Sensitivity of chondrocytes of growing cartilage to reactive oxygen species

Vascular invasion of calcified cartilage, during endochondral ossification, is initiated and sustained by invasive cells (endothelial cells and macrophages) which degrade the tissue by releasing lytic enzymes. Concurrently, reactive oxygen species (ROS) are also released by these cells and we hypoth...

Full description

Saved in:
Bibliographic Details
Published inBiochimica et biophysica acta Vol. 1425; no. 1; pp. 103 - 111
Main Authors Fragonas, Emanuela, Pollesello, Piero, Mlinárik, Vladimir, Toffanin, Renato, Grando, Cristina, Godeas, Cristiana, Vittur, Franco
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 16.09.1998
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Vascular invasion of calcified cartilage, during endochondral ossification, is initiated and sustained by invasive cells (endothelial cells and macrophages) which degrade the tissue by releasing lytic enzymes. Concurrently, reactive oxygen species (ROS) are also released by these cells and we hypothesize that ROS also contribute to the degradation of the tissue. As a preliminary approach to this problem, the antioxidant activities and the effect of ROS on hypertrophic cartilage and chondrocytes (HCs) were investigated. Compared to resting or articular chondrocytes, HCs exhibited higher catalase but lower SOD specific activities and lower PHGPx concentration, thus revealing a defence activity specific against H 2O 2. Moreover, dose-dependent depletion of ATP occurred after few minutes of exposure to ROS, and a long-term treatment (16 h incubation with ROS) promoted the release of LDH activity and a significant variation of the poly- to mono-unsaturated fatty acid ratio. Finally, the incubation of HCs with low ROS doses induced the release of sedimentable alkaline phosphatase activity (matrix vesicles). How the obtained results fit the in vivo occurring events is discussed.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0304-4165
0006-3002
1872-8006
DOI:10.1016/S0304-4165(98)00055-5