作者: N.C. Rath , M.P. Richards , W.E. Huff , G.R. Huff , J.M. Balog
DOI: 10.1016/J.JCPA.2005.01.005
关键词:
摘要: Tibial dyschondroplasia (TD) is a metabolic cartilage disease of young poultry in which endochondral bone formation disrupted leading to the retention non-calcified, avascular plug tibial growth plate. Chicks aged 7 days were fed either control diet or one containing thiram 100 ppm for 48 h induce TD. Cell multiplication plate was determined thereafter with bromodeoxyuridine (BrdU) labelling, and changes by measuring alkaline phosphatase (ALP), tartrate-resistant acid (TRAP), glutathione (GSH) activities. The effect on chondrocyte maturation examined reverse transcriptase-polymerase chain reaction (RT-PCR) analysis gene expression. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) DNA fragmentation used determine effects cell survival. results showed that thiram-induced TD not due cells post-proliferative zones. Thiram did affect ALP activity, would have indicated loss calcification potential, but it reduced both TRAP concentrations, suggesting metabolism remodelling functions adversely affected. appeared no expression type X collagen, transglutaminase, RUNX2, matrix metalloproteinase-2 (MMP) genes alter potential chondrocytes. On contrary, expressions MMP-13 vascular endothelial factor (VEGF) "up-regulated," has pro-angiogenic activity. However, TUNEL assay induced apoptosis capillary vessels plates, as early 10 age, when visually evident. death increased subsequent accompanied massive chondrocytes transition zone induction also demonstrated fragmentation. It concluded through an increase altering causing arrest prehypertrophic state, creating dysfunction led destruction blood capillaries