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Biomedical subjects

V H Bono

Publications and source records attributed to V H Bono.

At least 19 recordsLinked to original sources
PubMed1978

Effects of chartreusin on cell survival and cell cycle progression.

Chartreusin was lethal to both L1210 and P388 cells in culture with 90% of the cells being killed after a 24-hr exposure to 1.1 and 2.6 microgram/ml, respectively. The lethality of the drug increased in direct proportion to dose and exposure time. Both L1210 and Chinese hamster ovary cells in S phase were more sensitive to the lethality of the drug than were their corresponding non-S-phase cells. L1210 cells were partially synchronized by exposing an asynchronous culture to [methyl-3H]thymidine (20 Ci/mmol) and Colcemid for 3 hr. Synchronous culture of Chinese hamster ovary cells was established by planting mitotic cells. The progression of cells through the cell cycle was studied with flow microfluorometry both in the presence of the drug and after the drug had been washed off. In the presence of chartreusin the progression of mitotic cells into G1 was not affected. The movement of G1 cells into S was slower, and the movement of G2 cells into mitosis was blocked. When the drug was removed, the G2 to M block persisted for at least 4 hr but the progression of G1 cells to S was no longer inhibited.

Animals↗
PubMed1977

Control of growth by picolinic acid: differential response of normal and transformed cells.

Picolinic acid reversibly inhibits the growth of cultured cells. Fourteen other pyridine derivatives were ineffective or toxic. Untransformed normal rat kidney (NRK) cells are reversibly arrested in the G(1) stage of the growth cycle as shown by cell counts, mitotic index, [(3)H]thymidine incorporation, and flow microfluorometry. Flow microfluorometry was used to monitor the effects of picolinic acid on numerous other cell lines. Normal cells are blocked in G(1), whereas transformed cells show responses that are dependent upon the transforming virus and independent of species or origin of the cell line. Kirsten sarcoma virus-transformed cells are blocked in G(1). Simian virus 40-transformed cells progress to a G(2) block. Cells transformed by polyoma or Harvey sarcoma virus with Moloney virus coat have flow microfluorometry profiles that indicate blocks in both G(1) and G(2). Cells transformed with Moloney sarcoma virus are not blocked in a specific phase of the cell cycle. Picolinic acid does not change the levels of NAD(+) plus NADH; however, the growth inhibition by picolinic acid is partially overcome by nicotinamide. These results suggest that picolinic acid interacts with a specific growth control mechanism that may involve NAD(+) and that this control mechanism is altered by different transforming viruses in different manners.

Cell Division↗
PubMed1977

Partial synchronization of L1210 cells by 5-fluorouracil and its use in drug combinations.

When L1210 cells growing logarithmically were exposed for 8 hr to a nonlethal dose of 5-fluorouracil (FU) (0.25 microgram/ml), the percentage of cells in S phase increased from 74.9% in the asynchronous culture to 93% in the FU-treated culture. This resulted in increased cell-kill by S-phase-specific inhibitors [1-beta-D-arabinofuranosylcytosine (ara-C), 5-hydroxy-2-formylpyridinethiosemicarbazone] when they were added to a culture partially synchronized by pretreatment with FU. For example, 2 hr exposure to ara-C alone or ara-C plus FU (added simultaneously to asynchronous culture) gave 28.8 and 25.8% survival, respectively, compared to 6.8% survival when ara-C was added for 2 hr to the partially synchronized culture. Eight to 12 hr after FU removal, the culture became asynchronous, such that ara-C addition at this time did not result in increased cell-kill. Cultures pretreated with FU were also highly sensitive to vincristine and Adriamycin. Adriamycin acted synergistically with FU (after 8 hr pretreatment) in killing L1210 cells.

Animals↗
PubMed1976

Studies with 2,5-piperazinedione, 3,6-bis(5-chloro-2-piperidyl)-,dihydrochloride. I. Cell kinetic and biologic effects in cultured L1210, human epidermoid No. 2, and adenocarcinoma 755 cells.

Experimental results obtained with cultured L1210, human epidermoid No. 2, and Adenocarcinoma 755 cells are consistent in showing that inhibition of proliferation of the cells by 2,5-piperazinedione, 3,6-bis(5-chloro-2-piperidyl)-,dihydrochloride is accompanied by cell enlargement. Although cells initially in the G2 phase when exposure to the agent is begun can probably proceed through mitosis and divide, cells that are initially in G1 and S phases accumulate in the G2 phase. Progression of cells to G2 phase during the period of exposure to the agent is not a requisite for cell-killing, because cells exposed for periods insufficient to permit their accumulation in G2 are killed.

Adenocarcinoma↗
PubMed1976

Binding of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea to L1210 cell nuclear proteins.

The binding of 1-(2-chloroethyl)-3-(cyclohexyl)-1-nitrosourea (CCNU) to the proteins of the L1210 cell nucleus has been studied using both [cyclohexyl-14C]CCNU and [chloroethyl-14C]CCNU. Most of the bound [cyclohexyl-14C] moiety of CCNU was found to exist in a form that was stable in acid solution but labile and dialyzable in alkaline solution. A small amount of the cyclohexyl moiety was bound to histones in a stable, nondialyzable form. The drug/protein ratio for the H1 histone was about 0.01 to 0.02 mole/mole. No binding of the cyclohexyl group to acidic proteins or of the chloroethyl group to either histones or acidic proteins was observed. Thus, the interaction of CCNU with the proteins of the cell nucleus can be defined in terms of the modification of histones by the cyclohexyl moiety.

Animals↗