THE OXIDANT HYPOCHLORITE (OCL-), A PRODUCT OF THE MYELOPEROXIDASE SYSTEM, DEGRADES ARTICULAR-CARTILAGE PROTEOGLYCAN AGGREGATE

被引：66

作者：

KATRANTZIS, M ^{[1
]}

BAKER, MS ^{[1
]}

HANDLEY, CJ ^{[1
]}

LOWTHER, DA ^{[1
]}

机构：

[1] WODEN VALLEY HOSP,JOHN CURTIN SCH MED RES,DIV CLIN SCI,CANBERRA,AUSTRALIA

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 1991年 / 10卷 / 02期

基金：

英国医学研究理事会;

关键词：

MYELOPEROXIDASE; HYPOCHLORITE; PROTEOGLYCAN; CARTILAGE; FREE RADICALS;

D O I：

10.1016/0891-5849(91)90003-L

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The myeloperoxidase-derived oxidant, hypochlorite (OCl-) was shown to be able to degrade proteoglycan aggregate prepared from bovine articular cartilage. Exposure of proteoglycan aggregate to OCl- concentrations less than 10(-4) M resulted in a decrease in the size of the constituent proteoglycan monomers, which were unable to reaggregate with hyaluronate due to the loss of the hyaluronic acid binding region as indicated by immunoblotting using the monoclonal 1-C-6 antibody. Analysis of the [S-35]-labeled core proteins by SDS / polyacrylamide electrophoresis and fluorography indicated a decrease in the size of the core protein. These data suggest that concentrations of OCl- below 10(-3) M results in the cleavage of the proteoglycan core protein in or near the hyaluronic acid binding region. The physiological consequences of these data are discussed. Exposure to higher concentrations (> 10(-3)) of OCl- caused more extensive degradation of the core protein; however, there was no evidence to suggest that OCl- cleaves glycosaminoglycan (GAG) chains.

引用

页码：101 / 109

页数：9

共 47 条

[1]

Harris, Mobilization of defensive cells in inflammatory tissue, Bacteriol. Rev., 24, pp. 3-15, (1960)

[2]

Cochrane, Immunologic tissue injury mediated by neutrophilic leukocytes, Adv. Immunol., 9, pp. 97-162, (1968)

[3]

Santer, Sriratana, Lowther, Carrageenan-induced arthritis. 5. A morphologic study of the development of inflammation in acute arthritis, Semin. Arth. Rheum., 13, pp. 160-168, (1983)

[4]

Riley, Kerr, Oxidant injury of the extracellular matrix: potential role in the pahogenesis of pulmonary emphysema, Lung, 163, pp. 1-13, (1985)

[5]

Lucisano, Mantovani, Lysosomal-enzyme release from polymorphonuclear leukocytes induced by immune complexes IGM and of IGG, J. Immunol., 132, pp. 2015-2020, (1984)

[6]

Barrett, The possible role of neutrophil proteinases in damage to articular cartilage, Agents Actions, 8, pp. 11-18, (1978)

[7]

Sandy, Sriratana, Brown, Lowther, Evidence for polymorphonuclear-leucocyte-derived proteinases in arthritic cartilage, Biochem. J., 193, pp. 193-202, (1981)

[8]

Velvart, Fehr, Baici, Sommermeyer, Knopfel, Cancer, Salgam, Boni, Degradation in vivo of articulate cartilage in rheumatoid arthritis by leukocyte elastase from polymorphonuclear leukocytes, Rheum. Int., 1, pp. 121-130, (1981)

[9]

Henson, Immunologic release of constituents from neutrophil leukocytes. 1. Role of antibody and complement on nonphagocytosable surfaces or phagocytosable particles, J. Immunol., 107, pp. 1535-1546, (1971)

[10]

Henson, Immunologic release of constituents from neutrophil leukocytes. 2. Mechanism of release during phagocytosis and adherence to non-phagocytosable surfaces, J. Immunol., 107, pp. 1547-1557, (1971)

← 1 2 3 4 5 →