Protection by quercetin against cooking oil fumes-induced DNA damage in human lung adenocarcinoma CL-3 cells: Role of COX-2

Shwu Yuann Lin, Shun Jen Tsai, Lien Hui Wang, Ming Fang Wu, Huei Lee

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Epidemiological studies have shown that the incidence of lung cancer was associated with exposure to cooking oil fumes (COF) in nonsmoking Taiwanese women. We suspect that quercetin may be a potent inhibitor for reduction of COF-induced DNA damage and prevention of lung cancer development. Comet assay was used to evaluate the DNA damage induced by a relatively low dose of COF (100 μg/ml) in human lung adenocarcinoma CL-3 cells. To understand whether quercetin has the most potent protective effect on COF-induced DNA damage, the 50% inhibition concentration of quercetin for COF-induced DNA damage (IC50) was compared with IC50 values of α-naphthoflavone (α-NF), NS-398, and NaN3 (specific inhibitors) or scavengers of cytochrome P-450 1A1, cyclooxygenase-2 (COX-2), and reactive oxygen species. The IC50 of quercetin was only 1/2, 1/3, and 1/35 of IC50 values of α-NF, NS-398, and NaN3, respectively. Clearly, quercetin was the most effective inhibitor of COF-induced DNA damage, followed sequentially by α-NF, NS-398, and NaN3. To further elucidate whether inhibition of COF-induced DNA damage of quercetin is mediated through the inhibition of COX-2 gene expression by altering the nuclear factor-κB pathway, COX-2 mRNA and its protein expressions induced by COF were evaluated by reverse transcription-polymerase chain reaction and Western blot, respectively. Our data showed that COX-2 mRNA and protein levels were significantly repressed by addition of quercetin in a dose-dependent manner. Gel retardation assay showed that nuclear factor-κB DNA binding activity induced by COF was significantly inhibited by quercetin. From our previous and present studies, it is revealed that coexpression of COX-2 and cytochrome P-450 1A1 caused by COF may contribute to genomic instability in lung cancer development. Thus quercetin may act as a potent chemopreventive agent of lung cancer for nonsmoking Taiwanese women.

Original languageEnglish
Pages (from-to)95-101
Number of pages7
JournalNutrition and Cancer
Volume44
Issue number1
Publication statusPublished - 2002
Externally publishedYes

Fingerprint

cooking fats and oils
Quercetin
Cooking
prostaglandin synthase
Cyclooxygenase 2
adenocarcinoma
DNA damage
quercetin
DNA Damage
Oils
lungs
lung neoplasms
Sodium Azide
Inhibitory Concentration 50
cells
inhibitory concentration 50
Lung Neoplasms
cytochrome P-450
Cytochrome P-450 Enzyme System
B-DNA

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Oncology
  • Food Science

Cite this

Protection by quercetin against cooking oil fumes-induced DNA damage in human lung adenocarcinoma CL-3 cells : Role of COX-2. / Lin, Shwu Yuann; Tsai, Shun Jen; Wang, Lien Hui; Wu, Ming Fang; Lee, Huei.

In: Nutrition and Cancer, Vol. 44, No. 1, 2002, p. 95-101.

Research output: Contribution to journalArticle

Lin, Shwu Yuann ; Tsai, Shun Jen ; Wang, Lien Hui ; Wu, Ming Fang ; Lee, Huei. / Protection by quercetin against cooking oil fumes-induced DNA damage in human lung adenocarcinoma CL-3 cells : Role of COX-2. In: Nutrition and Cancer. 2002 ; Vol. 44, No. 1. pp. 95-101.
@article{124c5c8d8c9f49a9a60aaa1385610850,
title = "Protection by quercetin against cooking oil fumes-induced DNA damage in human lung adenocarcinoma CL-3 cells: Role of COX-2",
abstract = "Epidemiological studies have shown that the incidence of lung cancer was associated with exposure to cooking oil fumes (COF) in nonsmoking Taiwanese women. We suspect that quercetin may be a potent inhibitor for reduction of COF-induced DNA damage and prevention of lung cancer development. Comet assay was used to evaluate the DNA damage induced by a relatively low dose of COF (100 μg/ml) in human lung adenocarcinoma CL-3 cells. To understand whether quercetin has the most potent protective effect on COF-induced DNA damage, the 50{\%} inhibition concentration of quercetin for COF-induced DNA damage (IC50) was compared with IC50 values of α-naphthoflavone (α-NF), NS-398, and NaN3 (specific inhibitors) or scavengers of cytochrome P-450 1A1, cyclooxygenase-2 (COX-2), and reactive oxygen species. The IC50 of quercetin was only 1/2, 1/3, and 1/35 of IC50 values of α-NF, NS-398, and NaN3, respectively. Clearly, quercetin was the most effective inhibitor of COF-induced DNA damage, followed sequentially by α-NF, NS-398, and NaN3. To further elucidate whether inhibition of COF-induced DNA damage of quercetin is mediated through the inhibition of COX-2 gene expression by altering the nuclear factor-κB pathway, COX-2 mRNA and its protein expressions induced by COF were evaluated by reverse transcription-polymerase chain reaction and Western blot, respectively. Our data showed that COX-2 mRNA and protein levels were significantly repressed by addition of quercetin in a dose-dependent manner. Gel retardation assay showed that nuclear factor-κB DNA binding activity induced by COF was significantly inhibited by quercetin. From our previous and present studies, it is revealed that coexpression of COX-2 and cytochrome P-450 1A1 caused by COF may contribute to genomic instability in lung cancer development. Thus quercetin may act as a potent chemopreventive agent of lung cancer for nonsmoking Taiwanese women.",
author = "Lin, {Shwu Yuann} and Tsai, {Shun Jen} and Wang, {Lien Hui} and Wu, {Ming Fang} and Huei Lee",
year = "2002",
language = "English",
volume = "44",
pages = "95--101",
journal = "Nutrition and Cancer",
issn = "0163-5581",
publisher = "Routledge",
number = "1",

}

TY - JOUR

T1 - Protection by quercetin against cooking oil fumes-induced DNA damage in human lung adenocarcinoma CL-3 cells

T2 - Role of COX-2

AU - Lin, Shwu Yuann

AU - Tsai, Shun Jen

AU - Wang, Lien Hui

AU - Wu, Ming Fang

AU - Lee, Huei

PY - 2002

Y1 - 2002

N2 - Epidemiological studies have shown that the incidence of lung cancer was associated with exposure to cooking oil fumes (COF) in nonsmoking Taiwanese women. We suspect that quercetin may be a potent inhibitor for reduction of COF-induced DNA damage and prevention of lung cancer development. Comet assay was used to evaluate the DNA damage induced by a relatively low dose of COF (100 μg/ml) in human lung adenocarcinoma CL-3 cells. To understand whether quercetin has the most potent protective effect on COF-induced DNA damage, the 50% inhibition concentration of quercetin for COF-induced DNA damage (IC50) was compared with IC50 values of α-naphthoflavone (α-NF), NS-398, and NaN3 (specific inhibitors) or scavengers of cytochrome P-450 1A1, cyclooxygenase-2 (COX-2), and reactive oxygen species. The IC50 of quercetin was only 1/2, 1/3, and 1/35 of IC50 values of α-NF, NS-398, and NaN3, respectively. Clearly, quercetin was the most effective inhibitor of COF-induced DNA damage, followed sequentially by α-NF, NS-398, and NaN3. To further elucidate whether inhibition of COF-induced DNA damage of quercetin is mediated through the inhibition of COX-2 gene expression by altering the nuclear factor-κB pathway, COX-2 mRNA and its protein expressions induced by COF were evaluated by reverse transcription-polymerase chain reaction and Western blot, respectively. Our data showed that COX-2 mRNA and protein levels were significantly repressed by addition of quercetin in a dose-dependent manner. Gel retardation assay showed that nuclear factor-κB DNA binding activity induced by COF was significantly inhibited by quercetin. From our previous and present studies, it is revealed that coexpression of COX-2 and cytochrome P-450 1A1 caused by COF may contribute to genomic instability in lung cancer development. Thus quercetin may act as a potent chemopreventive agent of lung cancer for nonsmoking Taiwanese women.

AB - Epidemiological studies have shown that the incidence of lung cancer was associated with exposure to cooking oil fumes (COF) in nonsmoking Taiwanese women. We suspect that quercetin may be a potent inhibitor for reduction of COF-induced DNA damage and prevention of lung cancer development. Comet assay was used to evaluate the DNA damage induced by a relatively low dose of COF (100 μg/ml) in human lung adenocarcinoma CL-3 cells. To understand whether quercetin has the most potent protective effect on COF-induced DNA damage, the 50% inhibition concentration of quercetin for COF-induced DNA damage (IC50) was compared with IC50 values of α-naphthoflavone (α-NF), NS-398, and NaN3 (specific inhibitors) or scavengers of cytochrome P-450 1A1, cyclooxygenase-2 (COX-2), and reactive oxygen species. The IC50 of quercetin was only 1/2, 1/3, and 1/35 of IC50 values of α-NF, NS-398, and NaN3, respectively. Clearly, quercetin was the most effective inhibitor of COF-induced DNA damage, followed sequentially by α-NF, NS-398, and NaN3. To further elucidate whether inhibition of COF-induced DNA damage of quercetin is mediated through the inhibition of COX-2 gene expression by altering the nuclear factor-κB pathway, COX-2 mRNA and its protein expressions induced by COF were evaluated by reverse transcription-polymerase chain reaction and Western blot, respectively. Our data showed that COX-2 mRNA and protein levels were significantly repressed by addition of quercetin in a dose-dependent manner. Gel retardation assay showed that nuclear factor-κB DNA binding activity induced by COF was significantly inhibited by quercetin. From our previous and present studies, it is revealed that coexpression of COX-2 and cytochrome P-450 1A1 caused by COF may contribute to genomic instability in lung cancer development. Thus quercetin may act as a potent chemopreventive agent of lung cancer for nonsmoking Taiwanese women.

UR - http://www.scopus.com/inward/record.url?scp=0345700299&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0345700299&partnerID=8YFLogxK

M3 - Article

C2 - 12672646

AN - SCOPUS:0345700299

VL - 44

SP - 95

EP - 101

JO - Nutrition and Cancer

JF - Nutrition and Cancer

SN - 0163-5581

IS - 1

ER -