Effect of frying-meat emission particulate on 17β-estradiol 2- and 4-hydroxylation in human lung adenocarcinoma CL5 cells

Hui Wu Wang, Tzuu-Huei Ueng, Ta-Liang Chen, Pan Chyr Yang

Research output: Contribution to journalArticle

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Abstract

The effect of airborne frying-meat emission particulate (FMEP) on metabolism of 17β-estradiol (E2) to potentially toxic catechol estrogens 2- and 4-hydroxyestradiol (2- and 4-OH-E2) was determined using human lung adenocarcinoma CL5 cells treated with organic extracts of beef FMEP. E2 was incubated with microsomes prepared from untreated CL5 cells or cells treated with 200 μg/ml FMEP extract for 6 h. E2 metabolites formed were analyzed by high-performance liquid chromatography (HPLC). The results revealed that treatment with FMEP produced three-and twofold increases of 2- and 4-hydroxylation of E2, respectively. Monooxygenase activity and immunoblot analyses showed that FMEP markedly induced microsomal 7-ethoxyresorufin O-deethylase (EROD) activity and cytochrome P-450 (CYP) IAI and CYPIBI protein levels. Similar increases in E2 hydroxylation, EROD activity, and CYP protein levels were observed with HepG2 human hepatoma and MCF-7 human breast cancer cells treated with FMEP or 1 μM dibenz[a,h]anthracene. Cotreatment of CL5 cells with FMEP extract and 2 μM α-naphthoflavone, an arylhydrocarbon receptor antagonist, blocked the inductive effects of FMEP on E2 hydroxylation and EROD activity. Additions of 0.01, 0.1, or 1 μM α-naphthoflavone, a CYP inhibitor, to microsomes produced concentration-dependent decreases in E2 2-hydroxylation and EROD activity of CL5 cells induced by dibenz[a,h]anthracene. The present finding demonstrates that FMEP can increase formation of 2-OH-E2 and 4-OH-E2 by human lung cells, and induction of CYP1A1 and CYP1B1 is a potential mechanism underlying increased E2 metabolism. The toxicological significance of FMEP and estrogen interaction warrants further investigation.

Original languageEnglish
Pages (from-to)1175-1188
Number of pages14
JournalJournal of Toxicology and Environmental Health - Part A
Volume66
Issue number12
DOIs
Publication statusPublished - Jun 27 2003

Fingerprint

Hydroxylation
Particulate emissions
Meats
meat
Meat
Estradiol
Cytochrome P-450 CYP1A1
cytochrome
Anthracene
Microsomes
Metabolism
Cytochrome P-450 Enzyme System
metabolism
Catechol Estrogens
Adenocarcinoma of lung
effect
Proteins
Beef
protein
Poisons

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Public Health, Environmental and Occupational Health
  • Pollution
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Effect of frying-meat emission particulate on 17β-estradiol 2- and 4-hydroxylation in human lung adenocarcinoma CL5 cells. / Wang, Hui Wu; Ueng, Tzuu-Huei; Chen, Ta-Liang; Yang, Pan Chyr.

In: Journal of Toxicology and Environmental Health - Part A, Vol. 66, No. 12, 27.06.2003, p. 1175-1188.

Research output: Contribution to journalArticle

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abstract = "The effect of airborne frying-meat emission particulate (FMEP) on metabolism of 17β-estradiol (E2) to potentially toxic catechol estrogens 2- and 4-hydroxyestradiol (2- and 4-OH-E2) was determined using human lung adenocarcinoma CL5 cells treated with organic extracts of beef FMEP. E2 was incubated with microsomes prepared from untreated CL5 cells or cells treated with 200 μg/ml FMEP extract for 6 h. E2 metabolites formed were analyzed by high-performance liquid chromatography (HPLC). The results revealed that treatment with FMEP produced three-and twofold increases of 2- and 4-hydroxylation of E2, respectively. Monooxygenase activity and immunoblot analyses showed that FMEP markedly induced microsomal 7-ethoxyresorufin O-deethylase (EROD) activity and cytochrome P-450 (CYP) IAI and CYPIBI protein levels. Similar increases in E2 hydroxylation, EROD activity, and CYP protein levels were observed with HepG2 human hepatoma and MCF-7 human breast cancer cells treated with FMEP or 1 μM dibenz[a,h]anthracene. Cotreatment of CL5 cells with FMEP extract and 2 μM α-naphthoflavone, an arylhydrocarbon receptor antagonist, blocked the inductive effects of FMEP on E2 hydroxylation and EROD activity. Additions of 0.01, 0.1, or 1 μM α-naphthoflavone, a CYP inhibitor, to microsomes produced concentration-dependent decreases in E2 2-hydroxylation and EROD activity of CL5 cells induced by dibenz[a,h]anthracene. The present finding demonstrates that FMEP can increase formation of 2-OH-E2 and 4-OH-E2 by human lung cells, and induction of CYP1A1 and CYP1B1 is a potential mechanism underlying increased E2 metabolism. The toxicological significance of FMEP and estrogen interaction warrants further investigation.",
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