Lipid Peroxidation in Hyperlipidaemic Patients. A Study of Plasma using an HPLC-Based Thiobarbituric Acid Test

Chirico, S; Smith, Christian; Marchant, Christine E.; Mitchinson, M. J.; Halliwell, Barry

doi:10.3109/10715769309056498

Cited by 99 publications

(53 citation statements)

References 21 publications

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“…Traditional approaches to the assessment of oxidative stress in humans relied on ex vivo indices such as the lag time to oxidation of LDL 65 and in vivo indices of questionable veracity such as thiobarbituric acid reactive substances 66 and plasma malondialdehyde. 67 However, more contemporary biomarkers of increased ROS generation now suggest that elevated oxidant stress is a characteristic of a spectrum of cardiovascular diseases.…”

Section: Ros and Vascular Disease: Human Studiesmentioning

confidence: 99%

Oxidative Stress and Cardiovascular Injury

2003

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T his review so far has considered the role of vascular cells in the generation of reactive oxygen species (ROS) and novel approaches to their detection in integrated systems such as animal models of vascular disease and humans. We now turn attention to evidence consistent with a role for ROS in models of human disease and in discrete patient populations. We also briefly comment on the outcomes of clinical trials of antioxidants. Mainly, these have been disappointing. However, it is premature to conclude that the oxidation hypothesis of disease causality has been adequately tested. ROS and Vascular Disease: Animal StudiesAnimal studies, for the most part, support a fundamental role for ROS in cardiovascular disease. Any controversy could in part reflect the use of ineffective antioxidants and the selection of models in which ROS generation is of marginal relevance to the measured outcome. Both of these issues require a quantitatively accurate measurement of drug effect (ie, antioxidant capacity) before hypotheses relating to the role of oxidant stress can be addressed rationally. These issues pertain to clinical trials also, as we will discuss. However, animal studies permit administration of much more powerful antioxidants (eg, rate constant for interaction of superoxide dismutase (SOD) with O 2 ·Ϫ Ϸ1.6ϫ10 9 · mol/L Ϫ1 · s Ϫ1 ) than is possible in humans (eg, rate constant for vitamin E Ϸ0.59 mol/L Ϫ1 · s Ϫ1 ) or, like in the case of vitamin E, doses of the antioxidant in excess of those usually applied in clinical research. AtherosclerosisAnimal models of atherosclerosis have documented that all the constituents of the plaque produce and use ROS. Lesion formation is associated with the accumulation of lipid peroxidation products 1,2 and induction of inflammatory genes, 3 inactivation of NO · resulting in endothelial dysfunction, 4,5 activation of matrix metalloproteinases, 6 and increased smooth muscle cell growth. 7 Atherogenesis in rodents is accompanied by increasing lipid peroxidation in vivo. Thus, levels of the F 2 isoprostane (iP), iPF 2␣ -IV, are increased in both urine and aortic tissue as atherosclerosis evolves in both apolipoprotein E (ApoE)-and low-density lipoprotein (LDL) receptor-knockout mice. 8,9 Evidence exists for and against the efficacy of vitamin E in limiting atherogenesis. 10 -12 However, a rational basis for selection of the interventional regimens, or indeed the possibility of comparing treatment regimens across models and species by anything other than weight-corrected dosing, does not exist, pointing to the need for a much more rigorous approach to the development, application, and testing of antioxidant therapies. If a dosing regimen of vitamin E is selected on the basis of its ability to suppress elevated urinary iPF 2␣ -VI in atherosclerotic ApoE mice, vitamin E will retard atherosclerosis by Ϸ50% while leaving hypercholesterolemia unaffected. 8 However, administration of much lower doses of vitamin E to the same model failed to detect an impact on atherogenesis. 10 It is notew...

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Section: Ros and Vascular Disease: Human Studiesmentioning

confidence: 99%

Oxidative Stress and Cardiovascular Injury

2003

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“…However, interpretation of the relationship between lipid peroxidation and diabetes has yielded contradictory results [14,15,18,19]. The simple TBARS assay measures many parameters in addition to lipid peroxidation and is affected by the lipid content of the sample [20]. Thus, it is unclear to what extent plasma lipoprotein peroxidation assessed by this method accounts for biological changes associated with oxidative stress.…”

Section: © Springer-verlag 1997mentioning

confidence: 99%

Relationships between plasma measures of oxidative stress and metabolic control in NIDDM

et al. 1997

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“…Both mucosal and airway neutrophilia were absent 1.5 h after a 2-h exposure to 0.2 ppm O 3 in subjects performing moderate exercise (20 …”

Section: Discussionmentioning

confidence: 97%

“…Immediately prior to analysis, samples were reconstituted in 200 mL of methanol by vigorous agitation on a vortex mixer. HPLC determination of MDA was based on the method of CHIRICO et al [20] and has been described in detail for BAL fluid [11].…”

Section: Determination Of Antioxidants and Markers Of Damagementioning

confidence: 99%

Personally measured weekly exposure to NO<SUB>2</SUB> and respiratory health among preschool children

Mukala¹,

Pekkanen²,

Tiittanen³

et al. 1999

Eur Respir J

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This study sought to clarify the early events occurring within the airways of healthy human subjects performing moderate intermittent exercise following ozone challenge.Thirteen healthy nonsmoking subjects were exposed in a single blinded, crossover control fashion to 0.2 parts per million (ppm) O 3 and filtered air for 2 h, using a standard intermittent exercise and rest protocol. Lung function was assessed pre-and immediately post-exposure. Bronchoscopy was performed with endobronchial mucosal biopsies, bronchial wash (BW) and bronchoalveolar lavage (BAL) 1.5 h after the end of the exposure period. Respiratory tract lining fluid (RTLF) redox status was assessed by measuring a range of antioxidants and oxidative damage markers in BW and BAL fluid samples.There was a significant upregulation after O 3 exposure in the expression of vascular endothelial P-selectin (p<0.005) and intercellular adhesion molecule-1 (p<0.005). This was associated with a 2-fold increase in submucosal mast cells (p<0.005) in biopsy samples, without evidence of neutrophilic inflammation, and a decrease in BAL fluid macrophage numbers (1.6-fold, p<0.005), with an activation of the remaining macrophage subset (2.5-fold increase in % human leukocyte antigen (HLA)-DR+ cells, p<0.005). In addition, exposure led to a 4.5-fold and 3.1-fold increase of reduced glutathione (GSH) concentrations, in BW and BAL fluid respectively (p<0.05), with alterations in urate and a-tocopherol plasma/RTLF partitioning ratios (p<0.05). Spirometry showed reductions in forced vital capacity (p<0.05) and forced expiratory volume in one second (p<0.01), with evidence of small airway narrowing using forced expiratory flow values (p<0.005).Evidence was found of O 3 -induced early adhesion molecule upregulation, increased submucosal mast cell numbers and alterations to the respiratory tract lining fluid redox status. No clear relationship was demonstrable between changes in these early markers and the lung function decrements observed. The results therefore indicate that the initial lung function decrements are not predictive of, or causally related to the O 3 -induced inflammatory events in normal human subjects. Eur Respir J 1999; 13: 1418±1428.

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Lipid Peroxidation in Hyperlipidaemic Patients. A Study of Plasma using an HPLC-Based Thiobarbituric Acid Test

Cited by 99 publications

References 21 publications

Oxidative Stress and Cardiovascular Injury

Oxidative Stress and Cardiovascular Injury

Relationships between plasma measures of oxidative stress and metabolic control in NIDDM

Personally measured weekly exposure to NO<SUB>2</SUB> and respiratory health among preschool children

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