DMSO modifies structural and functional properties of RPMI-8402 cells by promoting programmed cell death.
Apoptosis in lymphoid cells can be induced in different ways depending on cell type and acquired signal. Biochemical modifications occur at an early phase of cell death while at late times the typical morphological features of apoptosis can be visualized. The aim of this study is to verify by multiparametric analyses the plasma membrane fluidity, the intracellular Ca2+ concentration and the nitric oxide synthase (NOS) activity during cell death progression induced by DMSO treatment. The RPMI-8402 human pre-T lymphoblastoid cell line was induced to cell death by DMSO. Analyses rescued at early times of treatment prove a substantial modification of plasma membrane fluidity associated with an increase of intracellular Ca2+. Moreover, these modifications are associated with an up regulation of NOS activity. Our results are consistent with the hypothesis that programmed cell death can be induced by up regulation of the intracellular Ca2+ associated with an increase of cell membrane fluidity. The apoptotic mechanisms seem to involve not only membrane damage and increased intracellular calcium levels but also production of nitric oxide.
Trubiani
O
O
Dipartimento di Scienze Odontostomatologiche, University of Chieti, Italy.
Salvolini
E
E
Staffolani
R
R
Di Primio
R
R
Mazzanti
L
L
D017209:Apoptosis / Q000187:drug effects* / Q000276:immunology; D002118:Calcium / Q000378:metabolism; D045744:Cell Line, Tumor; D002462:Cell Membrane / Q000187:drug effects / Q000276:immunology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology*; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D013601:T-Lymphocytes / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology*
D019001:Nitric Oxide Synthase; D002118:Calcium; D004121:Dimethyl Sulfoxide