Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học quốc tế đề tài : The effect of oxygen tension on calcium homeostasis in bovine articular chondrocytes | White and Gibson Journal of Orthopaedic Surgery and Research 2010 5 27 http content 5 1 27 éHMÌ JOURNAL OF ORTHOPAEDIC oo SURGERY AND RESEARCH RESEARCH ARTICLE Open Access The effect of oxygen tension on calcium homeostasis in bovine articular chondrocytes Rachel White and John S Gibson Abstract Background Articular chondrocytes normally experience a lower O2 tension compared to that seen by many other tissues. This level may fall further in joint disease. Ionic homeostasis is essential for chondrocyte function but at least in the case of H ions it is sensitive to changes in O2 levels. Ca2 homeostasis is also critical but the effect of changes in O2 tension has not been investigated on this parameter. Here we define the effect of hypoxia on Ca2 homeostasis in bovine articular chondrocytes. Methods Chondrocytes from articular cartilage slices were isolated enzymatically using collagenase. Cytoplasmic Ca2 levels Ca2 i were followed fluorimetrically using Fura-2 to determine the effect of changes in O2 tension. The effects of ion substitution replacing extracellular Na with NMDG and chelating Ca2 with EGTA were tested. Levels of reactive oxygen species ROS and the mitochondrial membrane potential were measured and correlated with Ca2 i. Results A reduction in O2 tension from 20 to 1 for 16-18 h caused Ca2 i to approximately double reaching 105 23 nM p . Ion substitutions indicated that Na Ca2 exchange activity was not inhibited at low O2 levels. At 1 O2 ROS levels fell and mitochondria depolarised. Restoring ROS levels with an oxidant H2O2 a non-specific ROS generator Co2 or the mitochondrial complex II inhibitor antimycin A concomitantly reduced Ca2 . Conclusions O2 tension exerts a significant effect on Ca2 i. The proposed mechanism involves ROS from mitochondria. Findings emphasise the importance of using realistic O2 tensions when studying the physiology and pathology of articular cartilage and the potential interactions between O2 ROS .
