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Decreased mitochondrial DNA content in association with exposure to polycyclic aromatic hydrocarbons in house dust during wintertime: from a population enquiry to cell culture.

Pieters N, Koppen G, Smeets K, Napierska D, Plusquin M, De Prins S, Van De Weghe H, Nelen V, Cox B, Cuypers A, Hoet P, Schoeters G, Nawrot TS - PLoS ONE (2013)

Bottom Line: During summer months no association was found between mtDNA content and PAH concentration.The ability of benzo(a)pyrene (range 0 µM to 500 µM) to lower mtDNA content was confirmed in vitro in human TK6 cells.Based on these findings, mtDNA content can be a target of PAH toxicity in humans.

View Article: PubMed Central - PubMed

Affiliation: Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium.

ABSTRACT
Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants that are formed in combustion processes. At the cellular level, exposure to PAHs causes oxidative stress and/or some of it congeners bind to DNA, which may interact with mitochondrial function. However, the influence of these pollutants on mitochondrial DNA (mtDNA) content remains largely unknown. We determined whether indoor exposure to PAHs is associated with mitochondrial damage as represented by blood mtDNA content. Blood mtDNA content (ratio mitochondrial/nuclear DNA copy number) was determined by real-time qPCR in 46 persons, both in winter and summer. Indoor PAH exposure was estimated by measuring PAHs in sedimented house dust, including 6 volatile PAHs and 8 non-volatile PAHs. Biomarkers of oxidative stress at the level of DNA and lipid peroxidation were measured. In addition to the epidemiologic enquiry, we exposed human TK6 cells during 24 h at various concentrations (range: 0 to 500 µM) of benzo(a)pyrene and determined mtDNA content. Mean blood mtDNA content averaged (± SD) 0.95 ± 0.185. The median PAH content amounted 554.1 ng/g dust (25(th)-75(th) percentile: 390.7-767.3) and 1385 ng/g dust (25(th)-75(th) percentile: 1000-1980) in winter for volatile and non-volatile PAHs respectively. Independent for gender, age, BMI and the consumption of grilled meat or fish, blood mtDNA content decreased by 9.85% (95% CI: -15.16 to -4.2; p = 0.002) for each doubling of non-volatile PAH content in the house dust in winter. The corresponding estimate for volatile PAHs was -7.3% (95% CI: -13.71 to -0.42; p = 0.04). Measurements of oxidative stress were not correlated with PAH exposure. During summer months no association was found between mtDNA content and PAH concentration. The ability of benzo(a)pyrene (range 0 µM to 500 µM) to lower mtDNA content was confirmed in vitro in human TK6 cells. Based on these findings, mtDNA content can be a target of PAH toxicity in humans.

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Median amount of each PAH-component in winter and in summer (ng/g dust).PHE, phenanthrene; FLU, fluoranthene; PYR, pyrene; BaA, benzo(a)anthracene; CHR, chrysene; BbF, benzo(b)fluoranthene; BkF, benzo(k)fluoranthene; BAP, benzo(a)pyrene; PIY, indenol(1,2,3-cd)pyrene; BPE, benzo(g,h,i)perylene; NAP, naphthalene; ACN, acenaphtylene; ACE, acenapthnene; FLE, fluorene; ANT, anthracene; dBA, dibenzo(a,h)anthracene.
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pone-0063208-g001: Median amount of each PAH-component in winter and in summer (ng/g dust).PHE, phenanthrene; FLU, fluoranthene; PYR, pyrene; BaA, benzo(a)anthracene; CHR, chrysene; BbF, benzo(b)fluoranthene; BkF, benzo(k)fluoranthene; BAP, benzo(a)pyrene; PIY, indenol(1,2,3-cd)pyrene; BPE, benzo(g,h,i)perylene; NAP, naphthalene; ACN, acenaphtylene; ACE, acenapthnene; FLE, fluorene; ANT, anthracene; dBA, dibenzo(a,h)anthracene.

Mentions: The non-volatile PAH en volatile PAH concentrations in house dust were higher in the winter period than in summer (table 3). The 3- and 4-ring phenanthrene, fluorene, pyrene (resp. ca. 12%, 17% and 12%) and the 4- and 5-ring structures chrysene and benzo[b]fluoranthene (resp. ca. 14% and 10%), made up the most important contribution to the measured PAH concentration in house dust (Figure 1). Sixteen participants (35%) lived in a house with regular use of a woodstove in winter. The volatile PAH, non-volatile PAH and benzo(a)pyrene concentration tended to be higher, although not significantly, in houses with this heating device compared to houses with another heating source in winter (data not shown).


Decreased mitochondrial DNA content in association with exposure to polycyclic aromatic hydrocarbons in house dust during wintertime: from a population enquiry to cell culture.

Pieters N, Koppen G, Smeets K, Napierska D, Plusquin M, De Prins S, Van De Weghe H, Nelen V, Cox B, Cuypers A, Hoet P, Schoeters G, Nawrot TS - PLoS ONE (2013)

Median amount of each PAH-component in winter and in summer (ng/g dust).PHE, phenanthrene; FLU, fluoranthene; PYR, pyrene; BaA, benzo(a)anthracene; CHR, chrysene; BbF, benzo(b)fluoranthene; BkF, benzo(k)fluoranthene; BAP, benzo(a)pyrene; PIY, indenol(1,2,3-cd)pyrene; BPE, benzo(g,h,i)perylene; NAP, naphthalene; ACN, acenaphtylene; ACE, acenapthnene; FLE, fluorene; ANT, anthracene; dBA, dibenzo(a,h)anthracene.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3643917&req=5

pone-0063208-g001: Median amount of each PAH-component in winter and in summer (ng/g dust).PHE, phenanthrene; FLU, fluoranthene; PYR, pyrene; BaA, benzo(a)anthracene; CHR, chrysene; BbF, benzo(b)fluoranthene; BkF, benzo(k)fluoranthene; BAP, benzo(a)pyrene; PIY, indenol(1,2,3-cd)pyrene; BPE, benzo(g,h,i)perylene; NAP, naphthalene; ACN, acenaphtylene; ACE, acenapthnene; FLE, fluorene; ANT, anthracene; dBA, dibenzo(a,h)anthracene.
Mentions: The non-volatile PAH en volatile PAH concentrations in house dust were higher in the winter period than in summer (table 3). The 3- and 4-ring phenanthrene, fluorene, pyrene (resp. ca. 12%, 17% and 12%) and the 4- and 5-ring structures chrysene and benzo[b]fluoranthene (resp. ca. 14% and 10%), made up the most important contribution to the measured PAH concentration in house dust (Figure 1). Sixteen participants (35%) lived in a house with regular use of a woodstove in winter. The volatile PAH, non-volatile PAH and benzo(a)pyrene concentration tended to be higher, although not significantly, in houses with this heating device compared to houses with another heating source in winter (data not shown).

Bottom Line: During summer months no association was found between mtDNA content and PAH concentration.The ability of benzo(a)pyrene (range 0 µM to 500 µM) to lower mtDNA content was confirmed in vitro in human TK6 cells.Based on these findings, mtDNA content can be a target of PAH toxicity in humans.

View Article: PubMed Central - PubMed

Affiliation: Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium.

ABSTRACT
Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants that are formed in combustion processes. At the cellular level, exposure to PAHs causes oxidative stress and/or some of it congeners bind to DNA, which may interact with mitochondrial function. However, the influence of these pollutants on mitochondrial DNA (mtDNA) content remains largely unknown. We determined whether indoor exposure to PAHs is associated with mitochondrial damage as represented by blood mtDNA content. Blood mtDNA content (ratio mitochondrial/nuclear DNA copy number) was determined by real-time qPCR in 46 persons, both in winter and summer. Indoor PAH exposure was estimated by measuring PAHs in sedimented house dust, including 6 volatile PAHs and 8 non-volatile PAHs. Biomarkers of oxidative stress at the level of DNA and lipid peroxidation were measured. In addition to the epidemiologic enquiry, we exposed human TK6 cells during 24 h at various concentrations (range: 0 to 500 µM) of benzo(a)pyrene and determined mtDNA content. Mean blood mtDNA content averaged (± SD) 0.95 ± 0.185. The median PAH content amounted 554.1 ng/g dust (25(th)-75(th) percentile: 390.7-767.3) and 1385 ng/g dust (25(th)-75(th) percentile: 1000-1980) in winter for volatile and non-volatile PAHs respectively. Independent for gender, age, BMI and the consumption of grilled meat or fish, blood mtDNA content decreased by 9.85% (95% CI: -15.16 to -4.2; p = 0.002) for each doubling of non-volatile PAH content in the house dust in winter. The corresponding estimate for volatile PAHs was -7.3% (95% CI: -13.71 to -0.42; p = 0.04). Measurements of oxidative stress were not correlated with PAH exposure. During summer months no association was found between mtDNA content and PAH concentration. The ability of benzo(a)pyrene (range 0 µM to 500 µM) to lower mtDNA content was confirmed in vitro in human TK6 cells. Based on these findings, mtDNA content can be a target of PAH toxicity in humans.

Show MeSH
Related in: MedlinePlus