Ferritin formation by synovial cells exposed to haemoglobin in vitro.

Muirden, K. D.; Fraser, J. R. E.; Clarris, B. J.

doi:10.1136/ard.26.3.251

Cited by 30 publications

(10 citation statements)

References 11 publications

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“…We favor the hypothesis that ferritin is synthesized by synovial membrane cells and enters SF by secretion or by release from dying cells. The high production of ferritin by synovial cells, as shown by Muirden et al (21), is a protective reaction to the continuous iron release in SF, due to blood loss and the resulting breakdown of hemoglobin. Ferritin and transferrin can both play a dual role: 1) protection against oxygen free radicals by binding free iron, or 2) stimulation of OH' production by release of free iron from the binding protein.…”

Section: Discussionmentioning

confidence: 99%

Protective factors against oxygen free radicals and hydrogen peroxide in rheumatoid arthritis synovial fluid

Biemond

Swaak

Koster

1984

Arthritis & Rheumatism

121

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Oxygen free radicals are probably involved in the pathogenesis of rheumatoid arthritis (RA). The enzymes involved in protection against oxygen free radicals and H2O2 (superoxide dismutase, catalase, and glutathione peroxidase) were measured. Superoxide dismutase was not increased, glutathione peroxidase was slightly and catalase was strongly elevated in RA synovial fluid (SF) compared with control SF. Although these enzymes are present in SF, the activities are insufficient to protect against oxygen free radicals and H2O2. In contrast to transferrin, ferritin was increased in RA synovial fluid. Ceruloplasmin was also elevated. When rat liver microsomes were used as a target for oxygen free radicals, serum and SF were both protective. Gel filtration experiments showed that the fraction pattern in which there was maximal protective potential against lipid peroxidation corresponded closely to the level of ceruloplasmin. After removal of ceruloplasmin from serum or SF, about 70% of the protective capacity disappeared. It is concluded that ceruloplasmin is an important protector against oxygen free radicals.

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Section: Discussionmentioning

confidence: 99%

Protective factors against oxygen free radicals and hydrogen peroxide in rheumatoid arthritis synovial fluid

Biemond

Swaak

Koster

1984

Arthritis & Rheumatism

121

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“…Catabolised erythrocytes arising from intermittent intra-articular haemorrhages'9 may also contribute to the iron present in synovial macrophages. 20 One of the most constant findings in chronic diseases (such as adjuvant arthritis) is hypoferraemia.2' Plasma iron concentrations in animals with adjuvant disease have been shown to decrease 14 days after adjuvant induction,22 a change also observed in our adjuvant rats (see results and table).…”

Section: Discussionmentioning

confidence: 65%

Effect of iron complexes on adjuvant arthritis in rats.

Dabbagh

Blake

Morris

1992

Annals of the Rheumatic Diseases

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When a total dose infusion of iron dextran is given to anaemic rheumatoid patients an exacerbation of inflammatory synovitis in previously affected joints is observed. The adjuvant arthritis model of inflammation in rats has been used to investigate the mechanism of iron promoted synovitis. Either iron dextran (5 mg injected intravenously) with a dextran C control, or iron sorbitol (7.5 mg injected intramuscularly) with a sorbitol citrate complex control was given at the onset of clinical joint inflammation. Iron dextran significantly increased joint inflammation (assessed by joint scoring) at days 12, 13, 14, and 16 after injection. Similarly, iron sorbitol produced a significant increase in the joint score at days 17, 18, 19, and 21. In addition, extensive osteoporosis was observed in the rats treated with iron sorbitol. These proinflammatory effects of iron coincide with the presence of positive results for synovial iron (III) using Perl's test and neutrophil infiltration. The results of this study suggest that the iron induced increase in synovitis in adjuvant arthritis is a result of iron promoted oxidative damage and is not likely to be due to the dextran C or the sorbitol citric acid components. It is suggested that a similar mechanism may occur in rheumatoid patients given iron supplements.

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“…Almost invariably light microscopy in these situations has shown the iron to occur predominantly in deep macrophages in contrast to the more frequent localization to synovial lining cells in haemochromatosis. Electron microscopic studies in rheumatoid arthritis (Hirohata and Kobayashi, 1964;Muirden, 1966), pigmented villonodular synovitis (Wyllie, 1969), and in experimental hemarthrosis (Roy, 1968) or intra-articular iron dextran injection (Ball, Chapman, and Muirden, 1964), have all shown the iron predominantly in phagocytic cells, whether deep in the synovium or in the synovial lining. The Type B cells were always relatively spared in contrast to the findings in haemochromatosis.…”

Section: Other Causes Of Iron Deposition In the Synoviummentioning

confidence: 99%

Ultrastructural characteristics of the synovial membrane in idiopathic haemochromatosis.

Schumacher¹

1972

Annals of the Rheumatic Diseases

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Ferritin formation by synovial cells exposed to haemoglobin in vitro.

Cited by 30 publications

References 11 publications

Protective factors against oxygen free radicals and hydrogen peroxide in rheumatoid arthritis synovial fluid

Protective factors against oxygen free radicals and hydrogen peroxide in rheumatoid arthritis synovial fluid

Effect of iron complexes on adjuvant arthritis in rats.

Ultrastructural characteristics of the synovial membrane in idiopathic haemochromatosis.

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