Our previous studies demonstrated that intracellular polyamine depletion blocked HL-60 cell apoptosis triggered by exposure to 2-deoxy- -ribose (dRib). Here, we have characterized the intracellular events underlying the apoptotic effects of dRib and the involvement of polyamines in these effects. Treatment of HL-60 cells with dRib induces loss of mitochondrial transmembrane potential, radical oxygen species production, intracellular glutathione depletion and translocation of Bax from cytosol to membranes. These effects are followed by cell death. However, the mode of cell death caused by dRib depends on intracellular levels of polyamines. -Rib-treated cells with normal polyamine levels, progressing through the G1 into the S and G2/M phases, undergo apoptosis, while in polyamine-depleted cells, being blocked at the G1 phase, cell death mechanisms are switched to necrosis. The present study points to a relationship between the cell cycle distribution and the mode of cell death, and suggests that the level of intracellular spermidine, essential to cell cycle progression, may determine whether a cell dies by apoptosis or necrosis in response to a death stimulus.

Polyamine depletion switches the form of 2-deoxy-D-ribose-induced cell death from apoptosis to necrosis in HL-60 cells / Monti, Maria Giuseppina; Ghiaroni, Stefania; Marverti, Gaetano; Montanari, Monica; Moruzzi, Maria Stella. - In: THE INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY. - ISSN 1357-2725. - STAMPA. - 36:7(2004), pp. 1238-1248. [10.1016/j.biocel.2003.09.011]

Polyamine depletion switches the form of 2-deoxy-D-ribose-induced cell death from apoptosis to necrosis in HL-60 cells.

MONTI, Maria Giuseppina;GHIARONI, Stefania;MARVERTI, Gaetano;MONTANARI, Monica;MORUZZI, Maria Stella
2004

Abstract

Our previous studies demonstrated that intracellular polyamine depletion blocked HL-60 cell apoptosis triggered by exposure to 2-deoxy- -ribose (dRib). Here, we have characterized the intracellular events underlying the apoptotic effects of dRib and the involvement of polyamines in these effects. Treatment of HL-60 cells with dRib induces loss of mitochondrial transmembrane potential, radical oxygen species production, intracellular glutathione depletion and translocation of Bax from cytosol to membranes. These effects are followed by cell death. However, the mode of cell death caused by dRib depends on intracellular levels of polyamines. -Rib-treated cells with normal polyamine levels, progressing through the G1 into the S and G2/M phases, undergo apoptosis, while in polyamine-depleted cells, being blocked at the G1 phase, cell death mechanisms are switched to necrosis. The present study points to a relationship between the cell cycle distribution and the mode of cell death, and suggests that the level of intracellular spermidine, essential to cell cycle progression, may determine whether a cell dies by apoptosis or necrosis in response to a death stimulus.
2004
36
7
1238
1248
Polyamine depletion switches the form of 2-deoxy-D-ribose-induced cell death from apoptosis to necrosis in HL-60 cells / Monti, Maria Giuseppina; Ghiaroni, Stefania; Marverti, Gaetano; Montanari, Monica; Moruzzi, Maria Stella. - In: THE INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY. - ISSN 1357-2725. - STAMPA. - 36:7(2004), pp. 1238-1248. [10.1016/j.biocel.2003.09.011]
Monti, Maria Giuseppina; Ghiaroni, Stefania; Marverti, Gaetano; Montanari, Monica; Moruzzi, Maria Stella
File in questo prodotto:
File Dimensione Formato  
IJBCB-Monti36-7-2004.pdf

Solo gestori archivio

Tipologia: Versione pubblicata dall'editore
Dimensione 191.03 kB
Formato Adobe PDF
191.03 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/455693
Citazioni
  • ???jsp.display-item.citation.pmc??? 3
  • Scopus 14
  • ???jsp.display-item.citation.isi??? 13
social impact