Density effect on newly identified high-n Rydberg series of krypton by a resonantly enhanced multiphoton ionization method.
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Journal Article↗
Biomedical subjects
M Pellarin
Publications and source records attributed to M Pellarin.
Effect of N1,N14-bis(ethyl)homospermine on the growth of U-87 MG and SF-126 human brain tumor cells.
The effect of the spermine analogue N1,N14-bis(ethyl)homospermine on the growth, polyamine levels, and survival of U-87 MG and SF-126 human brain tumor cells was examined in tissue culture. At concentrations of 10 mumols and above, N1,N14-bis(ethyl)homospermine inhibited growth significantly, caused a marked decrease in intracellular levels of the naturally occurring polyamines putrescine, spermidine, and spermine, and had a considerable cytotoxic effect on both cell lines after more than 96 h of treatment. In earlier studies we showed that the affinity of the analogue for calf thymus DNA was higher than the affinity of spermine, but that it did not aggregate DNA or release bound ethidium bromide from DNA as efficiently as spermine does. Therefore, the growth-inhibitory and cytotoxic effects of N1,N14-bis(ethyl)homospermine support our hypothesis that polyamine analogues that can enter cells, deplete intracellular levels of natural polyamines, and replace the natural polyamines from their binding sites on DNA without replacing function should act as antiproliferative agents.
Brain Neoplasms↗
Effect of alpha-difluoromethylornithine on 1,3-bis(2-chloroethyl)-1-nitrosourea and cis-diamminedichloroplatinum(II) cytotoxicity, DNA interstrand cross-linking, and growth in human brain tumor cell lines in vitro.
The polyamine biosynthesis inhibitor alpha-difluoromethylornithine (DFMO) has been shown to potentiate the cytotoxicity of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in 9L rat brain tumor cells and in non-central nervous system human cancer cells in vitro, but the effects on a human brain tumor cell line have not been reported. Because BCNU is one of the main chemotherapeutic agents used clinically for the treatment of brain tumors, the effect of DFMO treatment on cell growth and potentiation of cytotoxicity was studied in vitro in U-251 MG and SF-126 cells, human tumor cell lines derived from malignant glioma tissue. Pretreatment of U-251 MG with 1 mM DFMO depleted cells of putrescine and spermidine within 48 h but did not sensitize cells to BCNU treatment even after a pretreatment of 72 h. DFMO treatment had no effect on the number of interstrand cross-links formed in BCNU-treated cells. Even treatment with 5 mM DFMO for 72 h caused only the suggestion of potentiation of BCNU cell kill. In contrast, a 72-h pretreatment with 1 mM DFMO decreased the cytotoxic effect of cis-diammine-dichloroplatinum(II) and caused a 38% decrease in the number of DNA interstrand cross-links formed. The glutathione content and cell cycle distribution of U-251 MG cells were not affected by DFMO pretreatment. Because Phase II clinical trials with DFMO and BCNU have shown promise for the treatment of anaplastic astrocytomas in humans, a second brain tumor cell line, SF-126, was studied. In this cell line a consistent potentiation of BCNU cytotoxicity (dose enhancement of 1.2 at the 10% survival level) was observed in cells pretreated with 1 mM DFMO for 72 h.
Biogenic Polyamines↗
Direct measurement of nuclear magnetic moments of radium isotopes.
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Journal Article↗
Effects of the polyamine analogs BE-3-7-3, 3-8-3, and BE-3-8-3 on human brain tumor cell growth and survival.
Based on computer modeling, physicochemical studies of spermine-DNA interactions, and cell culture experiments, we hypothesized that polyamine analogs with hydrocarbon chain lengths differing from natural polyamines and a stronger affinity for nucleic acids than spermine should have a cellular antiproliferative effect. We tested three spermine analogs with long hydrocarbon chains, 1,16-diamino-4,12-diazahexadecane (3-8-3), 1,16-bis(ethyl)amino-4,12-diazahexadecane (BE-3-8-3), and 1,15-bis(ethyl)amino-4,11-diazapentadecane (BE-3-7-3) in human brain tumor cell lines U-251 MG, SF-126, and SF-188. Analog concentrations < or = 5 microM inhibited growth and colony-forming efficiency in each cell line by treatment day 5, with significant decreases in putrescine and spermidine, but not spermine, levels. These findings suggest that potentially cytotoxic polyamine analogs can be specified on the basis of their hydrocarbon chain length and DNA affinity.
Brain Neoplasms↗
The ability of polyamine analogues to induce Z-DNA structure in synthetic polynucleotides in vitro inversely correlates with their effects on cytotoxicity of cis-diaminedichloroplatinum (II) (CDDP) in human brain tumor cell lines.
We studied the effects of 72 h pretreatment with five polyamine analogues on the cytotoxicity of cis-diaminedichloroplatinum (II) (CDDP) in U-251 MG and SF-188 human brain tumor cells. A colony forming efficiency assay showed that the pretreatment with clinically important analogues 1,11-bis(ethylamino)-4, 8-diazaundecane (BE-3-3-3), 1,14-bis(ethylamino)-5,10-diazatetradecane (BE-4-4-4), and 1,l9-bis(ethylamino)-5,10,15-triazanonadecane (BE-4-4-4-4) increased the cytotoxicity of CDDP by 1.3 to 2.3-fold; 1,19-diamino-5,10, 15-triazanonadecane (4-4-4-4) did not affect CDDP cytotoxicity, and 1,11-diamino-4,8-diazaundecane (3-3-3) protected cells from the cytotoxic effects of CDDP. An alkaline elution assay detected a small increase in DNA interstrand crosslinks accompanying the enhancement of CDDP cytotoxicity only in cells pretreated with BE-3-3-3. This study is the first to show that the Z-DNA inducing abilities of the polyamine analogues in synthetic polynucleotides in vitro correlates inversely with their effects on CDDP cytotoxicity in human tumor cells in culture.
Antineoplastic Agents↗