Ca45 resorption and incoporration into albino rat-bones in tissue culture was considered in studying the pathogenesis of osteoporosiscaused by cotinued administration of glucocorticoid, hydrocortisone succinate. 18-day old tibias were cultured in a chemically defined media, (BGJb). Hydrocotisone showed no effect on Ca45 resorption and little increase of Ca45 incorporation into bone. This may suggest that hydrocortisone produces osteoporosis not by direct effect but by secondary effects on calcium metabolism.
Animal ; Bone Development ; Bone and Bones/embryology ; Bone and Bones/metabolism* ; Calcification, Physiologic/drug effects ; Calcium/metabolism* ; Calcium Radioisotopes ; Hydrocortisone/adverse effects ; Hydrocortisone/pharmacology* ; Osteoporosis/chemically induced* ; Rats ; Tibia ; Tissue Culture

OBJECTIVETo determine the effects of zinc-deficiency and zinc-excess on bone metabolism.

METHODSWe developed the culture model of fetal mouse limbs (16th day) cultivated in self-made rotator with continuing flow of mixed gas for six days in vitro. The cultured limbs were examined by the techniques of 45Ca tracer and X-roentgenography.

RESULTSThe right limbs cultivated had longer bone length, higher bone density than the left limbs uncultivated from the same embryo; and histologically, the right limbs had active bone cell differentiation, proliferation, increased bone trabecula, clearly calcified cartilage matrix, and osteogenic tissue. Compared with the control group, the zinc-deficient group and zinc-excess (Zn2+ 120 mumol/L) group contained less osteocalcin (BGP) and 45Ca content, and lower AKP activity; whereas zinc-normal (Zn2+ 45 mumol/L and Zn2+ 70 mumol/L) groups contained more BGP and 45Ca contents, and higher AKP (alkaline phosphatase) activity.

CONCLUSIONBoth zinc-deficiency and zinc-excess can alter bone growth and normal metabolism. The results indicate that the culture model of fetal mouse limbs (16th day) in vitro can be used as a research model of bone growth and development.

Alkaline Phosphatase ; pharmacology ; Animals ; Biomarkers ; analysis ; Bone and Bones ; embryology ; metabolism ; Calcium ; metabolism ; Cartilage ; metabolism ; Cell Differentiation ; Cell Division ; Culture Techniques ; Disease Models, Animal ; Embryonic and Fetal Development ; drug effects ; Female ; Mice ; embryology ; Pregnancy ; Zinc ; adverse effects ; deficiency

The objective of this investigation was to evaluate dose-incidence relationships on the prenatal effects of gamma-radiation. Pregnant ICR mice were exposed on day 11.5 after conception, coincident with the most sensitive stage for the induction of major congenital malformations, with 0.5-4.0 Gy of gamma-radiations. The animals were sacrificed on day 18 of gestation and the fetuses were examined for mortality, growth retardation, change in head size and any other morphological abnormalities. With increasing radiation dose, incidence of small head, growth retarded fetuses, cleft palate, dilatation of cerebral ventricle and abnormalities of the extremities in live fetuses rose. The threshold doses of radiation that induced cleft palate and dilatation of cerebral ventricle, and abnormal extremities were between 1.0 and 2.0 Gy, and between 0.5 and 1.0 Gy, respectively.
Animals ; Bone and Bones/*abnormalities/radiation effects ; Congenital Abnormalities/embryology/epidemiology/*radionuclide imaging ; Female ; Fetal Death ; Fetal Resorption/epidemiology/radionuclide imaging ; *Gamma Rays ; Incidence ; Mice ; Mice, Inbred ICR ; Pregnancy ; *Prenatal Exposure Delayed Effects ; *Whole-Body Irradiation