Programmed cell-death (apoptosis) in lymphoid and myeloid cell-lines during zinc-deficiency

SJ Martin, G Mazdai, JJ Strain, TG Cotter, BM Hannigan

Research output: Contribution to journalArticle

97 Citations (Scopus)

Abstract

Three human cell lines of lymphoid (Molt-3 and Raji) or myeloid (HL-60) origin were maintained in vitro under zinc-sufficient or zinc-deficient conditions. Under these conditions, cell proliferation, viability and mode of death (apoptotic or necrotic) were assessed. All three cell types decreased their proliferative capacity and viability under conditions of zinc deficiency. Cell death in the HL-60 and Raji cultures occurred primarily via apoptosis, while most cells in zinc-deficient Molt-3 cultures died via necrosis. Apoptosis in zinc-deficient cultures of HL-60 and Raji cells was characterized by a slow decline in culture viability as cells with condensed and fragmented nuclear DNA appeared. These morphological changes were accompanied by an increase in cell buoyant density, which allowed separation of viable apoptotic cells from their non-apoptotic counterparts by means of percoll step-density gradients. Necrosis in zinc-deficient Molt-3 cultures was characterized by rapid loss of cell culture viability as these cells underwent direct lysis. Intact necrotic cells were easily identified by the flocculated state of their chromatin as well as the decreased basophilia of their cytoplasm. Analysis of DNA from apoptotic HL-60 and Raji cells revealed that internucleosomal DNA degradation, indicative of endogenous endonuclease activation, had occurred, whereas the nuclear DNA of necrotic Molt-3 cells remained relatively unfragmented. The different modes of cell death evoked may reflect the relative sensitivities of cells of these lineages to zinc levels in vivo.
LanguageEnglish
Pages338-343
JournalClinical and Experimental Immunology
Volume83
Issue number2
Publication statusPublished - Feb 1991

Fingerprint

Myeloid Cells
Zinc
Cell Death
Lymphocytes
Apoptosis
Cell Line
Cell Survival
HL-60 Cells
DNA
Necrosis
Endonucleases
Cell Lineage
Chromatin
Cytoplasm
Cell Culture Techniques
Cell Count
Cell Proliferation

Cite this

Martin, SJ ; Mazdai, G ; Strain, JJ ; Cotter, TG ; Hannigan, BM. / Programmed cell-death (apoptosis) in lymphoid and myeloid cell-lines during zinc-deficiency. In: Clinical and Experimental Immunology. 1991 ; Vol. 83, No. 2. pp. 338-343.
@article{9842de1257d2488ba0e656237c617bf8,
title = "Programmed cell-death (apoptosis) in lymphoid and myeloid cell-lines during zinc-deficiency",
abstract = "Three human cell lines of lymphoid (Molt-3 and Raji) or myeloid (HL-60) origin were maintained in vitro under zinc-sufficient or zinc-deficient conditions. Under these conditions, cell proliferation, viability and mode of death (apoptotic or necrotic) were assessed. All three cell types decreased their proliferative capacity and viability under conditions of zinc deficiency. Cell death in the HL-60 and Raji cultures occurred primarily via apoptosis, while most cells in zinc-deficient Molt-3 cultures died via necrosis. Apoptosis in zinc-deficient cultures of HL-60 and Raji cells was characterized by a slow decline in culture viability as cells with condensed and fragmented nuclear DNA appeared. These morphological changes were accompanied by an increase in cell buoyant density, which allowed separation of viable apoptotic cells from their non-apoptotic counterparts by means of percoll step-density gradients. Necrosis in zinc-deficient Molt-3 cultures was characterized by rapid loss of cell culture viability as these cells underwent direct lysis. Intact necrotic cells were easily identified by the flocculated state of their chromatin as well as the decreased basophilia of their cytoplasm. Analysis of DNA from apoptotic HL-60 and Raji cells revealed that internucleosomal DNA degradation, indicative of endogenous endonuclease activation, had occurred, whereas the nuclear DNA of necrotic Molt-3 cells remained relatively unfragmented. The different modes of cell death evoked may reflect the relative sensitivities of cells of these lineages to zinc levels in vivo.",
author = "SJ Martin and G Mazdai and JJ Strain and TG Cotter and BM Hannigan",
year = "1991",
month = "2",
language = "English",
volume = "83",
pages = "338--343",
journal = "Clinical and Experimental Immunology",
issn = "0009-9104",
number = "2",

}

Programmed cell-death (apoptosis) in lymphoid and myeloid cell-lines during zinc-deficiency. / Martin, SJ; Mazdai, G; Strain, JJ; Cotter, TG; Hannigan, BM.

In: Clinical and Experimental Immunology, Vol. 83, No. 2, 02.1991, p. 338-343.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Programmed cell-death (apoptosis) in lymphoid and myeloid cell-lines during zinc-deficiency

AU - Martin, SJ

AU - Mazdai, G

AU - Strain, JJ

AU - Cotter, TG

AU - Hannigan, BM

PY - 1991/2

Y1 - 1991/2

N2 - Three human cell lines of lymphoid (Molt-3 and Raji) or myeloid (HL-60) origin were maintained in vitro under zinc-sufficient or zinc-deficient conditions. Under these conditions, cell proliferation, viability and mode of death (apoptotic or necrotic) were assessed. All three cell types decreased their proliferative capacity and viability under conditions of zinc deficiency. Cell death in the HL-60 and Raji cultures occurred primarily via apoptosis, while most cells in zinc-deficient Molt-3 cultures died via necrosis. Apoptosis in zinc-deficient cultures of HL-60 and Raji cells was characterized by a slow decline in culture viability as cells with condensed and fragmented nuclear DNA appeared. These morphological changes were accompanied by an increase in cell buoyant density, which allowed separation of viable apoptotic cells from their non-apoptotic counterparts by means of percoll step-density gradients. Necrosis in zinc-deficient Molt-3 cultures was characterized by rapid loss of cell culture viability as these cells underwent direct lysis. Intact necrotic cells were easily identified by the flocculated state of their chromatin as well as the decreased basophilia of their cytoplasm. Analysis of DNA from apoptotic HL-60 and Raji cells revealed that internucleosomal DNA degradation, indicative of endogenous endonuclease activation, had occurred, whereas the nuclear DNA of necrotic Molt-3 cells remained relatively unfragmented. The different modes of cell death evoked may reflect the relative sensitivities of cells of these lineages to zinc levels in vivo.

AB - Three human cell lines of lymphoid (Molt-3 and Raji) or myeloid (HL-60) origin were maintained in vitro under zinc-sufficient or zinc-deficient conditions. Under these conditions, cell proliferation, viability and mode of death (apoptotic or necrotic) were assessed. All three cell types decreased their proliferative capacity and viability under conditions of zinc deficiency. Cell death in the HL-60 and Raji cultures occurred primarily via apoptosis, while most cells in zinc-deficient Molt-3 cultures died via necrosis. Apoptosis in zinc-deficient cultures of HL-60 and Raji cells was characterized by a slow decline in culture viability as cells with condensed and fragmented nuclear DNA appeared. These morphological changes were accompanied by an increase in cell buoyant density, which allowed separation of viable apoptotic cells from their non-apoptotic counterparts by means of percoll step-density gradients. Necrosis in zinc-deficient Molt-3 cultures was characterized by rapid loss of cell culture viability as these cells underwent direct lysis. Intact necrotic cells were easily identified by the flocculated state of their chromatin as well as the decreased basophilia of their cytoplasm. Analysis of DNA from apoptotic HL-60 and Raji cells revealed that internucleosomal DNA degradation, indicative of endogenous endonuclease activation, had occurred, whereas the nuclear DNA of necrotic Molt-3 cells remained relatively unfragmented. The different modes of cell death evoked may reflect the relative sensitivities of cells of these lineages to zinc levels in vivo.

M3 - Article

VL - 83

SP - 338

EP - 343

JO - Clinical and Experimental Immunology

T2 - Clinical and Experimental Immunology

JF - Clinical and Experimental Immunology

SN - 0009-9104

IS - 2

ER -