Spectrophotometric Assay of Superoxide Dismutase Activity Based on the Activated Autoxidation of a Tetracyclic Catechol

Nebot, Carolina; Moutet, Marc; Huet, Pascal; Xu, Jinzhu; Yadan, Jean‐Claude; Chaudière, Jean

doi:10.1006/abio.1993.1521

Cited by 254 publications

(163 citation statements)

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“…After inactivation of Mn-SOD by ethanol-chloroform extraction, the SOD-1 activity in the upper aqueous layer was measured spectrophotometrically by using the commercial superoxide dismutase assay kit (Merck Biosciences, San Diego). Briefly, the assay is based on the SOD-1-mediated increase in the rate of autoxidation of 5,6,6a,11b-tetrahydro-3,9,10-trihydroxybenzo[c]fluorene (BXT-01050) (24). Autoxidation of BXT-01050 yields a chromophore, which absorbs maximally at 525 nm.…”

Section: Quantification Of A␤mentioning

confidence: 99%

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Bayer

Schäfer

Simons

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

320

255

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The Cu-binding ␤-amyloid precursor protein (APP), and the amyloid A␤ peptide have been proposed to play a role in physiological metal regulation. There is accumulating evidence of an unbalanced Cu homeostasis with a causative or diagnostic link to Alzheimer's disease. Whereas elevated Cu levels are observed in APP knockout mice, APP overexpression results in reduced Cu in transgenic mouse brain. Moreover, Cu induces a decrease in A␤ levels in APP-transfected cells in vitro. To investigate the influence of bioavailable Cu, transgenic APP23 mice received an oral treatment with Cu-supplemented sucrose-sweetened drinking water (1). Chronic APP overexpression per se reduced superoxide dismutase 1 activity in transgenic mouse brain, which could be restored to normal levels after Cu treatment (2). A significant increase of brain Cu indicated its bioavailability on Cu treatment in APP23 mice, whereas Cu levels remained unaffected in littermate controls (3). Cu treatment lowered endogenous CNS A␤ before a detectable reduction of amyloid plaques. Thus, APP23 mice reveal APP-induced alterations linked to Cu homeostasis, which can be reversed by addition of dietary Cu.

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Section: Quantification Of A␤mentioning

confidence: 99%

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Bayer

Schäfer

Simons

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

320

255

View full text Add to dashboard Cite

show abstract

“…SOD activity was determined by the rate of reduction of cytochrome c, with 1 unit (U) of SOD activity defined as the amount of SOD required to inhibit the rate of cytochrome c reduction by 50%. 23 The final reaction volume was 3 ml and included 50 mmol/L potassium phosphate buffer, 2 mmol/L cytochrome c, 0.05 mmol/L xanthine, and a 0.1 mmol/L ethylenediaminetetraacetic acid solution. Xan-thine oxidase (Sigma) was added at a concentration sufficient to induce a 0.020 per minute change in absorbance at 550 nm.…”

Section: Antioxidant Assaysmentioning

confidence: 99%

Superoxide Dismutase Inactivation in Pathophysiology of Asthmatic Airway Remodeling and Reactivity

Comhair

Ghosh

et al. 2005

The American Journal of Pathology

175

149

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Airway hyperresponsiveness and remodeling are defining features of asthma. We hypothesized that impaired superoxide dismutase (SOD) antioxidant defense is a primary event in the pathophysiology of hyperresponsiveness and remodeling that induces apoptosis and shedding of airway epithelial cells. Mechanisms leading to apoptosis were studied in vivo and in vitro. Asthmatic lungs had increased apoptotic epithelial cells compared to controls as determined by terminal dUTP nick-end labeling-positive cells. Apoptosis was confirmed by the finding that caspase-9 and -3 and poly (ADP-ribose) polymerase were cleaved. On the basis that SOD inactivation triggers cell death and low SOD levels occur in asthma, we tested whether SOD inactivation plays a role in airway epithelial cell death. SOD inhibition increased cell death and cleavage/activation of caspases in bronchial epithelial cells in vitro. Asthma is commonly diagnosed using physiological measures, but alterations in airway structure are the defining features of asthma. Damage to airway epithelium, eosinophil infiltration, smooth muscle hyperplasia, thickening and aberrant collagen, and protein composition of the basement membrane are well established elements of the asthmatic airway. 1,2 The injury to the bronchial epithelium in asthma is marked by loss of columnar epithelial cells. Extensive loss of cells and denuded basement membrane with few basal cells remaining on the airway surface are noted in severe asthma, but shedding of airway epithelium is present even in clinically mild asthma. 2,3 Physical loss of epithelial lining cells is considered one proximate cause of the airway hyperresponsiveness to inhaled mediators, and has been speculated to contribute to asthmatic airway remodeling, in particular abnormal collagen synthesis. Evidence from organ culture systems supports the concept of an epithelial-mesenchymal unit in which loss of epithelium leads to mucosal myofibroblast and fibroblast proliferation, and collagen deposition. 2,4 -6 Thus, if the epithelial injury and loss could be understood and prevented in asthma, the clinical symptoms of airway hyperresponsiveness and long-term progressive sequelae in the airways, which contribute to fixed airflow limitation, might be prevented.Several reports have proposed that loss of epithelial cells is because of apoptosis based on immunostaining for the proteins that regulate apoptosis, or by detection of DNA strand breaks by immunostaining with the terminal dUTP nick-end labeling (TUNEL) assay. 7-11 However, not all reports have confirmed increased TUNEL positivity in airways. 9 Furthermore, if airway epithelial cells are undergoing increased cell death, it is unclear whether this is because of an inherent cell defect or a response to the asthmatic airway environment. Although nonspecific events related to increased levels of reactive oxygen and

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“…A atividade enzimática da SOD em hemácias foi determinada espectrofotometricamente, segundo o ensaio descrito por Nebot et al 18 . A atividade de GSH-Px em hemácias foi quantificada por meio de ensaio colorimétrico, utilizando um método que tem por base a técnica desenvolvida por Paglia e Valentine 19 .…”

Section: Marcadores De Atividade Do Sistema Antioxidante Enzimáticounclassified

The role of oxidative stress in inflammation in patients with juvenile rheumatoid arthritis

Ramos¹,

Ramos²,

Dominguez³

2000

J Pediatr (Rio J)

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Objective: To determine the level of cellular oxidative stress blood markers and the enzymatic system of antioxidant defense establishing the oxidative profile in patients with Juvenile Rheumatoid Arthritis.Methods: Case-control study that included 64 patients (46 of female sex) with Juvenile Rheumatoid Arthritis (JRA) following clinical control in the Pediatric Rheumatology Service of the Vall d'Hebron Hospital, Barcelona, Spain. The patients were separated in three subtypes based on the pattern of onset within the first six months of disease: polyarticular, pauciarticular and systemic. The control group included 60 patients (38 of female sex) following clinical control to diseases of non inflammatory nature, in the same hospital. The plasmatic levels of malondialdehyde (MDA), lipoperoxide (LPO), hydroperoxide (HPX), carbonile groups (CG) of proteins and gluthathione and the enzymatic activities of Superoxide dismutase (SOD), gluthathione peroxidase (GSH-Px) and gluthathione reductase were determined.Results: The group of patients with JRA presented high concentrations of lipid peroxidation products, evaluated by determining the plasmatic levels of MDA, LPO, and HPX; oxidative damage of the circulate protein, determined by CG contents of plasma proteins; elevation of enzymatic activity of SOD and GSH-Red; decrease of GSH-Px activity and GSH levels.Conclusions: Our results show the presence of molecular damage determined by oxygen free radicals in the JRA patients. The SOD activity and the changes of gluthathione redox enzymatic cycle confirm the decrease of capacity of cellular defense system against the induced toxicity of oxidative stress in these patients. Resultados: Comparados aos controles, os pacientes portadores de ARJ apresentaram concentrações elevadas dos produtos derivados da lipoperoxidação, avaliada pela determinação dos níveis plasmáticos do MDA, HPX e LPO; dano oxidativo das proteínas circulantes, determinado pelo conteúdo de GC de proteínas plasmá-ticas; elevação da atividade enzimática da SOD e GSH-Red; e diminuição da atividade da GSH-Px e dos níveis do GSH. J. pediatr. (Rio J.Conclusões: Estes resultados demonstram a presença de dano molecular determinado pelos radicais livres de oxigênio em pacientes com ARJ. A atividade da SOD e as alterações do ciclo enzimático glutatião-redox confirmam uma diminuição da capacidade dos sistemas de defesa intracelular contra a toxicidade induzida pelo estresse oxidativo nestes pacientes. Introdução A geração de radicais livres ocorre como parte do processo fisiológico do metabolismo aeróbico, secundária à produção de radicais reativos de oxigênio. Desse modo, o metabolismo celular produz radicais livres em condições fisiológicas, e estes radicais ativos podem ter vários efeitos J. pediatr. (Rio J.

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Spectrophotometric Assay of Superoxide Dismutase Activity Based on the Activated Autoxidation of a Tetracyclic Catechol

Cited by 254 publications

References 0 publications

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Superoxide Dismutase Inactivation in Pathophysiology of Asthmatic Airway Remodeling and Reactivity

The role of oxidative stress in inflammation in patients with juvenile rheumatoid arthritis

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