette smoke-induced lung injury, deterioration in lung functions, and development of chronic obstructive pulmonary disease (COPD). In smokers and in patients with COPD, the increased oxidant burden derives from cigarette smoke per se, and from activated inflammatory cells releasing enhanced amounts of reactive oxygen and nitrogen species (ROS, RNS, respectively). Although mild oxidative stress resulting from cigarette smoking leads to the upregulation of the antioxidative enzymes synthesis in the lungs, high levels of ROS and RNS observed in patients with COPD overwhelm the antioxidant enzymes capacities, resulting in oxidant-mediated lung injury and cell death. In addition, depletion of antioxidative systems in the systemic circulation was consistently observed in such patients. The imbalance between the generation of ROS/RNS and antioxidant capacities -the state of "oxidative stress" -is one of the major pathophysiologic hallmarks in the development of COPD. Detrimental effects of oxidative stress include impairment of membrane functions, inactivation of membrane-bound receptors and enzymes, and increased tissue permeability. In addition, oxidative stress aggravates the inflammatory processes in the lungs, and contributes to the worsening of the protease-antiprotease imbalance. Several markers of oxidative stress, such as increases in lipid peroxidation products and reductions in glutathione peroxidase activity, have been shown to be related to the reductions in pulmonary functions. In the present article we review the current knowledge about the vicious cycle of cigarette smoking, oxidative stress, and inflammation in the pathogenesis of COPD.

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“…2 Furthermore, the method mostly used is thiobarbituric acid (TBA) reaction measuring TBA reactive substances (TBARS) and not specifically MDA. 3 Discrepancy was reported in biomarkers of LPO and oxdative stress between vascular dementia with much higher MDA levels than in Alzheimer patients. 4 However, McGrath, et al had already clarified that increased LPO and oxidative stress in Alzheimer's disease could be assessed with 4-hydroxynonenal 5 but not MDA, either substance reacting with TBA.…”

Section: Reconsidering Markers Of Oxidative Stressmentioning

confidence: 99%

Reconsidering markers of oxidative stress

Freisleben

2013

Med J Indones

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Comparison of Serum Malondialdehyde Levels Determined by Two Different Methods in Patients With COPD: HPLC or TBARS Methods

Cited by 26 publications

References 19 publications

A specific, accurate, and sensitive measure of total plasma malondialdehyde by HPLC

A specific, accurate, and sensitive measure of total plasma malondialdehyde by HPLC

The role of oxidative stress in lung injury induced by cigarette smoke

Reconsidering markers of oxidative stress

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