Polycyclic aromatic hydrocarbons and their quinones modulate the metabolic profile and induce DNA damage in human alveolar and bronchiolar cells

Deepak Gurbani, Santosh Kumar Bharti, Ashutosh Kumar, Alok K. Pandey, Godson R.E.E. Ana, Ambrish Verma, Altaf Husain Khan, Devendra K. Patel, M. K.R. Mudiam, Swatantra K. Jain, Raja Roy, Alok Dhawan

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

The release of particulate pollutants into the air through burning of coal, crude oil, diesel, coal tar, etc. raises concerns of potential health hazards to the exposed human population. Polycyclic aromatic hydrocarbons (PAHs) are major toxic constituents of particulate matter (PM), which upon ingestion get metabolized to even more toxic metabolites such as quinones. The PAHs levels were assessed in both respirable particulate matter (RSPM, <10μM size) and suspended particulate matter (SPM, >10μM size) of urban ambient air (UAA) and that of major contributors viz. diesel exhaust particles (DEPs) and coal tar combustions emissions (CTCE). Seven US Environmental Protection Agency (USEPA) prioritized PAHs in RSPM and 10 in SPM were detected in UAA. Ten and 15 prioritized PAHs, respectively, were also detected in diesel exhaust particles (DEP) and coal tar combustion emission (CTCE) evidencing their release in the air. These PM associated PAHs for UAA, DEP and CTCE showed significant increase (p<0.05) in mutagenicity and mammalian genotoxicity in the order CTCE>DEP>UAA. Human lung alveolar (A549) and bronchiolar (BEAS-2B) cells when treated with PAH-metabolites viz. 1,4-benzoquinone (1,4-BQ), hydroquinone (HQ), 1,2-naphthoquinone (1,2-NQ), 1,4-naphthoquinone (1,4-NQ) and 9,10-phenanthroquinone (9,10-PQ) showed metabolic modulation in these cell lines with significant depletion of principal cellular metabolites viz. NADP, uracil, asparagines, glutamine, and histidine and accumulation of di-methyl amine and beta-hydroxybutyrate, identified using 1H NMR spectroscopy. These results suggest that PAH-quinones induce genotoxic effects by modulating the metabolic machinery inside the cells by a combined effect of oxidative stress and energy depletion. Our data for metabolic profiling of human lung cells could also help in understanding the mechanism of toxicity of other xenobiotics.

Original languageEnglish (US)
Pages (from-to)553-565
Number of pages13
JournalInternational Journal of Hygiene and Environmental Health
Volume216
Issue number5
DOIs
StatePublished - Aug 1 2013
Externally publishedYes

Fingerprint

Alveolar Epithelial Cells
Quinones
Metabolome
Polycyclic Aromatic Hydrocarbons
DNA Damage
Coal Tar
Particulate Matter
Vehicle Emissions
Air
Poisons
United States Environmental Protection Agency
Lung
3-Hydroxybutyric Acid
Uracil
Coal
Asparagine
Petroleum
Xenobiotics
Glutamine
NADP

Keywords

  • Genotoxicity
  • Human lung cells
  • Metabolic profiling
  • Polycyclic aromatic hydrocarbons (PAHs)
  • Quinones

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health

Cite this

Polycyclic aromatic hydrocarbons and their quinones modulate the metabolic profile and induce DNA damage in human alveolar and bronchiolar cells. / Gurbani, Deepak; Bharti, Santosh Kumar; Kumar, Ashutosh; Pandey, Alok K.; Ana, Godson R.E.E.; Verma, Ambrish; Khan, Altaf Husain; Patel, Devendra K.; Mudiam, M. K.R.; Jain, Swatantra K.; Roy, Raja; Dhawan, Alok.

In: International Journal of Hygiene and Environmental Health, Vol. 216, No. 5, 01.08.2013, p. 553-565.

Research output: Contribution to journalArticle

Gurbani, Deepak ; Bharti, Santosh Kumar ; Kumar, Ashutosh ; Pandey, Alok K. ; Ana, Godson R.E.E. ; Verma, Ambrish ; Khan, Altaf Husain ; Patel, Devendra K. ; Mudiam, M. K.R. ; Jain, Swatantra K. ; Roy, Raja ; Dhawan, Alok. / Polycyclic aromatic hydrocarbons and their quinones modulate the metabolic profile and induce DNA damage in human alveolar and bronchiolar cells. In: International Journal of Hygiene and Environmental Health. 2013 ; Vol. 216, No. 5. pp. 553-565.
@article{2a351009ef7e4f6ca678a6fb760f0af4,
title = "Polycyclic aromatic hydrocarbons and their quinones modulate the metabolic profile and induce DNA damage in human alveolar and bronchiolar cells",
abstract = "The release of particulate pollutants into the air through burning of coal, crude oil, diesel, coal tar, etc. raises concerns of potential health hazards to the exposed human population. Polycyclic aromatic hydrocarbons (PAHs) are major toxic constituents of particulate matter (PM), which upon ingestion get metabolized to even more toxic metabolites such as quinones. The PAHs levels were assessed in both respirable particulate matter (RSPM, <10μM size) and suspended particulate matter (SPM, >10μM size) of urban ambient air (UAA) and that of major contributors viz. diesel exhaust particles (DEPs) and coal tar combustions emissions (CTCE). Seven US Environmental Protection Agency (USEPA) prioritized PAHs in RSPM and 10 in SPM were detected in UAA. Ten and 15 prioritized PAHs, respectively, were also detected in diesel exhaust particles (DEP) and coal tar combustion emission (CTCE) evidencing their release in the air. These PM associated PAHs for UAA, DEP and CTCE showed significant increase (p<0.05) in mutagenicity and mammalian genotoxicity in the order CTCE>DEP>UAA. Human lung alveolar (A549) and bronchiolar (BEAS-2B) cells when treated with PAH-metabolites viz. 1,4-benzoquinone (1,4-BQ), hydroquinone (HQ), 1,2-naphthoquinone (1,2-NQ), 1,4-naphthoquinone (1,4-NQ) and 9,10-phenanthroquinone (9,10-PQ) showed metabolic modulation in these cell lines with significant depletion of principal cellular metabolites viz. NADP, uracil, asparagines, glutamine, and histidine and accumulation of di-methyl amine and beta-hydroxybutyrate, identified using 1H NMR spectroscopy. These results suggest that PAH-quinones induce genotoxic effects by modulating the metabolic machinery inside the cells by a combined effect of oxidative stress and energy depletion. Our data for metabolic profiling of human lung cells could also help in understanding the mechanism of toxicity of other xenobiotics.",
keywords = "Genotoxicity, Human lung cells, Metabolic profiling, Polycyclic aromatic hydrocarbons (PAHs), Quinones",
author = "Deepak Gurbani and Bharti, {Santosh Kumar} and Ashutosh Kumar and Pandey, {Alok K.} and Ana, {Godson R.E.E.} and Ambrish Verma and Khan, {Altaf Husain} and Patel, {Devendra K.} and Mudiam, {M. K.R.} and Jain, {Swatantra K.} and Raja Roy and Alok Dhawan",
year = "2013",
month = "8",
day = "1",
doi = "10.1016/j.ijheh.2013.04.001",
language = "English (US)",
volume = "216",
pages = "553--565",
journal = "International Journal of Hygiene and Environmental Health",
issn = "1438-4639",
publisher = "Urban und Fischer Verlag Jena",
number = "5",

}

TY - JOUR

T1 - Polycyclic aromatic hydrocarbons and their quinones modulate the metabolic profile and induce DNA damage in human alveolar and bronchiolar cells

AU - Gurbani, Deepak

AU - Bharti, Santosh Kumar

AU - Kumar, Ashutosh

AU - Pandey, Alok K.

AU - Ana, Godson R.E.E.

AU - Verma, Ambrish

AU - Khan, Altaf Husain

AU - Patel, Devendra K.

AU - Mudiam, M. K.R.

AU - Jain, Swatantra K.

AU - Roy, Raja

AU - Dhawan, Alok

PY - 2013/8/1

Y1 - 2013/8/1

N2 - The release of particulate pollutants into the air through burning of coal, crude oil, diesel, coal tar, etc. raises concerns of potential health hazards to the exposed human population. Polycyclic aromatic hydrocarbons (PAHs) are major toxic constituents of particulate matter (PM), which upon ingestion get metabolized to even more toxic metabolites such as quinones. The PAHs levels were assessed in both respirable particulate matter (RSPM, <10μM size) and suspended particulate matter (SPM, >10μM size) of urban ambient air (UAA) and that of major contributors viz. diesel exhaust particles (DEPs) and coal tar combustions emissions (CTCE). Seven US Environmental Protection Agency (USEPA) prioritized PAHs in RSPM and 10 in SPM were detected in UAA. Ten and 15 prioritized PAHs, respectively, were also detected in diesel exhaust particles (DEP) and coal tar combustion emission (CTCE) evidencing their release in the air. These PM associated PAHs for UAA, DEP and CTCE showed significant increase (p<0.05) in mutagenicity and mammalian genotoxicity in the order CTCE>DEP>UAA. Human lung alveolar (A549) and bronchiolar (BEAS-2B) cells when treated with PAH-metabolites viz. 1,4-benzoquinone (1,4-BQ), hydroquinone (HQ), 1,2-naphthoquinone (1,2-NQ), 1,4-naphthoquinone (1,4-NQ) and 9,10-phenanthroquinone (9,10-PQ) showed metabolic modulation in these cell lines with significant depletion of principal cellular metabolites viz. NADP, uracil, asparagines, glutamine, and histidine and accumulation of di-methyl amine and beta-hydroxybutyrate, identified using 1H NMR spectroscopy. These results suggest that PAH-quinones induce genotoxic effects by modulating the metabolic machinery inside the cells by a combined effect of oxidative stress and energy depletion. Our data for metabolic profiling of human lung cells could also help in understanding the mechanism of toxicity of other xenobiotics.

AB - The release of particulate pollutants into the air through burning of coal, crude oil, diesel, coal tar, etc. raises concerns of potential health hazards to the exposed human population. Polycyclic aromatic hydrocarbons (PAHs) are major toxic constituents of particulate matter (PM), which upon ingestion get metabolized to even more toxic metabolites such as quinones. The PAHs levels were assessed in both respirable particulate matter (RSPM, <10μM size) and suspended particulate matter (SPM, >10μM size) of urban ambient air (UAA) and that of major contributors viz. diesel exhaust particles (DEPs) and coal tar combustions emissions (CTCE). Seven US Environmental Protection Agency (USEPA) prioritized PAHs in RSPM and 10 in SPM were detected in UAA. Ten and 15 prioritized PAHs, respectively, were also detected in diesel exhaust particles (DEP) and coal tar combustion emission (CTCE) evidencing their release in the air. These PM associated PAHs for UAA, DEP and CTCE showed significant increase (p<0.05) in mutagenicity and mammalian genotoxicity in the order CTCE>DEP>UAA. Human lung alveolar (A549) and bronchiolar (BEAS-2B) cells when treated with PAH-metabolites viz. 1,4-benzoquinone (1,4-BQ), hydroquinone (HQ), 1,2-naphthoquinone (1,2-NQ), 1,4-naphthoquinone (1,4-NQ) and 9,10-phenanthroquinone (9,10-PQ) showed metabolic modulation in these cell lines with significant depletion of principal cellular metabolites viz. NADP, uracil, asparagines, glutamine, and histidine and accumulation of di-methyl amine and beta-hydroxybutyrate, identified using 1H NMR spectroscopy. These results suggest that PAH-quinones induce genotoxic effects by modulating the metabolic machinery inside the cells by a combined effect of oxidative stress and energy depletion. Our data for metabolic profiling of human lung cells could also help in understanding the mechanism of toxicity of other xenobiotics.

KW - Genotoxicity

KW - Human lung cells

KW - Metabolic profiling

KW - Polycyclic aromatic hydrocarbons (PAHs)

KW - Quinones

UR - http://www.scopus.com/inward/record.url?scp=84880046089&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84880046089&partnerID=8YFLogxK

U2 - 10.1016/j.ijheh.2013.04.001

DO - 10.1016/j.ijheh.2013.04.001

M3 - Article

C2 - 23735462

AN - SCOPUS:84880046089

VL - 216

SP - 553

EP - 565

JO - International Journal of Hygiene and Environmental Health

JF - International Journal of Hygiene and Environmental Health

SN - 1438-4639

IS - 5

ER -