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PubMed1954

Vitamin A and endochondral ossification in the rat as indicated by the use of sulfur-35 and phosphorus-32.

The administration of vitamin A to vitamin A-deficient rats resulted in a decreased concentration of inorganic sulfate-sulfur in the serum from a value of 2.5 mg. per cent to 1.8 mg. per cent, the latter being close to the value of 2.0 mg. per cent found in normal rats of the same age. The uptake of sulfate and phosphate by femurs and tibiae of vitamin A-deficient rats was less than that in normal rats of the same age. An increased uptake followed the administration of vitamin A: radioautography indicated that in the case of sulfate, its uptake was particularly increased in the epiphyseal cartilage; an increased uptake of phosphate was particularly evident in the diaphysis immediately adjacent to the epiphyseal cartilage plate. The specific activity of the sulfate-sulfur in the chondroitin sulfate samples isolated from the skeletons of vitamin A-deficient rats fell progressively as the deficiency continued. Following administration of vitamin A, the specific activity approached and exceeded the value given by the sample from the skeletons of normal rats of the same age. A substantial increase was found in the value of the specific activity of the sulfate-sulfur of sulfomucopolysaccharides isolated from skins of vitamin A-deficient rats that had been given vitamin A. Following administration of vitamin A to rats deficient in this vitamin, an increased accumulation of some sulfur-containing material was found in regions of active calcification.

Animals↗
PubMed1954

Vitamin D and endochondral ossification in the rat as indicated by the use of sulfur-35 and phosphorus-32.

The concentration of inorganic sulfate-sulfur in the serum of vitamin D-deficient rats, 2.6 to 3.5 mg. per cent, was found to be higher than that in the serum of normal rats of the same age, 2.0 mg. per cent. No change was observed following the administration of 25 gamma of vitamin D(2). In accord with the results of others, it was found that a definitely increased deposition of phosphorus in femurs and tibiae had occurred 36 to 48 hours after the administration of vitamin D(2) to vitamin D-deficient rats. An immediate increase in the uptake of sulfate by the skeleton was found using sodium sulfate-S(35). As measured by the specific activity of sulfate-sulfur in samples of chondroitin sulfate isolated from the skeletons of the vitamin D-deficient animals and from normal controls receiving equal doses of sulfur-35, the rate of synthesis of chondroitin sulfate in rachitic rats is similar to the rate in normal rats of the same age. Likewise, the incorporation of labelled sulfate into the sulfomuco-polysaccharides of the pelts was found to be equal at 12 hours to that in normal rats. Following the administration of vitamin D(2) to deficient animals an increase in the rate of synthesis of the chondroitin sulfate of the skeletons was noted. The radiochemical and radioautographic evidence suggest that there is in vitamin D-deficient rats an impaired utilization of chondroitin sulfate and that vitamin D(2) is able to accelerate this process.

Animals↗
PubMed1955

Inactivation of bacteriophages by decay of incorporated radioactive phosphorus.

The inactivation of the phages T1, T2, T3, T5, T7, and lambda by decay of incorporated P(32) has been studied. It was found that these phages fall into two classes of sensitivity to P(32) decay: at the same specific activity of P(32) in their deoxyribonucleic acid (DNA), T2 and T5 are inactivated three times as rapidly as T1, T3, T7, and lambda. Since the strains of the first class were found to contain about three times as much total phosphorus per phage particle as those of the second) it appears that the fraction of all P(32) disintegrations which are lethal is very nearly the same in all the strains. This fraction alpha depends on the temperature at which decay is allowed to proceed, being 0.05 at -196 degrees C., 0.1 at +4 degrees C., and 0.3 at 65 degrees C. Decay of P(32) taking place only after the penetration of the DNA of a radioactive phage particle into the interior of the bacterial cell can still prevent the reproduction of the parental phage, albeit inactivation now proceeds at a slightly reduced rate. T2 phages inactivated by decay of P(32) can be cross-reactivated; i.e., donate some of their genetic characters to the progeny of a mixed infection with a non-radioactive phage. They do not, however, exhibit any multiplicity reactivation or photoreactivation. The fact that at low temperatures less than one-tenth of the P(32) disintegrations are lethal to the phage particle and the dependence of the fraction of lethal disintegrations on temperature can be accounted for by the double stranded structure of the DNA macromolecule.

Bacteriophages↗
PubMed1955

Decay of incorporated radioactive phosphorus during reproduction of bacteriophage T2.

The multiplication of vegetative T2 bacteriophage in B/r bacteria has been followed by studying the lethal effects of decay of incorporated radiophosphorus P(32) at various stages of the eclipse period. Experiment I. Non-radioactive B/r bacteria were infected with highly radioactive (i.e. P(32)-unstable) T2 and infection allowed to proceed at 37 degrees C. for various numbers of minutes before freezing the infected cells and storing them in liquid nitrogen. The longer development had been allowed to proceed at 37 degrees C. before freezing, the slower the inactivation of the frozen infective centers by P(32) decay. Samples which were frozen after incubation for 9 minutes were completely stable. Experiment II. Radioactive B/r bacteria in radioactive growth medium were infected with non-radioactive (i.e. stable) T2 and incubated for various lengths of time before being frozen and stored in liquid nitrogen, like those of Experiment I. In this case, the infective centers were stable to P(32) decay as long as they were frozen before the end of the eclipse period. The T2 progeny phages issuing from the infected bacteria were P(32)-unstable. Experiment III. Radioactive B/r bacteria in radioactive medium were infected with radioactive (i.e. P(32)-unstable) T2 and otherwise incubated and frozen like those of the first two experiments. In this case, the same progressive stabilization, of the infective centers towards inactivation by P(32) decay was observed as that found in Experiment I. The ability to yield infective progeny of infected bacteria incubated for 10 minutes at 37 degrees C. before freezing could no longer be destroyed by P(32) decay. The progeny issuing from the infected cells were as unstable as the parental phage. These results could be explained by one of three general hypotheses. As vegetative phage begins to multiply, it is possible that: (a) there is a high probability that any part of the vegetative phage already duplicated can be saved after its destruction by P(32) decay through a process analogous to multiplicity reactivation or, (b) there occurs a change in state of the deoxyribonucleic acid (DNA) preliminary to or in the course of its replication that renders it refractory to destruction by P(32) decay, or, finally (c) there occurs a transfer of the genetic factors from the DNA of the infecting phage to another substance not sensitive to destruction by P(32) decay.

Bacteria↗
PubMed1956

Inactivation of bacteria by decay of incorporated radioactive phosphorus.

Cultures of Escherichia coli will not grow in media containing very high specific activities of radiophosphorus P(32), the inhibition of growth being due to the decay of assimilated P(32) atoms. Experiments with a differentially labeled thymineless strain of E. coli show that the P(32) disintegrations which occur in the bacterial deoxyribonucleic acid, i.e. in the nucleus, are mainly responsible for the inactivation of the cell. The kinetics with which radioactive bacterial populations are inactivated indicate that the function of several nuclei per bacterial cell must be eliminated by P(32) decay before the ability to generate a colony is lost. The efficiency with which each P(32) disintegration inactivates the nucleus in which it has occurred is calculated to be 0.02 (at -196 degrees ), i.e., similar in magnitude to the killing efficiency of P(32) decay in bacteriophages. P(32) decay and thymine starvation cooperate in bringing about the death of individuals of the thymineless strain, from which observation it is inferred that "thymineless death" is likewise a nuclear inactivation. The descendants of a non-radioactive bacterial culture grown for several generations in the presence of P(32) and the descendants of a radioactive culture grown in the absence of P(32) are inactivated by P(32) decay in a manner which indicates that the phosphorus atoms of bacterial nuclei are dispersed among the progeny nuclei in their line of descendance.

Bacteria↗