The measurement of free radical reactions in humans

Halliwell, Barry; Grootveld, Martin

doi:10.1016/0014-5793(87)81455-2

Cited by 304 publications

(145 citation statements)

References 56 publications

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“…However, the measurement of malondialdehyde is not an accurate indicator of lipid peroxidation in biologic samples (24,25). Furthermore, as mentioned above, evidence from previous studies suggests enhanced platelet activation in vivo in patients with scleroderma (13).…”

Section: Discussionmentioning

confidence: 99%

Evidence of free radical–mediated injury (isoprostane overproduction) in scleroderma

Stein

Tanner

Awad

et al. 1996

Arthritis & Rheumatism

154

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Objective. Free radical–induced oxidative stress with consequent lipid peroxidation and resultant tissue damage has been suggested as a potential mechanism of the pathogenesis of scleroderma. However, because reliable measurement of lipid peroxidation in vivo is difficult, it has not been possible to adequately examine this hypothesis. We have previously described a series of bioactive prostaglandin F2–like compounds, termed F2‐isoprostanes, produced in vivo in humans by the noncyclooxygenase, free radical–catalyzed, peroxidation of arachidonic acid and have shown them to be a reliable measure of lipid peroxidation in vivo. In the present study, we determined whether scleroderma is associated with enhanced oxidative stress.Methods. As a measure of oxidative stress, we determined urinary concentrations of a tetranordicarboxylic acid metabolite of F2‐isoprostanes (F2IP‐M) by mass spectrometry in 8 patients with scleroderma (representing a wide spectrum of disease, including limited disease with refractory digital ulceration or pulmonary hypertension, and diffuse disease) and in 10 healthy control subjects.Results. F2IP‐M concentrations were significantly higher in patients with scleroderma (mean ± SEM 3.41 ± 0.64 ng/mg of creatinine) than in healthy controls (1.22 ± 0.14 ng/mg of creatinine) (P = 0.002). These elevations occurred in patients with limited disease and in those with diffuse disease.Conclusion. The increased level of urinary F2IP‐M supports the hypothesis that free radical–induced oxidative injury occurs in scleroderma and provides a biologic marker whose relationship to disease activity and disease therapy may be important. These findings may also provide a rationale for exploring whether antioxidant therapy may influence the natural course of the disease.

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Section: Discussionmentioning

confidence: 99%

Evidence of free radical–mediated injury (isoprostane overproduction) in scleroderma

Stein

Tanner

Awad

et al. 1996

Arthritis & Rheumatism

154

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“…Expression of the gene encoding eNOS is increased in endothelial cells exposed to estrogen (9,10). In addition, estrogen might modulate NO synthesis through its direct antioxidant effects (11) and by regulating the expression of genes encoding essential co-factor or enzymes that increase eNOS activity by post-translational modification (12). Enhancement of endothelial function by estrogen is potentiated by a concomitant rise in the synthesis of prostacyclin (PGI 2 ) through the activation of the gene encoding cyclooxygenase in endothelial cells (13).…”

Section: Introductionmentioning

confidence: 99%

Endothelial mediators of 17ß-estradiol-induced coronary vasodilation in the isolated rat heart

Santos

Abreu

Bissoli

et al. 2004

Braz J Med Biol Res

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The present study was designed to determine relaxation in response to 17ß-estradiol by isolated perfused hearts from intact normotensive male and female rats as well as the contribution of endothelium and its relaxing factors to this action. Baseline coronary perfusion pressure was determined and the vasoactive effects of 17ß-estradiol (10 µM) were assessed by in bolus administration before and after endothelium denudation by infusion of 0.25 µM sodium deoxycholate or perfusion with 100 µM L-NAME, 2.8 µM indomethacin, 0.75 µM clotrimazole, 100 µM L-NAME plus 2.8 µM indomethacin, and 100 µM L-NAME plus 0.75 µM clotrimazole. Baseline coronary perfusion pressure differed significantly between males (84 ± 2 mmHg, N = 61) and females (102 ± 2 mmHg, N = 61). Bolus injection of 10 µM 17ß-estradiol elicited a transient relaxing response in all groups, which was greater in coronary beds from females. For both sexes, the relaxing response to 17ß-estradiol was at least in part endothelium-dependent. In the presence of the nitric oxide synthase inhibitor L-NAME, the relaxing response to 17ß-estradiol was reduced only in females. Nevertheless, in the presence of indomethacin, a cyclooxygenase inhibitor, or clotrimazole, a cytochrome P450 inhibitor, the 17ß-estradiol response was significantly reduced in both groups. In addition, combined treatment with L-NAME plus indomethacin or L-NAME plus clotrimazole also reduced the 17ß-estradiol response in both groups. These results indicate the importance of prostacyclin and endothelium-derived hyperpolarizing factor in the relaxing response to 17ß-estradiol. 17ß-estradiol-induced relaxation may play an important role in the regulation of coronary tone and this may be one of the reasons why estrogen replacement therapy reduces the risk of coronary heart disease in postmenopausal women.

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“…Oxygen centered free radicals may play a central role in the initiation or exacerbation of tissue damage in heart attack, stroke, organ transplantation, acute pancreatitis, liver cirrhosis, arthritis, Parkinson's disease, and the toxicity of and redox cycling drugs and chemicals. [1][2][3][4][5][6][7][8][9][10][11] Perhaps of greatest clinical importance is the amplification of tissue damage during reperfusion of previously ischemic tissues, including heart, 12 kidney, [13][14] small intestine, [15][16][17] skin, 18 and skeletal muscle. 19 Widespread acceptance of pathogenic mechanisms invoking formation of oxygen radicals has been limited by their inability of investigators to convincingly detect and quantify such radicals in isolated tissues or in animal models.…”

Section: Introductionmentioning

confidence: 99%

Scatchard analysis of methane sulfinic acid production from dimethyl sulfoxide: A method to quantify hydroxyl radical formation in physiologic systems

Babbs

Griffin

1989

Free Radical Biology and Medicine

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A major impediment to the confirmation of free radical mechanisms in pathogenesis is a lack of direct, chemical evidence that oxygen centered free radicals actually arise in living tissues in quantities sufficient to cause serious damage. This investigation was conducted to validate the use of dimethyl sulfoxide (DMSO) as a quantitative molecular probe for the generation of hydroxyl radicals (HO*) under physiologic conditions. Reaction of HO* with DMSO produces methane sulfinic acid (MSA) as a primary product, which can be detected by a simple colorimetric assay. To develop a method for estimating total HO* production, we studied two model systems: the superoxide driven Fenton reaction in vitro, using xanthine oxidase as the source of superoxide, and a computer model of Fenton chemistry. Measured MSA production both in vitro and in the computer model was a predictable function of the concentrations of DMSO and competing scavengers of HO*, according to the principle of competition kinetics. Both experimental results and model calculations showed that Scatchard analysis may be used to infer total HO* generation, despite the presence of scavengers other than DMSO, such as mannitol. Thus, methane sulfinic acid production from DMSO holds promise as an easily measured marker for HO* formation in biologic systems pretreated with DMSO, and Scatchard analysis of repeated experiments with varying DMSO concentrations can yield an estimate of total HO* generation.

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The measurement of free radical reactions in humans

Cited by 304 publications

References 56 publications

Evidence of free radical–mediated injury (isoprostane overproduction) in scleroderma

Evidence of free radical–mediated injury (isoprostane overproduction) in scleroderma

Endothelial mediators of 17ß-estradiol-induced coronary vasodilation in the isolated rat heart

Scatchard analysis of methane sulfinic acid production from dimethyl sulfoxide: A method to quantify hydroxyl radical formation in physiologic systems

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