Inhibition of proteoglycan synthesis by hydrogen peroxide in cultured bovine articular cartilage

Bates, Edna J.; Johnson, Colin C.; Lowther, Dennis A.

doi:10.1016/0304-4165(85)90082-0

Cited by 80 publications

(53 citation statements)

References 29 publications

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“…Reactive oxygen metabolites produced during the respiratory burst may also be involved (13)(14)(15). Myeloperoxidase (MPO) produced by neutrophils may react with H2O2 and Cl" to generate OHCI which has been shown to be relevant to the neutrophiPs capacity to kill amoebae (16).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of human neutrophil‐mediated cartilage damage in vitro: The role of lysosomal enzymes, hydrogen peroxide and hypochlorous acid

1989

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Summary Cartilage is a focal point of attack by cellular and molecular elements of the inflammatory response which occurs in arthritic diseases. Neutrophils damage articular cartilage by degrading matrix components and inhibiting their synthesis. The aim of this study was to elucidate mechanisms of this damage. Human neutrophils were isolated from blood by centrifuging through Ficoll-Hypaque and granule extract prepared from them. Articular cartilage from adult humans and cattle was maintained in organ culture. Cartilage degradation (release of 35S-labelled proteoglycan) or synthesis (incorporation of ^^S into proteoglycan) was determined after various treatments. Human neutrophils and neutrophil granule extract degraded proteoglycan and inhibited proteoglycan synthesis. The specific leucocyte elastasc inhibitor A'-methoxysuccinyl-(ala)2-pro-vaI-chloromethylketone (MAAPV-CMK) partially reversed these effects. H2O2. a product of the neutrophi! respiratory burst, when added directly at 10" ^mol/L, or generated by glucose oxidase (GO)/glucose inhibited proteoglycan synthesis but had no effect on degradation. Hypochlorous acid (OHCI), a product of the myeloperoxidase (MPO)/H2O2/C1 system at 50 |imol/L degraded proteoglycan and inhibited its synthesis. OHCI produced by granule extract (as a source of MPO) + GO-generated H2O2+C1~ degraded proteoglycan. The results indicate that neutrophii-mediated proteoglycan degradation and inhibition of synthesis Is largely attributable to elastase and secondarily to OHCI, whereas H2O2 impairs synthesis without affecting degradation of proteoglycan.

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Section: Introductionmentioning

confidence: 99%

Mechanisms of human neutrophil‐mediated cartilage damage in vitro: The role of lysosomal enzymes, hydrogen peroxide and hypochlorous acid

1989

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“…Os radicais hidroxil podem degradar a cartilagem 6 . O ácido hipocloroso pode atacar proteoglicanos, e o peróxido de hidrogênio (H 2 O 2 ) inibe a sua síntese 8 . A aplicação intra-articular de H 2 O 2 , em ratas, induz à produção da enzima glicose oxidase, que causa grave lesão articular e morte de condrócitos 9 .…”

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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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“…OH may inhibit cartilage proteoglycan synthesis, e.g., by interfering with ATP synthesis, in part by inhibiting the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase in chondrocytes. [45][46][47][48] Alpaslan et al 49 found that intraarticular use of hyaluronan significantly decreased concentration This would suggest that membrane lipids are only one of the possible targets of oxidative damage, and compounds of SF such as hyaluronic acid would be more susceptible to oxidative stress. The production of ROS in synovial fluid is difficult to detect because ROS are extremely labile.…”

Section: Discussionmentioning

confidence: 99%

Oxidant and anti‐oxidant systems of synovial fluid from patients with knee post‐traumatic arthritis

Ostałowska

Kasperczyk

et al. 2007

Journal Orthopaedic Research

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It has been suggested that patients with knee post-traumatic arthritis (PA), associated or not to haemarthrosis (HA), display altered oxidant and anti-oxidant systems in their synovial fluid. This study aimed to establish whether this is really the case. Synovial fluid samples were obtained by transdermal arthrocentesis from 69 patients with PA (36 of them had HA) and 22 control subjects. The activities of synovial fluid zinc-copper superoxide dismutase (ZnCuSOD) and manganese superoxide dismutase (MnSOD) isoenzymes, catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione-S-transferase (GST) enzymes, and malondialdehyde (MDA) concentration and synovial fluid viscosity were measured in the study groups. Patients with PA had significantly increased activities of all antioxidant enzymes, except CAT, and MDA concentration than did the controls. However, synovial fluid viscosity was found to be decreased in the study group, mainly in the HA subgroup. Results suggest that excessive free radicals production may exist in synovial fluid of PA patients and may contribute to knee joint destruction.

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Inhibition of proteoglycan synthesis by hydrogen peroxide in cultured bovine articular cartilage

Cited by 80 publications

References 29 publications

Mechanisms of human neutrophil‐mediated cartilage damage in vitro: The role of lysosomal enzymes, hydrogen peroxide and hypochlorous acid

Mechanisms of human neutrophil‐mediated cartilage damage in vitro: The role of lysosomal enzymes, hydrogen peroxide and hypochlorous acid

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

Oxidant and anti‐oxidant systems of synovial fluid from patients with knee post‐traumatic arthritis

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