acid-phosphatase and Magnesium-Deficiency

Magnesium (Mg(2+)) deficiency is a frequently occurring disorder that leads to loss of bone mass, abnormal bone growth and skeletal weakness. It is not clear whether Mg(2+) deficiency affects the formation and/or activity of osteoclasts. We evaluated the effect of Mg(2+) restriction on these parameters. Bone marrow cells from long bone and jaw of mice were seeded on plastic and on bone in medium containing different concentrations of Mg(2+) (0.8 mM which is 100% of the normal value, 0.4, 0.08 and 0 mM). The effect of Mg(2+) deficiency was evaluated on osteoclast precursors for their viability after 3 days and proliferation rate after 3 and 6 days, as was mRNA expression of osteoclastogenesis-related genes and Mg(2+)-related genes. After 6 days of incubation, the number of tartrate resistant acid phosphatase-positive (TRACP(+)) multinucleated cells was determined, and the TRACP activity of the medium was measured. Osteoclastic activity was assessed at 8 days by resorption pit analysis. Mg(2+) deficiency resulted in increased numbers of osteoclast-like cells, a phenomenon found for both types of marrow. Mg(2+) deficiency had no effect on cell viability and proliferation. Increased osteoclastogenesis due to Mg(2+) deficiency was reflected in higher expression of osteoclast-related genes. However, resorption per osteoclast and TRACP activity were lower in the absence of Mg(2+). In conclusion, Mg(2+) deficiency augmented osteoclastogenesis but appeared to inhibit the activity of these cells. Together, our in vitro data suggest that altered osteoclast numbers and activity may contribute to the skeletal phenotype as seen in Mg(2+) deficient patients.

Topics: Acid Phosphatase; Animals; Bone and Bones; Bone Development; Bone Marrow Cells; Calcium; Cell Proliferation; Cell Survival; Cells, Cultured; Isoenzymes; Magnesium; Magnesium Deficiency; Male; Mice; Mice, Inbred C57BL; Osteoclasts; RNA, Messenger; Tartrate-Resistant Acid Phosphatase

In the present study, we used osteoprotegerin (OPG), which blocks osteoclastogenesis, to correct and thus explain the hypercalcemia that is seen during dietary Mg deficiency in the mouse. Control and Mg-deficient mice received injections for 12 days of either OPG or vehicle only. Serum Ca was similar in Mg-deficient mice treated with OPG and in control mice receiving OPG (9.2 +/- 0.3 mg/dl vs. 9.2 +/- 0.5). Both groups had significantly higher serum Ca than controls or Mg-deficient animals receiving vehicle alone. Surprisingly, Mg-depleted mice that received OPG in doses that inhibit osteoclastic bone resorption remained hypercalcemic. Because mature osteoclasts still present in the marrow might be hyperactive, we examined osteoclast morphology at the light microscopic and ultrastructural level. Light microscopic examination of trabecular bone showed few osteoclasts in OPG-treated mice. Ultrastructural examination revealed that osteoclasts in OPG-treated mice have decreased contact with the endosteal bone surface and absence of a ruffled border. Because the morphology of the existing pool of mature osteoclasts did not enhance resorption, another mechanism, such as increased intestinal absorption of Ca in Mg-deficient mice, likely contributes to the hypercalcemia observed during Mg deficiency.

Topics: Acid Phosphatase; Animals; Calcium; Female; Glycoproteins; Hypercalcemia; Isoenzymes; Magnesium Deficiency; Mice; Osteoclasts; Osteoprotegerin; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor; Tartrate-Resistant Acid Phosphatase

Topics: Acid Phosphatase; Animals; Lysosomes; Magnesium Deficiency; Mice; Neutrophils; Zinc

In rats with induced syndrome of chronic magnesium deficiency, occurrence of haemolytic anaemia in conjuction with a shortening of the erythrocyte survival time and marked reticulocytosis among other symptoms became noticeable. In the present experiment the authors undertook to study the behaviour of the lysosomal enzymes in the erythrocytes of magnesium-deficient rats. In these animals anaemia and reticulocytosis as well as a marked increase in the percentage of the erythrocytes showing positive reactions to the acid phosphatase and beta-glucuronidase tests developed. It seems likely that the positive lysosomal reactions were obtained with younger blood cells which did not stain with brilliant cresyl blue but still retained single lysosomes in their cytoplasm. This assumption was confirmed by ultrastructural studies which demonstrated the presence of siderosomes inside both the reticulocytes and the mature erythrocytes. The changes in the percentages of reticulocytes and enzyme-positive erythrocytes were independent of the histological structure of the experimental rat's thymus. In the reticulocytes as well as in the mature erythrocytes, the noteworthy presence of degenerated mitochondria containing electron-dense material seems to be a morphological sign of impairment of the magnesium-deficient rat's erythrocytes.

Topics: Acid Phosphatase; Animals; Erythrocyte Count; Erythrocytes; Female; Glucuronidase; Lysosomes; Magnesium Deficiency; Rats; Reticulocytes; Thymus Gland

A magnesium deficient diet caused transient but marked degenerative changes in the rat hypothalamo-hypophysial neurosecretory system which strongly resembled in many ultrastructural respects those induced by a prolonged administration of aldosterone as previously reported by us. The possible mechanism for this selective alteration in the neurosecretory neurons has been briefly discussed with regard to aldosterone secretion.

Topics: Acid Phosphatase; Aldosterone; Animals; Axons; Cell Nucleus; Cytoplasmic Granules; Endoplasmic Reticulum; Golgi Apparatus; Hypothalamo-Hypophyseal System; Magnesium Deficiency; Male; Nerve Degeneration; Neurons; Pituitary Gland, Posterior; Pituitary-Adrenal System; Rats; Supraoptic Nucleus; Time Factors

Topics: Acid Phosphatase; Animals; Body Weight; Calcium; Cell Fractionation; Cell Nucleus; Centrifugation; Diet; Disease Models, Animal; Electron Transport Complex IV; Glucosephosphate Dehydrogenase; Kidney; Magnesium; Magnesium Deficiency; Male; Mitochondria; Nephrocalcinosis; Parathyroid Hormone; Proteins; Rats; Tissue Extracts

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Calcium; Electrolytes; Enzymes; Fructose-Bisphosphate Aldolase; Hydroxybutyrate Dehydrogenase; Isocitrate Dehydrogenase; L-Lactate Dehydrogenase; Magnesium; Magnesium Deficiency; Potassium; Rats; Rodent Diseases

Topics: Acid Phosphatase; Calcium; Drug Therapy; Feces; Humans; Hypocalcemia; Infant, Newborn; Intestinal Absorption; Magnesium; Magnesium Deficiency; Malabsorption Syndromes; Male; Metal Metabolism, Inborn Errors; Radioisotopes; Seizures; Tetany; Time Factors