Abstract
Similarities in morphology between copper-deficient cartilage and abnormal cartilage associated with tibial dyschondroplasia (TD) led to studies dealing with copper metabolism and its possible relation to TD.Abnormal cartilage and copper deficient cartilage cells both oxidize significantly less glucose to CO2 and water when compared to normal epiphyseal and day-old hypertrophic cartilage cells. Plasma ceruloplasmin levels and cartilage copper content were not different between normal birds and those affected with TD, which seemed to rule out a genetic defect in copper metabolism as being partly responsible for the abnormal cartilage occurrence.Mitochondrial marker enzyme activities were investigated, and abnormal cartilage showed a significant decrease in activity of both cytochrome oxidase and citrate synthase. The yield of mitochondria on a percent of total activity basis was quite low from both normal and abnormal cartilages and, thus, an absolute conclusion with regard to mitochondrial impairment cannot be made at this time.
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