Changes in polyamine catabolism in HL-60 human promyelogenous leukaemic cells in response to etoposide-induced apoptosis

G S Lindsay, H M Wallace

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

The topoisomerase II inhibitor etoposide induced apoptosis in HL-60 cells within 4 h of exposure to the drug, as measured by changes in morphology, DNA fragmentation and cytotoxicity assays. Etoposide-induced apoptosis was accompanied by an increase in polyamine efflux from the cells and a decrease in total polyamine content during the first 24 h of exposure to the drug. Although both enzyme activities increased slightly, there were no significant changes in spermidine/spermine N-1-acetyltransferase activity or polyamine oxidase activity. After longer exposures (48-72 h), significant induction of spermidine/spermine N-1-acetyltransferase activity and loss of polyamine content occurred. These results suggest that polyamine oxidation and the resultant hydrogen peroxide produced may be associated with the initiation of apoptosis, while induction of the acetyltransferase and overall loss of intracellular polyamines may be involved in the final, possibly necrotic, stages of cell death.

Original languageEnglish
Pages (from-to)83-87
Number of pages5
JournalBiochemical Journal
Volume337
Publication statusPublished - 1999

Keywords

  • cancer
  • cell death
  • polyamine efflux
  • polyamine
  • oxidase
  • spermidine/spermine N-1-acetyltransferase
  • SPERMIDINE/SPERMINE N-1-ACETYLTRANSFERASE
  • MAMMALIAN-CELLS
  • BREAST-CANCER
  • GROWTH
  • ANALOG
  • DEATH
  • INDUCTION
  • ACETYLATION
  • BHK-21/C13
  • EXCRETION

Cite this

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title = "Changes in polyamine catabolism in HL-60 human promyelogenous leukaemic cells in response to etoposide-induced apoptosis",
abstract = "The topoisomerase II inhibitor etoposide induced apoptosis in HL-60 cells within 4 h of exposure to the drug, as measured by changes in morphology, DNA fragmentation and cytotoxicity assays. Etoposide-induced apoptosis was accompanied by an increase in polyamine efflux from the cells and a decrease in total polyamine content during the first 24 h of exposure to the drug. Although both enzyme activities increased slightly, there were no significant changes in spermidine/spermine N-1-acetyltransferase activity or polyamine oxidase activity. After longer exposures (48-72 h), significant induction of spermidine/spermine N-1-acetyltransferase activity and loss of polyamine content occurred. These results suggest that polyamine oxidation and the resultant hydrogen peroxide produced may be associated with the initiation of apoptosis, while induction of the acetyltransferase and overall loss of intracellular polyamines may be involved in the final, possibly necrotic, stages of cell death.",
keywords = "cancer, cell death, polyamine efflux, polyamine, oxidase, spermidine/spermine N-1-acetyltransferase, SPERMIDINE/SPERMINE N-1-ACETYLTRANSFERASE, MAMMALIAN-CELLS, BREAST-CANCER, GROWTH, ANALOG, DEATH, INDUCTION, ACETYLATION, BHK-21/C13, EXCRETION",
author = "Lindsay, {G S} and Wallace, {H M}",
year = "1999",
language = "English",
volume = "337",
pages = "83--87",
journal = "Biochemical Journal",
issn = "0264-6021",
publisher = "Portland Press Ltd.",

}

TY - JOUR

T1 - Changes in polyamine catabolism in HL-60 human promyelogenous leukaemic cells in response to etoposide-induced apoptosis

AU - Lindsay, G S

AU - Wallace, H M

PY - 1999

Y1 - 1999

N2 - The topoisomerase II inhibitor etoposide induced apoptosis in HL-60 cells within 4 h of exposure to the drug, as measured by changes in morphology, DNA fragmentation and cytotoxicity assays. Etoposide-induced apoptosis was accompanied by an increase in polyamine efflux from the cells and a decrease in total polyamine content during the first 24 h of exposure to the drug. Although both enzyme activities increased slightly, there were no significant changes in spermidine/spermine N-1-acetyltransferase activity or polyamine oxidase activity. After longer exposures (48-72 h), significant induction of spermidine/spermine N-1-acetyltransferase activity and loss of polyamine content occurred. These results suggest that polyamine oxidation and the resultant hydrogen peroxide produced may be associated with the initiation of apoptosis, while induction of the acetyltransferase and overall loss of intracellular polyamines may be involved in the final, possibly necrotic, stages of cell death.

AB - The topoisomerase II inhibitor etoposide induced apoptosis in HL-60 cells within 4 h of exposure to the drug, as measured by changes in morphology, DNA fragmentation and cytotoxicity assays. Etoposide-induced apoptosis was accompanied by an increase in polyamine efflux from the cells and a decrease in total polyamine content during the first 24 h of exposure to the drug. Although both enzyme activities increased slightly, there were no significant changes in spermidine/spermine N-1-acetyltransferase activity or polyamine oxidase activity. After longer exposures (48-72 h), significant induction of spermidine/spermine N-1-acetyltransferase activity and loss of polyamine content occurred. These results suggest that polyamine oxidation and the resultant hydrogen peroxide produced may be associated with the initiation of apoptosis, while induction of the acetyltransferase and overall loss of intracellular polyamines may be involved in the final, possibly necrotic, stages of cell death.

KW - cancer

KW - cell death

KW - polyamine efflux

KW - polyamine

KW - oxidase

KW - spermidine/spermine N-1-acetyltransferase

KW - SPERMIDINE/SPERMINE N-1-ACETYLTRANSFERASE

KW - MAMMALIAN-CELLS

KW - BREAST-CANCER

KW - GROWTH

KW - ANALOG

KW - DEATH

KW - INDUCTION

KW - ACETYLATION

KW - BHK-21/C13

KW - EXCRETION

M3 - Article

VL - 337

SP - 83

EP - 87

JO - Biochemical Journal

JF - Biochemical Journal

SN - 0264-6021

ER -