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PubMed1996

Studies on the mechanisms of tumorigenesis induced by polyetherurethanes in rats: leachable and biodegradable oligomers involving the diphenyl carbamate structure acted as an initiator on the transformation of Balb 3T3 cells.

The tumor-initiating activities of the methanol extracts of polyetherurethanes (PEUs) were first detected in the presence of 12-0-tetradecanyl-phorbol-13-acetate (TPA) using Balb 3T3 transformation assay. A model hard segment of PEUs, 4,4'-di(ethoxycarboamide) diphenylmethane (MDU), showed initiating activity, while chemical moieties other than the hard segment were shown to be negative in the test. The transformation assay was carried out using glass dishes half coated with two different PEUs, PU4 and PU8. In the presence of TPA, the transforming activities correlated with the tumorigenic potential in the rat implantation study on the coated surface of PEUs, but not on the uncoated glass area. From these results it was concluded that initiation was caused by the hard-segment moiety such as MDU structure derived not only from the leachable extracts but also from the biodegradable substances by the direct interaction of cells with the coated materials.

3T3 Cells↗
PubMed1994

Altered oxidative stress responses in nickel-resistant mammalian cells.

BALB 3T3 cells exposed to NiCl2 acquired resistance to concentrations as high as 200 microM and retain resistance for many generations in the absence of nickel. This resistance was not due to alterations in uptake or to metallothionein overexpression. The nickel-resistant B200 cell line was found to also exhibit cross-resistance to hydrogen peroxide and menadione. These nickel-resistant cells had 1.8 times higher basal levels of glutathione compared to wild-type cells. Studies with the glutathione synthesis inhibitor buthionine sulfoximine showed that while glutathione turnover was more rapid in the nickel-resistant cells, its depletion following NiCl2 treatment of the parental BALB 3T3 cell line was greater than in the nickel-resistant B200 cells. The reduced level of binding of NFkB and AP-1 transcription factors to their DNA consensus sequences in B200 cells compared to wild-type cells, and their more reactive response following treatment of resistant cells with H2O2 or buthionine sulfoximine, strengthens the hypothesis that nickel resistance is closely allied to oxidative stress responses.

3T3 Cells↗
PubMed1981

Distinct mechanisms of hypoxanthine and inosine transport in membrane vesicles isolated from Chinese hamster ovary and Balb 3T3 cells.

Both enzyme-mediated group translocation and facilitated diffusion have been proposed as mechanisms by which mammalian cells take up purine bases and nucleosides. We have investigated the mechanisms for hypoxanthine and inosine transport by using membrane vesicles from Chinese hamster ovary cells (CHO), Balb/c 3T3 and SV3T3 cells prepared by identical procedures. Uptake mechanisms were characterized by analyzing intravesicular contents, determining which substrates could exchange with the transport products, assaying for hypoxanthine phosphoribosyltransferase activity, and measuring the stimulation of uptake of hypoxanthine by phosphoribosyl pyrophosphate (PRib-PP). We found that the uptake of hypoxanthine in Balb 3T3 vesicles was stimulated 3--4-fold by PRib-PP. The intravesicular product was predominantly IMP. The hypoxanthine phosphoribosyltransferase activity copurified with the vesicle preparation. These results suggest the possible involvement of this enzyme in hypoxanthine uptake in 3T3 vesicles. In contrast to the 3T3 vesicles, CHO vesicles prepared under identical procedures did not retain hypoxanthine phosphoribosyltransferase activity and did not demonstrate PRib-PP-stimulated hypoxanthine uptake. The intravesicular product of hypoxanthine uptake in CHO vesicles was hypoxanthine. These results and data from our kinetic and exchange studies indicated that CHO vesicles transport hypoxanthine via facilitated diffusion. An analogous situation was observed for inosine uptake; CHO vesicles accumulated inosine via a facilitated diffusion mechanism, while in the same experiments SV3T3 vesicles exhibited a purine nucleoside phosphorylase-dependent translocation of the ribose moiety of inosine. Vesicles prepared from a CHO cell line temperature-sensitive for hypoxanthine uptake (Azarts) showed a temperature-sensitivity in Km for uptake parallel to that of the intact cells. This suggests that the defect in Azarts may be caused by a missense mutation in the gene coding for the hypoxanthine transport carrier.

Animals↗
PubMed1974

Selection of revertants of Kirsten sarcoma virus transformed nonproducer BALB-3T3 cells.

Revertants of Kirsten sarcoma virus transformed nonproducer BALB/3T3 cells (KA31 cells) were isolated after exposing the transformed cells to 5-fluorodeoxyuridine at high cell density, or when suspended in methylcellulose. Revertants were also isolated by treating KA31 cells with the lectin, concanavalin A, which is manyfold more toxic to transformed cells than for normal cells. The revertants resemble BALB/3T3 cells in their morphology and growth characteristics in that they have a low saturation density, fail to grow in 1% calf serum or when suspended in methylcellulose, and cease to synthesize DNA after reaching their saturation density. Infection by murine leukemia virus rescues Kirsten sarcoma virus from only the concanavalin-A-selected variants, though all the revertants are susceptible to infection by leukemia virus. The concanavalin A revertants also become transformed after infection with murine leukemia virus. All the revertants can be transformed by Kirsten sarcoma virus but not by simian virus 40.

Animals↗
PubMed1970

Murine sarcoma virus transformation of BALB-3T3 cells: lack of dependence on murine leukemia virus.

Murine sarcoma virus induces foci of morphologically altered cells in BALB/3T3 cultures. Focus formation in mouse cells has been thought to require the presence of a helper, murine leukemia virus, which is present in murine sarcoma virus stocks but by itself does not induce any morphological transformation of mouse cells. The present studies show that early after infection, the titration pattern for murine sarcoma virus in BALB/3T3 cells is "two-hit" since only foci produced by virus spread can be detected. Such foci require the presence of both viruses in the initially infected cell. By seven days the titration pattern is "one-hit" under culture conditions which allow the growth and detection of small foci of transformed cells induced by murine sarcoma virus alone. The "two-hit" titration pattern results from the inability to detect these foci. We conclude that murine sarcoma virus is able to transform mouse cells without requiring murine leukemia virus.

Animals↗
PubMed1973

A scanning electron microscope study of surface features of viral and spontaneous transformants of mouse Balb-3T3 cells.

Cells of the mouse line Balb/3T3 as well as three virus-induced transformants and two spontaneous transformants grown in vitro have been studied for their topography by scanning electron microscopy. The parent cell in confluent culture closely resembles an endothelial cell in its form and in the structure of its association with adjacent cells. The tumorigenic transformants produced by SV40, murine sarcoma virus, or polyoma viruses are fusiform to pleomorphic and distinctly different from the cell of origin. They show relatively smooth surfaces except for blebs and marginal microvilli. Perhaps most surprising is the similarity they bear to one another. This is made the more singular by the very different form shown by the tumorigenic transformants of spontaneous origin. One of these, S2-4, possesses a thickened rather than the lamellar form of the parent A31 cell and is covered by long microvilli and many spherical blebs. The other, TuT(3), more closely resembles the cell of origin but shows extensive ruffling at its margins. All transformants grow without evidence of contact inhibition. The significance of the surface morphologies and the factors influencing cell form are discussed.

Animals↗
PubMed1972

Genetic analysis of simian virus 40. IV. Inhibited transformation of Balb-3T3 cells by a temperature-sensitive early mutant.

The temperature-sensitive early mutant, ts(*)101, was characterized during productive infection in monkey cells, and the results are presented in an accompanying paper. This paper demonstrates that although 101 mutant virions adsorb normally to confluent Balb/3T3 mouse cells at both permissive (33 C) and restrictive (38.5 C) temperatures, T antigen synthesis and transformation, abortive and stable, are inhibited at both temperatures (host-range inhibition). T antigen synthesis is temperature sensitive, whereas abortive and stable transformation are not. Clones of 101-transformed Balb/3T3 cells were isolated, and virus was rescued from all clones at both permissive and restrictive temperatures. The rescued virus was as temperature sensitive as the original transforming 101 virions.

Adsorption↗