[Adsorption of Saccharomyces cerevisiae cells by carbon sorbents].
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Biomedical subjects
Publications and source records attributed to V N Shvets.
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For 10 days rats were subcutaneously injected with alpha-hydroxydimethyl-gamma-aminopropylidene biphosphonate in the dose range 0.005 to 5 mg/kg/day. As shown morphometrically, the mass of spongy bone increased linearly with the dose. It was found that the drug affected primarily the highly metabolic component of spongy bone. The drug had a systemic osteotrophic effect and modified the number of osteocytes significantly. When the drug was injected for a long time (up to 60 days), the number of osteoclasts decreased and the proportion of cells containing more than one nucleus remained within normal limits. The number of osteoblasts either diminished (in long bones) or remained unchanged (in torso and pelvic bones). It is concluded that the osteotrophic effect of the drug is mediated via its action on bone resorption the rate of which is inhibited; this is responsible for bone mass growth.
The role of ksidifon in the prevention of immobilization-induced osteoporosis was investigated. Osteoporosis was produced by placing animals (Wistar male rats weighing 200-230 g) into small-size cages for 60 days. Every day the rats were injected subcutaneously with ksidifon (hydroxyethylidene bisphosphonic acid) at a dose of 1 or 5 mg/kg. It was found histomorphometrically that ksidifon in these doses inhibited losses of cancellous bone from tubular bones, trunk and pelvic bones. The ksidifon effect was closely correlated with the initial metabolic state of bones. The drug changed the balance of bone cells. The population of osteoblasts decreased greatly whereas that of osteoclasts either remained unchanged or increased slightly. It is concluded that ksidifon is an agent that can be used to prevent osteoporosis, provided that the physiological state of bone and the organism as a whole is taken into consideration.
Preventive administration of vitamin D3 active metabolites 1.25(OH)2D3 and 24.25(OH)2D3 into growing rats, kept under conditions of long-term hard hypokinesia, normalized Ca metabolism and the state of bone tissue depending on the preparations dose and their combination. 1.25(OH)2D3 at a dose of 0.03 microgram per an animal daily augmented effectively the Ca absorption in small intestine, corrected hypocalcemia, increased slightly the bone tissue density and the Ca and P content in the tissue as well as it elevated the volume of spongiosa, width of the epiphysial growth plate (EGP) and the amount of osteoclasts. After an increase of the metabolite dose up to 0.15 microgram hypercalcemia, hyperphosphatemia, intensive resorption of bone tissue, distinct increase in the osteoclasts content and ectopic calcification were observed. Administration of 1.35(OH)2D3 and 24.25(OH)2D3 combination (0.03 microgram and 0.25 or 1.25 micrograms, respectively) or only 24.25(OH)2D3 at a dose of 1.25 micrograms caused a restoration of Ca absorption in intestine and of its level in blood as well as mineral composition, density of bone tissue, volume of primary and secondary spongiosa were normalized, while the EGP width and amount of osteoclasts remained decreased. Synergic effect of 1.25(OH)2D3 and 24.25(OH)2D3 in rats appears to depend on their various functions in regulation of Ca metabolism, in development and remodelation of bone tissue, thus indicating that these metabolites of vitamin D3 should be used simultaneously under conditions of hypokinesia for prophylactic purposes.
The experiments were carried out on Wistar SPF rats that were immobilized for 35 days. By heterotopic marrow cell transplantation under the kidney capsule to the normal rats and by cloning these cells in vitro it was found that osteogenetic potentials were significantly inhibited and the amount of osteogenetic precursor cells was reduced. The addition of 24,25(OH)2D3 vitamin (at a dose of 1.25 micrograms per day) to the animal diet led to the normalization of the above parameters. It is assumed that immobilization-associated osteoporosis develops via, among other mechanisms, inhibition of histogenesis of stromal precursor cells. The beneficial role of vitamin D3 is actually the activation of histogenesis of these cells which results in the recovery of bone remodelling during immobilization.
The unrestrained rats were rotated for 21 and 30 days at 1.1 and 2.0 G. The exposure did not deteriorate their equilibrium function or physical condition, i. e. static and dynamic endurance. However, the exposure decreased the reactivity and sensitivity of the semicircular canals. Bone parameters-longitudinal and transverse bone growth, metaepiphysis morphometry-indicated that the rats developed an acute stress-reaction accompanied by an inhibited growth of limb bones during the first 7 days of rotation. By experimental day 30 the animals became adapted to the new environment.
Examination of spongy bones of rats exposed to clino- and antiorthostatic hypokinesia showed that changes in bone mass, bone cells and their precursors were similar in both cases. The bone resorption-bone formation process remained balanced. However, bone responses clino- and antiorthostatic hypokinesia exhibited certain differences. Clinostatic hypokinesia produced greater osteoporosis in the femoral bone, whereas bone losses in the humerus, sternum and pelvis were identical. Antiorthostatic hypokinesia led to osteoporosis that was identical in every bone examined. In addition, clino- and antiorthostatic hypokinesia caused different reactions of stromal precursor cells, the latter model producing a greater effect on them. It is concluded that immobilization-induced skeletal disorders are associated with a decreased rate of bone histogenesis which proceeds at a lower level rather than with the stress-reaction.
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Immunological reactivity of rats flown aboard the biosatellites Cosmos-605 and Cosmos-690 was compared with respect to the complementary activity of serum and frequency antibodies to sheep red blood cells. Cosmos-605 rats showed changes that rapidly returned to the normal whereas Cosmos-690 rats irradiated inflight with a dose of 800 rad exhibited significant and stable changes in immunological reactivity. Those latter seemed to be associated with the combined effect of ionizing radiation and other space flight factors.
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The tubular bones of the fore- and hindlimbs of rats immobilized for 5 weeks were examined morphometrically and histologically. The rats were regularly given per os 1,25(OH)2D3, 24,25(OH)2D3 or their combination. The uptake of 24,25(OH)2D3 at a dose of 1.25 micrograms or a combination of 1,25(OH)2D3 and 24,25(OH)2D3 at a dose of 0.03 + 0.25 micrograms led to the recovery of the linear and volume-weight rates of bone formation that changed during hypokinesia. However, these D3 metabolites did not restore the width of the epiphyseal growth plate, whereas the size of the primary and secondary spongiosa returned to normal or exceeded it in response to 24,25(OH)2D3 at a dose of 1.25 micrograms and 1,25(OH)2D3 at a dose of 0.15 micrograms, respectively (only these two doses were used); in other words, the D3 metabolites prevented osteoporosis which is typical of hypokinesia. It is assumed that hypokinesia may produce either disorders in D3 metabolism or changes in the sensitivity of bone cells to active D3 metabolites and other hormones that are directly or indirectly involved in osteogenesis regulation.