Peripheral erythrocyte levels, hemolysis and three vanadium compounds

Three vanadium compounds of different valence states were administered to adult mice. Two, four, and eight days following treatment of vanadium, cardiac blood was collected. The blood sample was used to ascertain the peripheral erythrocyte count (cell/mm3) and to determine the in vitro hemolytic index of erythrocytes obtained from mice treated in vivo with either the tri-, tetra-, or pentavalent vanadium compound. Data indicate that the tetravalent form was the most effective test substance in 1) promoting rupture of isolated erythrocytes compared to red cells retrieved from control mice and 2) depressing the erythrocyte count obtained from heart blood; maximum effects were manifest four days post-treatment. For all treatments there appeared to be a good correlation between the degree of vanadium-induced hemolysis and the peripheral erythrocyte count reduction following exposure to the vanadium.     

Neutrophilic granulocytosis following lead acetate in female mice

Lead induces an abrupt neutrophilic granulocytosis with the peak response detected 4 days after treatment. Using the incorporation of tritiated thymidine as an index of neutrophil production, autoradiographic analysis revealed that only about 16% of the total neutrophil increase is associated with a stimulatory effect on production. The remainder of the increase appears to be linked to the panhistotoxic action of lead, promoting migration of neutrophils from reserve sites in the wake of tissue damage.     

Lamin B1 duplications cause autosomal dominant leukodystrophy

Adult-onset autosomal dominant leukodystrophy (ADLD) is a slowly progressive neurological disorder characterized by symmetrical widespread myelin loss in the central nervous system, with a phenotype similar to chronic progressive multiple sclerosis. In this study, we identify a genomic duplication that causes ADLD. Affected individuals carry an extra copy of the gene for the nuclear laminar protein lamin B1, resulting in increased gene dosage in brain tissue from individuals with ADLD. Increased expression of lamin B1 in Drosophila melanogaster resulted in a degenerative phenotype. In addition, an abnormal nuclear morphology was apparent when cultured cells overexpressed this protein. This is the first human disease attributable to mutations in the gene encoding lamin B1. Antibodies to lamin B are found in individuals with autoimmune diseases, and it is also an antigen recognized by a monoclonal antibody raised against plaques from brains of individuals with multiple sclerosis. This raises the possibility that lamin B may be a link to the autoimmune attack that occurs in multiple sclerosis.     

Peripheral erythrocyte levels,hemolysis and three vanadium compounds

Summary Three vanadium compounds of different valence states were administered to adult mice. Two, four, and eight days following treatment of vanadium, cardiac blood was collected. The blood sample was used to ascertain the peripheral erythrocyte count (cell/mm³) and to determine the in vitro hemolytic index of erythrocytes obtained from mice treated in vivo with either the tri-, tetra- or pentavalent vanadium compound. Data indicate that the tetravalent form was the most effective test substance in 1) promoting rupture of isolated erythrocytes compared to red cells retrieved from control mice and 2) depressing the erythrocyte count obtained from heart blood; maximum effects were manifest four days post-treatment. For all treatments there appeared to be a good correlation between the degree of vanadium-induced hemolysis and the peripheral erythrocyte count reduction following exposure to the vanadium.