The Molecular Mechanism Of Neuropathic Injury In Dairy Cattle With Copper Deficiency

The principle focus of this study was to clarify the mechanism of neuropathic injury in dairy cattle with copper deficiency on condition that the primary factors of biogeochemical agents causing copper deficiency of dairy cattle were analyzed systematically, so were the mechanism of copper dysbolism and changes of physiological and biochemical indexes. Specimen were collected from nine morbid cows with ataxia and six clinically healthy ones to determine the indices mainly relating to neural lesions while 25 dairy cattle with sublinical copper deficiency from affected areas were selected for copper supplementation experiment and 25 clinically healthy ones from nonffected areas were used as control. The chief methods and schemes were showed as follows: The concentration of free radicals were determined by Electron Spin Resonance (RSR), function of ion pump and subnit composition of cell membrane by enzyme assay and differential centrifugation respectively; Myelin basic protein and ganglioside were separated and studied by Sephadex150 and Sephadex75 gel column chromatography respectively in neural tissue of cows with copper deficiency; phospholipid in neural cell membrane by high performancehin layer chromatography; The means of Enzymeinked Immunosorbent assay (Elisa) was first established for analyzing the autontibodies to myelin basic protein and ganglioside in copper deficient cows. The oligoclone band protein and some important isoenzymes were detected by polymethacrylate gel electrophoresis. Pathological examination was carried out by microscopic and ultramicroscopic observation. Results and conclusions:1.The content of copper in waterarthood chain is marginally deficient and high level of molybdenum in diets is the primary condition resulting in subsequent copper deficiency. however, the geogrophical envirorunent of sufficient fluorine and deficient selenium exacerbate the duration of copper deficiency. The over synthesis of metallothionein (MT) is mainly caused by deposition of iron in liver due to copper deficiency. The abnormal component of MT induces the dysbolism of copper, zinc, iron and manganese leading to imbalance of multiple trace elements while the normal physiological function of nervous system is affected. The changes of physiological and biochemical indexes in serum were manifested by the abnormity of hepatic function, serum thyriod hormone level, lipid metabolism and immunologic function.2.Excessive free radicals and dysfunction of antioxidant defense system induced lipid peroxidat ion attacking membrane system, causing the abnormity of membraneAfluidity and ion pump function, destructing the sub梪nit component of phospholipid and ganglioside on the axolemnia and myelin membrane.3.The changes of physiological and biochemical indexes in neural system were manifested by high level of oligoclone band protein in cerebrospinal fluid, positive colloidal gold test, characteristic changes of isozymography, abnormal alterations in content of ferritin, component of free amino acid and immunological indexes in CSF.4.Characteristic changes were also found in the sub梪nit component of myelin basic protein, ganglioside and membrane phospholipid in neural system, so were the high level of auto梐ntibodies to myelin basic protein and ganglioside in serum and cerebrospinal fluid. There was abnormal histochemical characteristic of oxidoreductase and nervous transmitter enzyme in neural tissue.5.The ultramicroscopic pathological changes in neural system were manifested by rarefaction and exfoliation of medullary sheath, degeneration and necrosis in part of neuronal and neuroglial cells, neurotropic phenomenon and corpuscula of programmed cell death existing in the karyon of neuronal and endothenial cells.The mechanism of neural injury can be summed up from these results: Neural tissue especially the axolemma and myelin membrane is vulnerable to attacking of free radicals due to the copper deficiency and their integrity is damaged which leads to exposing the myelin basic protein, g...