Suppression of nitric oxide-induced apoptosis by N-acetyl-L-cysteine through modulation of glutathione, bcl-2, and bax protein levels

Yuan Soon Ho, Horng Mo Lee, Tung Chang Mou, Ying-Jan Wang, Jen Kun Lin

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

It has been demonstrated that nitric oxide (NO) can promote apoptosis in human cancer cells. To test the protective effects of antioxidants (N-acetyl-L-cysteine (LNAC)) and free-radical spin traps (5,5-dimethyl-1-pyrroline N-oxide and 2,2,6,6,-tetramethyl-1-piperidinyloxy) against NO-induced apoptosis, a human colon cancer cell line (COLO 205) was treated with NO, and its survival rate was evaluated both with and without antioxidant therapy. LNAC arrested the development of progression of apoptosis in COLO 205 cells in a dose-dependent manner, promoted long-term survival, and prevented the internucleosomal DNA cleavage induced by NO. The intracellular level of glutathione (GSH) was found to be elevated in cells after exposure to LNAC. The bax protein levels were elevated by NO treatment, and this effect was blocked by LNAC. On the other hand, the bcl-2 oncoprotein level in the LNAC-pretreated cells was significantly elevated in a time-dependent manner compared to cells that received NO pretreatment. In summary, our results suggest that the protective effect of LNAC may be linked to its inducement of increases in cellular GSH and bcl-2 protein levels and to its suppression of cellular bax protein in treated cells.

Original languageEnglish
Pages (from-to)101-113
Number of pages13
JournalMolecular Carcinogenesis
Volume19
Issue number2
DOIs
Publication statusPublished - 1997 Jul 28

Fingerprint

bcl-2-Associated X Protein
Acetylcysteine
Glutathione
Nitric Oxide
Apoptosis
Antioxidants
DNA Cleavage
Oncogene Proteins
Colonic Neoplasms
Free Radicals
Cell Line
Survival
Neoplasms
Proteins

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cancer Research

Cite this

@article{a371506ac4344a60b8dc91fcd4de7a07,
title = "Suppression of nitric oxide-induced apoptosis by N-acetyl-L-cysteine through modulation of glutathione, bcl-2, and bax protein levels",
abstract = "It has been demonstrated that nitric oxide (NO) can promote apoptosis in human cancer cells. To test the protective effects of antioxidants (N-acetyl-L-cysteine (LNAC)) and free-radical spin traps (5,5-dimethyl-1-pyrroline N-oxide and 2,2,6,6,-tetramethyl-1-piperidinyloxy) against NO-induced apoptosis, a human colon cancer cell line (COLO 205) was treated with NO, and its survival rate was evaluated both with and without antioxidant therapy. LNAC arrested the development of progression of apoptosis in COLO 205 cells in a dose-dependent manner, promoted long-term survival, and prevented the internucleosomal DNA cleavage induced by NO. The intracellular level of glutathione (GSH) was found to be elevated in cells after exposure to LNAC. The bax protein levels were elevated by NO treatment, and this effect was blocked by LNAC. On the other hand, the bcl-2 oncoprotein level in the LNAC-pretreated cells was significantly elevated in a time-dependent manner compared to cells that received NO pretreatment. In summary, our results suggest that the protective effect of LNAC may be linked to its inducement of increases in cellular GSH and bcl-2 protein levels and to its suppression of cellular bax protein in treated cells.",
author = "Ho, {Yuan Soon} and Lee, {Horng Mo} and Mou, {Tung Chang} and Ying-Jan Wang and Lin, {Jen Kun}",
year = "1997",
month = "7",
day = "28",
doi = "10.1002/(SICI)1098-2744(199707)19:2<101::AID-MC5>3.0.CO;2-I",
language = "English",
volume = "19",
pages = "101--113",
journal = "Molecular Carcinogenesis",
issn = "0899-1987",
publisher = "Wiley-Liss Inc.",
number = "2",

}

Suppression of nitric oxide-induced apoptosis by N-acetyl-L-cysteine through modulation of glutathione, bcl-2, and bax protein levels. / Ho, Yuan Soon; Lee, Horng Mo; Mou, Tung Chang; Wang, Ying-Jan; Lin, Jen Kun.

In: Molecular Carcinogenesis, Vol. 19, No. 2, 28.07.1997, p. 101-113.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Suppression of nitric oxide-induced apoptosis by N-acetyl-L-cysteine through modulation of glutathione, bcl-2, and bax protein levels

AU - Ho, Yuan Soon

AU - Lee, Horng Mo

AU - Mou, Tung Chang

AU - Wang, Ying-Jan

AU - Lin, Jen Kun

PY - 1997/7/28

Y1 - 1997/7/28

N2 - It has been demonstrated that nitric oxide (NO) can promote apoptosis in human cancer cells. To test the protective effects of antioxidants (N-acetyl-L-cysteine (LNAC)) and free-radical spin traps (5,5-dimethyl-1-pyrroline N-oxide and 2,2,6,6,-tetramethyl-1-piperidinyloxy) against NO-induced apoptosis, a human colon cancer cell line (COLO 205) was treated with NO, and its survival rate was evaluated both with and without antioxidant therapy. LNAC arrested the development of progression of apoptosis in COLO 205 cells in a dose-dependent manner, promoted long-term survival, and prevented the internucleosomal DNA cleavage induced by NO. The intracellular level of glutathione (GSH) was found to be elevated in cells after exposure to LNAC. The bax protein levels were elevated by NO treatment, and this effect was blocked by LNAC. On the other hand, the bcl-2 oncoprotein level in the LNAC-pretreated cells was significantly elevated in a time-dependent manner compared to cells that received NO pretreatment. In summary, our results suggest that the protective effect of LNAC may be linked to its inducement of increases in cellular GSH and bcl-2 protein levels and to its suppression of cellular bax protein in treated cells.

AB - It has been demonstrated that nitric oxide (NO) can promote apoptosis in human cancer cells. To test the protective effects of antioxidants (N-acetyl-L-cysteine (LNAC)) and free-radical spin traps (5,5-dimethyl-1-pyrroline N-oxide and 2,2,6,6,-tetramethyl-1-piperidinyloxy) against NO-induced apoptosis, a human colon cancer cell line (COLO 205) was treated with NO, and its survival rate was evaluated both with and without antioxidant therapy. LNAC arrested the development of progression of apoptosis in COLO 205 cells in a dose-dependent manner, promoted long-term survival, and prevented the internucleosomal DNA cleavage induced by NO. The intracellular level of glutathione (GSH) was found to be elevated in cells after exposure to LNAC. The bax protein levels were elevated by NO treatment, and this effect was blocked by LNAC. On the other hand, the bcl-2 oncoprotein level in the LNAC-pretreated cells was significantly elevated in a time-dependent manner compared to cells that received NO pretreatment. In summary, our results suggest that the protective effect of LNAC may be linked to its inducement of increases in cellular GSH and bcl-2 protein levels and to its suppression of cellular bax protein in treated cells.

UR - http://www.scopus.com/inward/record.url?scp=0030748314&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030748314&partnerID=8YFLogxK

U2 - 10.1002/(SICI)1098-2744(199707)19:2<101::AID-MC5>3.0.CO;2-I

DO - 10.1002/(SICI)1098-2744(199707)19:2<101::AID-MC5>3.0.CO;2-I

M3 - Article

VL - 19

SP - 101

EP - 113

JO - Molecular Carcinogenesis

JF - Molecular Carcinogenesis

SN - 0899-1987

IS - 2

ER -