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Biomedical subjects

H Rubin

Publications and source records attributed to H Rubin.

At least 235 records · Page 13Linked to original sources

Ultrastructure of developing Ascaris larvae undergoing lipid to carbohydrate interconversion.

Triglyceride utilization is correlated with glycogen resynthesis in developing Ascaris suum larvae. Glycogen content, determined by amyloglucosidase hydrolysis at 2-day intervals, decreases sharply during embryonation from 15% (per mg dry weight) at day 4 to 2% at day 12. Thereafter glycogen increases 3-fold through day 20, marking the resynthesis period. Triglyceride lipid droplets are confirmed primarily to the posterior half of the larvae and mark the site of the interconversion. Although they serve as precursors to glycogen, only a small diminution was observed ultrastructurally. Glycogen accumulation, on the other hand, correlates well with increases determined biochemically. alpha-glycogen builds up among lipid droplets, while beta-glycogen concentrates in the cytoplasm of somatic muscle cells paralleling myofibril development. Dense granules, restricted to the lipid body region, are considered as the possible subcellular site for the enzymatic conversion.

Ascaris↗

Effects of glucose starvation on normal and rous sarcoma virus-transformed chick cells.

We studied the effect of glucose starvation on glucose uptake and thymidine uptake and incorporation in cultures of normal chicken embryo cells and those transformed by Rous sarcoma virus. Resting normal fibroblasts increased the rate of glucose transport up to tenfold when they were starved for glucose, whereas fast-growing normal cells doubled the rate of uptake after starvation. Transformed cells did not show any change in the rate of glucose uptake during starvation. Thymidine uptake and incorporation by normal and transformed cells were not affected by glucose starvation. These results showed that a decrease in the glucose concentration of the medium induced a specific increase in the rate of glucose transport by normal chick fibroblasts, but did not change the transport of glucose by transformed cells. Therefore, it is suggested that glucose or one of its metabolic products regulated the hexose uptake of normal chick fibroblasts. Virus-transformed cells were insensitive to this regulation.

Animals↗

Sugar transport in normal and Rous sarcoma virus-transformed chick-embryo fibroblasts.

3-O-methylglucose (3-OMeG) is a nonmetabolizable glucose analog and is, therefore, suitable for transport studies. 3-OMeG and glucose compete for entry into normal and Rous sarcoma virus (RSV)-transformed chick-embryo fibroblasts. Therefore, 3-OMeG can be used to study the transport of glucose in these cells. Chickembryo fibroblasts infected and transformed by RSV take up 3-OMeG at a faster rate than uninfected cells when both cell types are growing at the same rate. The rate of efflux of 3-OMeG also increases after transformation. When the uptake and the efflux reach a steady state, the intracellular concentration of 3-OMeG is equal to the concentration in the medium. This finding indicates that glucose is transported across the plasma membrane by facilitated diffusion. The V(max) of the transport system for 3-OMeG increases after transformation, while the affinity or K(m) of the system remains unchanged. We conclude that viral transformation causes a change in the plasma membrane of the infected cells by increasing either the number of molecules or the mobility of the glucose carrier.

Animals↗

Inhibition of DNA synthesis in chick embryo cultures by deprivation of either serum or zinc.

The rate of DNA synthesis in cultures of chick embryo cells is proportional to the concentration of serum added. The concentration of serum required to stimulate DNA synthesis increases with cell population density and with the duration of culture after trypsinization. The increase of the serum requirement with population density is not caused by the depletion of serum constituents. The requirement of cells for external zinc in DNA synthesis also increases with population density and duration of culture. The kinetics of inhibition of DNA synthesis by deprivation of serum or zinc are similar. Serum deprivation, however, inhibits 2-deoxyglucose uptake and cell movement, but zinc deprivation does not. The deprivation of either serum or zinc inhibits RNA synthesis about twofold. Very low concentrations of actinomycin D prevent the resumption of RNA and DNA synthesis upon restoration of serum or zinc to deprived cultures.

Animals↗

Inhibition of DNA synthesis in animal cells by ethylene diamine tetraacetate, and its reversal by zinc.

During an investigation of the role of ions in growth regulation, it was found that ethylene diamine tetraacetate (EDTA) inhibits DNA synthesis about 10-fold in cultures of chick embryo cells, while ethylene glycol bis(beta-amino ethyl ether)-N,N'-tetraacetate has no effect. RNA synthesis is only slightly inhibited by EDTA, and protein synthesis is unaffected. EDTA is inhibitory to DNA synthesis at a concentration much lower than that of either Ca(++) or Mg(++) present in the growth medium. The inhibition is prevented by the addition of Zn(++) at a much lower concentration than that of the EDTA. Other metal ions are ineffective. The inhibition of DNA synthesis only becomes apparent after more than 6 hr of incubation with EDTA, and descends to its final level by 15 hr. Complete restoration of the original rate of DNA synthesis is achieved within 8-10 hr by the addition of Zn(++). The low rate of DNA synthesis that occurs in a density-inhibited culture, is refractory to further inhibition by EDTA. Rous sarcoma cells are less sensitive to inhibition by EDTA than normal cells, but the sensitivity of both is increased by reducing the concentration of Ca(++) in the medium. DNA synthesis in mouse 3T3 cells is also inhibited by EDTA. It is concluded that Zn(++) is a continuing requirement for DNA synthesis in cultured vertebrate cells, and it is suggested that the availability of Zn(++) within the cell may play a role in the regulation of cell multiplication.

Acetates↗