Thymidine transport by Novikoff rat hepatoma cells synchronized by double hydroxyurea treatment

Plagemann, Peter G.W.; Richey, David P.; Zylka, J M; Erbe, John

doi:10.1016/0014-4827(74)90343-7

Cited by 48 publications

(21 citation statements)

References 16 publications

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“…HU is a known, selective inhibitor of semiconservative DNA replication in various mitotic and meiotic cell lines (9,10,15). In lily microsporocytes, this drug also inhibits DNA synthesis during the premeiotic S phase and the zygotene stage (3).…”

Section: Discussionmentioning

confidence: 99%

Effect of hydroxyurea on mitotic and meiotic divisions in explanted lily microsporocytes.

Takegami

Ito

1982

Cell Struct. Funct.

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ABSTRACT. The cytological effects of hydroxyurea (HU), an inhibitor of DNA synthesis, were examined on mitotic and meiotic divisions in lily microsporocytes. Microsporocytes in premeiotic stages and meiotic prophase were cultured in vitro for discrete periods in the presence of the inhibitor at various concentrations.Hydroxyurea interfered with mitotic development if administered to cells during the late S or early G2 phase of premeiosis, when cells undergo mitotic division by explantation. When applied during leptonema, the main effects were the suppression of meiotic development and the production of sticky chromosomes.The affected cells progressed through early prophase without showing any gross cytological abnormalities ; the inhibition of DNA synthesis by hydroxyurea during zygonema did not interfere with synapsis. On further culture, cells did not progress beyond prophase; but remained suspended in some stage of late prophase. Chromosome stickiness was the response of cells cultured with hydroxyurea during pachynema for a prolonged period. The relevance of these observations to microsporocyte development is discussed.

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Section: Discussionmentioning

confidence: 99%

Effect of hydroxyurea on mitotic and meiotic divisions in explanted lily microsporocytes.

Takegami

Ito

1982

Cell Struct. Funct.

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“…Growth-arrested rat aortic SMC were exposed to 100 pgiml heparin for 2 h a t 37°C. Uptake of the indicated metabolites was then measured using tritiumlabeled probes according to the methods described by Pardee (1976) and Plagemann et al (1974). The data shown was obtained using a 5-min transport assay time; similar results were obtained at all time points tested (15 sec-60 min).…”

Section: Uptake Of Metabolitesmentioning

confidence: 92%

Effect of heparin on vascular smooth muscle cells. I. Cell metabolism

Castellot

Cochran

Karnovsky

1985

Journal Cellular Physiology

216

110

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Previous work from our laboratory has shown that heparin inhibits the proliferation of vascular smooth muscle cells in vivo and in vitro. The mechanism of action of this glycosaminoglycan is unknown. In this communication, we have examined the antiproliferative effect of heparin on smooth muscle and other cell types, and have investigated several aspects of heparin on smooth muscle cell metabolism. Smooth muscle and closely related cell types from several species, including human, were much more sensitive to heparin than any other cell type tested, including primary and established cell lines, normal and transformed cell pairs, fibroblasts, epithelial, and endothelial cells. Flow microfluorimetric analysis of cell cycle distribution indicated that heparin blocked either the G0----S transition or a very early S-phase event in smooth muscle cells. Heparin rapidly inhibited DNA and RNA synthesis, but did not affect the rate of protein synthesis. The decrease in nucleic acid synthesis could be accounted for by an inhibition of thymidine and uridine uptake. Interestingly, heparin did not block amino acid or glucose transport. Although no change in the overall rate of protein synthesis was observed in the presence of heparin, we noted at least two changes in the synthesis of specific proteins by smooth muscle cells: two 35,000-dalton proteins which appeared in the culture medium of heparin-treated cells, and the transient disappearance of a 48,000-dalton protein in the substrate attached material of smooth muscle cells exposed to heparin. The role of the observed changes in smooth muscle cell metabolism is yet to be determined, but they may provide valuable clues to the molecular mechanisms controlling the antiproliferative activity of heparin.

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“…Measurement of thymidine-uptake kinetics several hours after irradiation should show any effect of radiation on the synthesis of new transport sites, since transport sites for nucleotides have a fast turnover (Plagemann, Richey, Zylka and Erbe 1975), and their numbers increase rapidly in S phase (Hopwood et al 1975) . Thus, if radiation inhibits the synthesis of new sites, a decrease in transport of thymidine should occur .…”

Section: Discussionmentioning

confidence: 99%

“…The Vmax values for transport of thymidine vary during the cell-cycle in proportion to the acid-insoluble incorporation of the precursor (Plagemann, Richey, Zylka andErbe 1974, Hopwood et al 1976) . Here we report the effects of moderate and high doses of X-irradiation on the transport of thymidine into both asynchronous and S-phase CHO cells .…”

Section: Introductionmentioning

confidence: 99%

Effect of X-irradiation on the Transport of Thymidine into Asynchronous and S Phase CHO Cells

Hopwood

Dewey

1976

International Journal of Radiation Biology and Related Studies

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Thymidine transport by Novikoff rat hepatoma cells synchronized by double hydroxyurea treatment

Cited by 48 publications

References 16 publications

Effect of hydroxyurea on mitotic and meiotic divisions in explanted lily microsporocytes.

Effect of hydroxyurea on mitotic and meiotic divisions in explanted lily microsporocytes.

Effect of heparin on vascular smooth muscle cells. I. Cell metabolism

Effect of X-irradiation on the Transport of Thymidine into Asynchronous and S Phase CHO Cells

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