Reactive Oxygen Species and Drug Therapy for Inflammatory Diseases

Mw, Whitehouse; Lg, Cleland

doi:10.1007/978-3-0348-7720-6_22

Cited by 6 publications

(7 citation statements)

References 14 publications

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“…The therapeutic effect of these measures is, at least partially, connected with influence on ROS generation systems, what was suggested for corticotherapy [15], as well as for radiation [44]. However, the favourable effect of corticosteroids alone is reported only in about 60% of cases, growing when corticotherapy is combined with orbital irradiation [45].…”

Section: Discussionmentioning

confidence: 97%

“…In vitro studies suggest that the anti-inflammatory action of corticosteroids depends, at least partially, on an interference with the formation of ROS by phagocytes [15]. Corticosteroids produce significant inhibition of superoxide anion release by human monocytes in normal subjects [16] or asthmatic patients [17], as well as human granulocytes [18].…”

Section: Introductionmentioning

confidence: 99%

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Peripheral parameters of oxidative stress in patients with infiltrative Graves’ ophthalmopathy treated with corticosteroids

2004

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Peripheral parameters of oxidative stress in patients with infiltrative Graves’ ophthalmopathy treated with corticosteroids

2004

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“…The anti-inflammatory effects of corticosteroids on ROS inhibition in various cell types are controversial [21]. In vitro studies have suggested that the anti-inflammatory action of corticosteroids depends at least partially on an interference with the formation of reactive oxygen species by phagocytes [26].…”

Section: Discussionmentioning

confidence: 99%

Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

Majori

Vachier²,

Godard³

et al. 1998

Eur Respir J

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Bronchial asthma is a chronic inflammatory disease of the airways characterized by an increased recruitment of inflammatory cells, including mononuclear phagocytic cells such as monocytes [1]. The ability of these cells to generate highly reactive oxygen species (ROS), including super-oxide anion, following activation of a membraneassociated reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important part of the host defence system, and has also been implicated in inflammation in a variety of pulmonary diseases [2,3], including asthma [4,5]. Oxygen metabolites cause tissue injury, smooth muscle contraction, increased airway vascular permeability, and may increase airway responsiveness and release of var-ious mediators [4].In previous studies, it has been shown that alveolar macrophages [6], blood monocytes [5] and eosinophils [7] from asthmatic patients were able to produce high amounts of ROS. Alveolar macrophage activation was correlated with the severity of asthma [6]. This activation occurred immediately after antigen challenge, and the appearance of high-density macrophages which release higher amounts of superoxide anion occurred during the late airway response [8]. Several investigators have also suggested that polymorphonuclear leucocytes from asthmatic patients generated more ROS than control subjects [9,10]. This activation was correlated with the level of bronchial hyperreactivity [11].Corticosteroids are the most potent anti-inflammatory agents available for the treatment of asthma [12], but little is known about their molecular mechanism of action in improving symptoms or the way they reduce hyperresponsiveness. It has been proposed that corticosteroids inhibit the inflammatory process by redirection of lymphocyte traffic, inhibition of cytokine gene expression [13] and inhibition of the expression of adhesion molecules [14].The effect of anti-inflammatory corticosteroids on oxygen radical production by phagocytes has been less extensively studied, and the results are contradictory. In vitro studies have demonstrated an inhibitory effect of high corticosteroid concentrations on oxygen radical production in human granulocytes [15]. In contrast, dexamethasone treatment has been reported to have no effect on ROS secretion in human blood-derived macrophages [16], but have a stimulatory effect on human monocytes [17]. It has been reported that in vivo corticosterone had no effect on murine peritoneal inflammatory cells [18]. Ex vivo inhaled steroid treatment had no effect on superoxide anion production in human alveolar macrophages [19,20]. In contrast, a recent study showed that in vivo administration of dexamethasone or methylprednisolone led to a dose-dependent inhibition of rat peritoneal leucocyte chemiluminescence [21]. Moreover, hydrocortisone was found to inhibit superoxide anion production during an asthma attack [22].Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients. M. Majori, I. Vachier, P. Godard, M. Farce, J. Bousquet, P. Chanez. ...

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“…Systemic corticosteroids are a fundamental therapeutic tool for active GO, and their use is associated with interference in the formation of ROS or an effect on ROS scavenging enzymes. 13,14 Among the various types of oxidative damage in cellular structures or biomolecules induced by ROS, 8-hydroxy-2Ј-deoxyguanosine (8-OHdG) is one of the most abundant oxidative products of DNA and represents a noninvasive and sensitive biomarker of oxidative stress. 15 In this study, we measured the 8-OHdG levels in urine of patients having active GO treated with systemic corticosteroids with an aim to determine whether 8-OHdG level could be used as a biomarker in the management of GO.…”

mentioning

confidence: 99%

Oxidative Stress Change by Systemic Corticosteroid Treatment Among Patients Having Active Graves Ophthalmopathy

et al. 2007

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To measure the 8-hydroxy-2Ј-deoxyguanosine (8-OHdG) level in patients having active Graves ophthalmopathy (GO) and to compare this oxidative stress biomarker and the clinical evolution of patients after systemic corticosteroid treatment. Methods: In 8 euthyroid patients having active GO, we determined the 8-OHdG levels in urine before, during, and after intensive corticosteroid therapy. Clinical activity and ophthalmopathy index scores were assessed. Nine age-and sex-matched healthy volunteers served as control subjects. Results: The mean 8-OHdG level was statistically significantly increased in patients having active GO compared with that of controls (17.47 vs 5.97 ng/mg of creatinine, P Ͻ .001). During and after maximal systemic corticosteroid treatment, patients had statistically significantly lower mean 8-OHdG levels (7.19 and 10.18 ng/mg of creatinine, respectively) compared with the mean level before treatment. These changes were accompanied by decreases in clinical activity and ophthalmopathy index scores. The urinary 8-OHdG levels were subsequently elevated in 2 patients having recurrent active GO when corticosteroid therapy was tapered or withdrawn. Conclusions: Oxidative stress may have a role in the pathogenesis of GO. Urinary 8-OHdG level can be used not only as a noninvasive biomarker of oxidative stress in patients having GO but also as an objective and quantitative parameter in the follow-up of patients during immunosuppressive treatment.

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Reactive Oxygen Species and Drug Therapy for Inflammatory Diseases

Cited by 6 publications

References 14 publications

Peripheral parameters of oxidative stress in patients with infiltrative Graves’ ophthalmopathy treated with corticosteroids

Peripheral parameters of oxidative stress in patients with infiltrative Graves’ ophthalmopathy treated with corticosteroids

Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

Oxidative Stress Change by Systemic Corticosteroid Treatment Among Patients Having Active Graves Ophthalmopathy

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