PubMed Health⌕ Search

Biomedical subjects

I A Bolotnikov

Publications and source records attributed to I A Bolotnikov.

12 recordsLinked to original sources
PubMed2000

[Interaction of tumor cell differentiation induced in vitro and sensitivity of them to nonspecific lysis by natural killer cells. Possible mechanisms].

The literature data on the influence of a large group of cancer cell differentiation inducers on the modulation of their susceptibility to non-MHC-restricted lysis (non-specific cytotoxicity, NCT) by natural killer (NK) cells have been analysed. A possible association between the apoptogenic action of differentiation inducers and their ability to modulate the NCT of cell targets by NK cells is discussed.

Animals↗
PubMed1999

[Treatment of synchronized K562 cells by tetrafluoroaluminate does not modulate the fluorescence of ethidium bromide and 4'6-diamidine-2-phenylindole in case of the binding with nucleoid DNA].

Earlier we showed that 4-hours treatment of cells K562 with the GTP-binding protein activator AlF4- (10 mM NaF + 20 microM AlCl3) increased the DNA fragmentation on an average to 5% of the total 3H-thymidine-labeled DNA. The viability of cells under these conditions did not change. It has been suggested that gene toxic action of AlF4- is a result of cell proliferation block induced by AlF4-. In the present work we tried to determine possible changes in the ethidium bromide and 4',6-diamidine-2-phenylindole (DAPI) fluorescence when they bind with nucleoid DNA of synchronized cells K562 treated with AlF4-. Cells K562 were incubated for synchronization with 2 mM thymidine during 15 hours. Under these conditions DNA synthesis (3H-thymidine uptake) was suppressed by 94-99%. It has been found that the treatment of "cool" thymidine-incubated cells K562 with AlF4- did not change the fluorescence of either ethidium or DAPI. The presence of phorbol-12-myristate-13-acetate (PMA) in the incubation medium did not influence the results. On the other, hand the rat thymocytes incubated with dexametazone (2 microM) during 4 hours (positive control of DNA fragmentation) demonstrated the increase in both parameters. PMA decreased the ethidium fluorescence that correspond to its (PMA) ability to suppress fragmentation of thymocyte DNA. On the base of the results we suggested that AlF4- did not induce DNA fragmentation in the cells K562 with the blocked DNA synthesis.

Aluminum Compounds↗
PubMed1997

[Nicotinamide decreases DNA destabilization in K562 cells treated with AlF(-4)].

Using trypan blue exclusion test it has been shown that a 18 hour incubation of human erythromyeloleukosis cell line K562 together with AlF(-4) (10 mM NaF + 20 mkM AlCl3) reduced cell proliferation and survival. However, the latter parameter did not change during 4 hours of incubation. Nevertheless, AlF(-4) increased fragmentation of 3H-thymidine-labelled DNA by 2-4 times. This effect may be suppressed by cultivation of cells with 20 mkM nicotinamide (inhibitor of poly(ADP-ribose)polymerase enzyme). We found that incubation of K562 and YAC-1 cells with 10 mM nicotinamide for 24 hours much reduced their susceptibility to non-MHC-restricted lysis by rat spleen cells. This effect may be induced by a share of intracellular NAD+ and NADH from destroyed K562 cells; their concentration in cells increased under the influence of nicotinamide by 3 times, but this effect should be the least because in these conditions nicotinamide does not influence the survival of K562 cells. The effect of nicotinamide in both cases may be explained by suppression of poly(ADP-ribose)polymerase activity and, thus, the rate of DNA reparation. Analysis of AlF(-4) and nicotinamide effects on the K562 cells enables us to suppose that suppression of the K562 proliferation by tetrafluoroaluminate results in accumulation of reversed damages of DNA.

Aluminum Compounds↗
PubMedDate not supplied

[Changes in the K562 cell sensitivity to nonspecific lysis by human and rat leukocytes under the influence of sodium butyrate, dimethyl sulfoxide and phorbol-12-myristate-13-acetate].

We studied the ability of inducers and inhibitors of erythroid differentiation of K562 leukemia cells, such as sodium butyrate, dimethyl sulfoxide, and phorbol-12-myristate-13-acetate, respectively, to modulate sensitivity of these cells to non-specific lysis (non-restricted with respect to antigens of the major histocompatibility complex) mediated by natural human or rat killer cells. Unfractionated leukocytes from human peripheral blood or rat splenocytes were used as sources of natural killers. The induction of erythroid differentiation by sodium butyrate was accompanied by a significant increase in cell sensitivity to lysis with human peripheral blood lymphocytes; incubation of K562 cells in the mixture of sodium butyrate and dimethyl sulfoxide did not change cell sensitivity to lysis by both types of effector cells. The inhibition of sodium butyrate-induced erythroid differentiation with high doses of phorbol-12-myristate-13-acetate (100 nM; incubation was in the presence of both these agents simultaneously) resulted in an increased cell sensitivity to lysis with rat splenocytes. Incubation of K562 cells in a mixture of sodium butyrate, dimethyl sulfoxide, and phorbol-12-myristate-13-acetate (100 nM) produced greater lysis by human leukocytes, as compared with incubation in the mixture of sodium butyrate and dimethyl sulfoxide.

Animals↗