Effect of cadmium on cell cycle progression in chinese hamster ovary cells

Pei Ming Yang, Shu Jun Chiu, Kwei Ann Lin, Lih Yuan Lin

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Chinese hamster ovary K1 (CHO K1) cells are very sensitive to cadmium (Cd) toxicity. They were used to investigate the effect of Cd on cell cycle progression. Cells were cultured with 0.1, 0.4, 1 or 4 μM Cd for various time intervals. There was no difference in growth rate when less than 0.4 μM Cd was given within 24 h. A dose-dependent reduction of cell proliferation was observed when more than 0.4 μM of Cd was given. The cells were pulse-labeled with 5-bromodeoxyuridine (BrdU), and the labeled cells were cultured in the presence of increasing concentrations of Cd. Cell cycle progression was retarded as a function of Cd concentration. G2/M arrest was observed when the BrdU-labeled cells were treated with 1 μM Cd for 8 h, whereas cells receiving 4 μM Cd stopped at the S phase within 4 h. Cell cycle analysis of cells treated with Cd for 24 h showed that G2/M arrest occurred only when cells received 0.8 to 2 μM Cd. Despite the occurrence of G2/M arrest in the Cd treatment, only a limited proportion of the cells were blocked in the M phase. However, the increase in M phase cells coincided with an elevation in the cyclin-dependent kinase 1 activity. To examine whether Cd acts on cells at a specific cell stage, they were synchronized at the G1 or G2/M phase then treated with 1 μM Cd for 12 h. The cells were blocked at the G2/M and G1/S phase, respectively. This finding indicates that Cd toxicity is global and not cell phase specific. We also investigated the involvement of Cd-induced reactive oxygen species (ROS) with the occurrence of G2/M block and found a lack of correlation between cell cycle arrest and ROS production. We measured the Cd content that caused G2/M arrest from a series of Cd treatments and determined the ranges of cumulative Cd concentrations that could result in cell cycle arrest.

Original languageEnglish
Pages (from-to)125-136
Number of pages12
JournalChemico-Biological Interactions
Volume149
Issue number2-3
DOIs
Publication statusPublished - Oct 15 2004
Externally publishedYes

Fingerprint

Cricetulus
Cadmium
Ovary
Cell Cycle
Cells
Cell Division
Bromodeoxyuridine
Cell Cycle Checkpoints
S Phase
Toxicity
Cultured Cells
Reactive Oxygen Species
CDC2 Protein Kinase
G2 Phase
Cell proliferation
G1 Phase

Keywords

  • Cadmium
  • Cdk1
  • Cell cycle
  • CHO cells
  • G2/M arrest

ASJC Scopus subject areas

  • Toxicology

Cite this

Effect of cadmium on cell cycle progression in chinese hamster ovary cells. / Yang, Pei Ming; Chiu, Shu Jun; Lin, Kwei Ann; Lin, Lih Yuan.

In: Chemico-Biological Interactions, Vol. 149, No. 2-3, 15.10.2004, p. 125-136.

Research output: Contribution to journalArticle

Yang, Pei Ming ; Chiu, Shu Jun ; Lin, Kwei Ann ; Lin, Lih Yuan. / Effect of cadmium on cell cycle progression in chinese hamster ovary cells. In: Chemico-Biological Interactions. 2004 ; Vol. 149, No. 2-3. pp. 125-136.
@article{11f0ce9349ec4bd093fb5e87a1fc2506,
title = "Effect of cadmium on cell cycle progression in chinese hamster ovary cells",
abstract = "Chinese hamster ovary K1 (CHO K1) cells are very sensitive to cadmium (Cd) toxicity. They were used to investigate the effect of Cd on cell cycle progression. Cells were cultured with 0.1, 0.4, 1 or 4 μM Cd for various time intervals. There was no difference in growth rate when less than 0.4 μM Cd was given within 24 h. A dose-dependent reduction of cell proliferation was observed when more than 0.4 μM of Cd was given. The cells were pulse-labeled with 5-bromodeoxyuridine (BrdU), and the labeled cells were cultured in the presence of increasing concentrations of Cd. Cell cycle progression was retarded as a function of Cd concentration. G2/M arrest was observed when the BrdU-labeled cells were treated with 1 μM Cd for 8 h, whereas cells receiving 4 μM Cd stopped at the S phase within 4 h. Cell cycle analysis of cells treated with Cd for 24 h showed that G2/M arrest occurred only when cells received 0.8 to 2 μM Cd. Despite the occurrence of G2/M arrest in the Cd treatment, only a limited proportion of the cells were blocked in the M phase. However, the increase in M phase cells coincided with an elevation in the cyclin-dependent kinase 1 activity. To examine whether Cd acts on cells at a specific cell stage, they were synchronized at the G1 or G2/M phase then treated with 1 μM Cd for 12 h. The cells were blocked at the G2/M and G1/S phase, respectively. This finding indicates that Cd toxicity is global and not cell phase specific. We also investigated the involvement of Cd-induced reactive oxygen species (ROS) with the occurrence of G2/M block and found a lack of correlation between cell cycle arrest and ROS production. We measured the Cd content that caused G2/M arrest from a series of Cd treatments and determined the ranges of cumulative Cd concentrations that could result in cell cycle arrest.",
keywords = "Cadmium, Cdk1, Cell cycle, CHO cells, G2/M arrest",
author = "Yang, {Pei Ming} and Chiu, {Shu Jun} and Lin, {Kwei Ann} and Lin, {Lih Yuan}",
year = "2004",
month = "10",
day = "15",
doi = "10.1016/j.cbi.2004.08.001",
language = "English",
volume = "149",
pages = "125--136",
journal = "Chemico-Biological Interactions",
issn = "0009-2797",
publisher = "Elsevier Ireland Ltd",
number = "2-3",

}

TY - JOUR

T1 - Effect of cadmium on cell cycle progression in chinese hamster ovary cells

AU - Yang, Pei Ming

AU - Chiu, Shu Jun

AU - Lin, Kwei Ann

AU - Lin, Lih Yuan

PY - 2004/10/15

Y1 - 2004/10/15

N2 - Chinese hamster ovary K1 (CHO K1) cells are very sensitive to cadmium (Cd) toxicity. They were used to investigate the effect of Cd on cell cycle progression. Cells were cultured with 0.1, 0.4, 1 or 4 μM Cd for various time intervals. There was no difference in growth rate when less than 0.4 μM Cd was given within 24 h. A dose-dependent reduction of cell proliferation was observed when more than 0.4 μM of Cd was given. The cells were pulse-labeled with 5-bromodeoxyuridine (BrdU), and the labeled cells were cultured in the presence of increasing concentrations of Cd. Cell cycle progression was retarded as a function of Cd concentration. G2/M arrest was observed when the BrdU-labeled cells were treated with 1 μM Cd for 8 h, whereas cells receiving 4 μM Cd stopped at the S phase within 4 h. Cell cycle analysis of cells treated with Cd for 24 h showed that G2/M arrest occurred only when cells received 0.8 to 2 μM Cd. Despite the occurrence of G2/M arrest in the Cd treatment, only a limited proportion of the cells were blocked in the M phase. However, the increase in M phase cells coincided with an elevation in the cyclin-dependent kinase 1 activity. To examine whether Cd acts on cells at a specific cell stage, they were synchronized at the G1 or G2/M phase then treated with 1 μM Cd for 12 h. The cells were blocked at the G2/M and G1/S phase, respectively. This finding indicates that Cd toxicity is global and not cell phase specific. We also investigated the involvement of Cd-induced reactive oxygen species (ROS) with the occurrence of G2/M block and found a lack of correlation between cell cycle arrest and ROS production. We measured the Cd content that caused G2/M arrest from a series of Cd treatments and determined the ranges of cumulative Cd concentrations that could result in cell cycle arrest.

AB - Chinese hamster ovary K1 (CHO K1) cells are very sensitive to cadmium (Cd) toxicity. They were used to investigate the effect of Cd on cell cycle progression. Cells were cultured with 0.1, 0.4, 1 or 4 μM Cd for various time intervals. There was no difference in growth rate when less than 0.4 μM Cd was given within 24 h. A dose-dependent reduction of cell proliferation was observed when more than 0.4 μM of Cd was given. The cells were pulse-labeled with 5-bromodeoxyuridine (BrdU), and the labeled cells were cultured in the presence of increasing concentrations of Cd. Cell cycle progression was retarded as a function of Cd concentration. G2/M arrest was observed when the BrdU-labeled cells were treated with 1 μM Cd for 8 h, whereas cells receiving 4 μM Cd stopped at the S phase within 4 h. Cell cycle analysis of cells treated with Cd for 24 h showed that G2/M arrest occurred only when cells received 0.8 to 2 μM Cd. Despite the occurrence of G2/M arrest in the Cd treatment, only a limited proportion of the cells were blocked in the M phase. However, the increase in M phase cells coincided with an elevation in the cyclin-dependent kinase 1 activity. To examine whether Cd acts on cells at a specific cell stage, they were synchronized at the G1 or G2/M phase then treated with 1 μM Cd for 12 h. The cells were blocked at the G2/M and G1/S phase, respectively. This finding indicates that Cd toxicity is global and not cell phase specific. We also investigated the involvement of Cd-induced reactive oxygen species (ROS) with the occurrence of G2/M block and found a lack of correlation between cell cycle arrest and ROS production. We measured the Cd content that caused G2/M arrest from a series of Cd treatments and determined the ranges of cumulative Cd concentrations that could result in cell cycle arrest.

KW - Cadmium

KW - Cdk1

KW - Cell cycle

KW - CHO cells

KW - G2/M arrest

UR - http://www.scopus.com/inward/record.url?scp=6344226159&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=6344226159&partnerID=8YFLogxK

U2 - 10.1016/j.cbi.2004.08.001

DO - 10.1016/j.cbi.2004.08.001

M3 - Article

C2 - 15501434

AN - SCOPUS:6344226159

VL - 149

SP - 125

EP - 136

JO - Chemico-Biological Interactions

JF - Chemico-Biological Interactions

SN - 0009-2797

IS - 2-3

ER -