Induction of apoptosis by S-nitrosoglutathione and Cu2+ or Ni2+ ion through modulation of bax, bad, and bcl-2 proteins in human colon adenocarcinoma cells

Yuan Soon Ho, Hsu Ling Liu, Jiing Shium Duh, Rong-Jane Chen, Wei Lu Ho, Jiiang Huei Jeng, Ying-Jan Wang, Jen Kun Lin

Research output: Contribution to journalArticle

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Abstract

In this study, the amount of S-nitrosoglutathione (GSNO) was measured spectrophotometrically at 334 nm. A spontaneous decrease in absorbency at 334 nm was detected when GSNO was exposed to 37 °C and a high pH (pH 8.0). We investigated the catalytic roles of various metal ions on the decomposition of GSNO. The degradation of GSNO (0.5 mM) was enhanced by the presence of Cu2+ and Ni2+ ions. The amount of nitric oxide (NO) released from GSNO degradation was estimated by the Griess reaction based on nitrite accumulation. The results indicated that nitrite production was elevated at least twofold in the presence of Cu2+. Our study further indicated that Cu2+ enhanced GSNO-induced apoptosis in human colon adenocarcinoma HT 29 cells. We also found that copper ions modulated the expression of bad, bax, and bcl-2 in GSNO-treated HT 29 cells. The levels of bax and bad proteins in treated cells were significantly elevated about fourfold to sixfold when compared with mock-treated cells 24 h after combined treatment with GSNO plus Cu2+ or Ni2+. On the other hand, significant inhibition of bcl-2 occurred in HT 29 cells with simultaneous treatment of GSNO with Cu2+ (or Ni2+). It seemed that Cu2+ and Ni2+ can enhance the decomposition of GSNO, which liberates NO to activate the pathways. Our results demonstrated that the apoptotic effects induced by GSNO were promoted by Ni2+ and Cu2+ through two different mechanisms: depletion of intracellular glutathione and triggering of NO release from GSNO, which then promotes NO-induced apoptosis in human cells.

Original languageEnglish
Pages (from-to)201-211
Number of pages11
JournalMolecular Carcinogenesis
Volume26
Issue number3
DOIs
Publication statusPublished - 1999 Nov 22

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S-Nitrosoglutathione
HT29 Cells
Nitric Oxide
Colon
Adenocarcinoma
Ions
Apoptosis
Nitrites
Proteins
bcl-Associated Death Protein
bcl-2-Associated X Protein
Glutathione
Copper
Metals

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cancer Research

Cite this

Ho, Yuan Soon ; Liu, Hsu Ling ; Duh, Jiing Shium ; Chen, Rong-Jane ; Ho, Wei Lu ; Jeng, Jiiang Huei ; Wang, Ying-Jan ; Lin, Jen Kun. / Induction of apoptosis by S-nitrosoglutathione and Cu2+ or Ni2+ ion through modulation of bax, bad, and bcl-2 proteins in human colon adenocarcinoma cells. In: Molecular Carcinogenesis. 1999 ; Vol. 26, No. 3. pp. 201-211.
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abstract = "In this study, the amount of S-nitrosoglutathione (GSNO) was measured spectrophotometrically at 334 nm. A spontaneous decrease in absorbency at 334 nm was detected when GSNO was exposed to 37 °C and a high pH (pH 8.0). We investigated the catalytic roles of various metal ions on the decomposition of GSNO. The degradation of GSNO (0.5 mM) was enhanced by the presence of Cu2+ and Ni2+ ions. The amount of nitric oxide (NO) released from GSNO degradation was estimated by the Griess reaction based on nitrite accumulation. The results indicated that nitrite production was elevated at least twofold in the presence of Cu2+. Our study further indicated that Cu2+ enhanced GSNO-induced apoptosis in human colon adenocarcinoma HT 29 cells. We also found that copper ions modulated the expression of bad, bax, and bcl-2 in GSNO-treated HT 29 cells. The levels of bax and bad proteins in treated cells were significantly elevated about fourfold to sixfold when compared with mock-treated cells 24 h after combined treatment with GSNO plus Cu2+ or Ni2+. On the other hand, significant inhibition of bcl-2 occurred in HT 29 cells with simultaneous treatment of GSNO with Cu2+ (or Ni2+). It seemed that Cu2+ and Ni2+ can enhance the decomposition of GSNO, which liberates NO to activate the pathways. Our results demonstrated that the apoptotic effects induced by GSNO were promoted by Ni2+ and Cu2+ through two different mechanisms: depletion of intracellular glutathione and triggering of NO release from GSNO, which then promotes NO-induced apoptosis in human cells.",
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Induction of apoptosis by S-nitrosoglutathione and Cu2+ or Ni2+ ion through modulation of bax, bad, and bcl-2 proteins in human colon adenocarcinoma cells. / Ho, Yuan Soon; Liu, Hsu Ling; Duh, Jiing Shium; Chen, Rong-Jane; Ho, Wei Lu; Jeng, Jiiang Huei; Wang, Ying-Jan; Lin, Jen Kun.

In: Molecular Carcinogenesis, Vol. 26, No. 3, 22.11.1999, p. 201-211.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Induction of apoptosis by S-nitrosoglutathione and Cu2+ or Ni2+ ion through modulation of bax, bad, and bcl-2 proteins in human colon adenocarcinoma cells

AU - Ho, Yuan Soon

AU - Liu, Hsu Ling

AU - Duh, Jiing Shium

AU - Chen, Rong-Jane

AU - Ho, Wei Lu

AU - Jeng, Jiiang Huei

AU - Wang, Ying-Jan

AU - Lin, Jen Kun

PY - 1999/11/22

Y1 - 1999/11/22

N2 - In this study, the amount of S-nitrosoglutathione (GSNO) was measured spectrophotometrically at 334 nm. A spontaneous decrease in absorbency at 334 nm was detected when GSNO was exposed to 37 °C and a high pH (pH 8.0). We investigated the catalytic roles of various metal ions on the decomposition of GSNO. The degradation of GSNO (0.5 mM) was enhanced by the presence of Cu2+ and Ni2+ ions. The amount of nitric oxide (NO) released from GSNO degradation was estimated by the Griess reaction based on nitrite accumulation. The results indicated that nitrite production was elevated at least twofold in the presence of Cu2+. Our study further indicated that Cu2+ enhanced GSNO-induced apoptosis in human colon adenocarcinoma HT 29 cells. We also found that copper ions modulated the expression of bad, bax, and bcl-2 in GSNO-treated HT 29 cells. The levels of bax and bad proteins in treated cells were significantly elevated about fourfold to sixfold when compared with mock-treated cells 24 h after combined treatment with GSNO plus Cu2+ or Ni2+. On the other hand, significant inhibition of bcl-2 occurred in HT 29 cells with simultaneous treatment of GSNO with Cu2+ (or Ni2+). It seemed that Cu2+ and Ni2+ can enhance the decomposition of GSNO, which liberates NO to activate the pathways. Our results demonstrated that the apoptotic effects induced by GSNO were promoted by Ni2+ and Cu2+ through two different mechanisms: depletion of intracellular glutathione and triggering of NO release from GSNO, which then promotes NO-induced apoptosis in human cells.

AB - In this study, the amount of S-nitrosoglutathione (GSNO) was measured spectrophotometrically at 334 nm. A spontaneous decrease in absorbency at 334 nm was detected when GSNO was exposed to 37 °C and a high pH (pH 8.0). We investigated the catalytic roles of various metal ions on the decomposition of GSNO. The degradation of GSNO (0.5 mM) was enhanced by the presence of Cu2+ and Ni2+ ions. The amount of nitric oxide (NO) released from GSNO degradation was estimated by the Griess reaction based on nitrite accumulation. The results indicated that nitrite production was elevated at least twofold in the presence of Cu2+. Our study further indicated that Cu2+ enhanced GSNO-induced apoptosis in human colon adenocarcinoma HT 29 cells. We also found that copper ions modulated the expression of bad, bax, and bcl-2 in GSNO-treated HT 29 cells. The levels of bax and bad proteins in treated cells were significantly elevated about fourfold to sixfold when compared with mock-treated cells 24 h after combined treatment with GSNO plus Cu2+ or Ni2+. On the other hand, significant inhibition of bcl-2 occurred in HT 29 cells with simultaneous treatment of GSNO with Cu2+ (or Ni2+). It seemed that Cu2+ and Ni2+ can enhance the decomposition of GSNO, which liberates NO to activate the pathways. Our results demonstrated that the apoptotic effects induced by GSNO were promoted by Ni2+ and Cu2+ through two different mechanisms: depletion of intracellular glutathione and triggering of NO release from GSNO, which then promotes NO-induced apoptosis in human cells.

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