Effects Of Manganese Deficiency On Serum Biochemical Index Of Bone Metabolism In Chicken

The purpose of this study was to elucidate the mechanism of bone and cartilagemetabolism on Perosis by feeding chicks on a low-Mn diets, which can provides the scientificfoundation for further study of bone and cartilage development in the conditions ofmanganese deficiency.Ninety1-d-old male Arbor Acre chicks were randomly divided into3groups and eachgroup were treated with diet, which had different concentration of Mn (Mn60mg/kg, controlgroup; Mn40mg/kg, Mn deficient group Ⅰ; Mn8.7mg/kg, Mn deficient group Ⅱ). Allthe animals were fed the feed as the basal diet recommended by NRC (1994) aboutMeat-Type Chicken except Mn, and living conditions and habitat met the guiding principlesof chicks. Both diet and water were provided ad libitum; After42days, the chicks wereslaughtered after collecting15ml blood and then sera were collected for evaluating the makerof bone metabolism and ion concentration. In the study, serum parathyroid hormone,calcitonin, tumor necrosis factor alpha and osteocalcin contents were determined byradioimmunoassay method; serum transforming growth factor alpha, basic fibroblast growthfactor, matrix metallopeptidase9, tissue inhibitors of metalloproteinase1and bonemorphogenetic protein were determined by ELISA; The method of chloramine T was used forestimating Hydroxyproline; Serum tartrate-resistant acid phosphatase activity weredetermined by colorimetry; The serum of alkaline phosphatase and phosphorus levels weredetermined by autoanalyzer; The levels of serum calcium magnesium copper zinc andmanganese were determined by atomic absorption spectrophotometry. Results show that:Compared to control group, serum calcitonin, transforming growth factor alpha,hydroxyproline tartrate-resistant acid phosphatase alkaline phosphatase and manganese weredecreased remarkably (P<0.05), while serum parathyroid hormone, tumor necrosis factoralpha, tissue inhibitors of metalloproteinase1, and serum calcium, magnesium and zinc wereincreased remarkably (P<0.05). However, there were no remarkable differences (P>0.05) ofosteocalcin, basic fibroblast growth factor, matrix metallopeptidase9, and bonemorphogenetic protein in serum between three groups.In conclusion, our study demonstrate that Mn deficiency induces in the disorder of boneregulatory hormones in serum, which might elevate the content of serum calcium magnesiumand zinc and affect the balance of bone and cartilage on internal environment. So we can speculate the disorder of regulators of bone hormonal might be a reason of tibialdyschondroplasia resulted from manganese deficiency. In addition, the changes of serummarkers of bone and cartilage metabolism break the microenvironment of cartilage and bonedevelopment, which may affects the proliferation and differentiation of cartilage. Therefore,the reason of perosis has not only to do with the decreasing of the organic matrix formationbut also with serum markers of bone metabolism, which might have a tiny effect on themicroenvironment of bone and chondrocyte development.