Effects of airborne pollutants on mitochondrial DNA Methylation

Byun, Hyang‐Min; Panni, Tommaso; Motta, Valeria; Hou, Lifang; Nordio, Francesco; Apostoli, Pietro; Bertazzi, Pier Alberto; Baccarelli, Andrea

doi:10.1186/1743-8977-10-18

Cited by 178 publications

(146 citation statements)

References 37 publications

(46 reference statements)

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“…Our group previously reported that blood platelet mtDNA methylation levels are higher in CVD patients compared with healthy persons 12. Possibly because of the use of a single blood cell type (platelets), the observed differences in mtDNA methylation between CVD patients and healthy persons were relatively larger (20%) than other studies that have used mixed cell–type populations, such as buffy coat 25.…”

Section: Discussionmentioning

confidence: 73%

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Effects of Air Pollution and Blood Mitochondrial DNA Methylation on Markers of Heart Rate Variability

Byun

Colicino

Trevisi

et al. 2016

JAHA

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BackgroundThe mitochondrion is the primary target of oxidative stress in response to exogenous environments. Mitochondrial DNA (mtDNA) is independent from nuclear DNA and uses separate epigenetic machinery to regulate mtDNA methylation. The mtDNA damage induced by oxidative stress can cause mitochondrial dysfunction and is implicated in human diseases; however, mtDNA methylation has been largely overlooked in environmental studies relating to human disease. The purpose of this study was to examine the association between exposure to fine metal‐rich particulates (particulate matter <2.5 µm in diameter [PM 2.5]) from welding in a boilermaker union and blood mtDNA methylation in relation to heart rate variability.Methods and ResultsForty‐eight healthy men were recruited on multiple sampling cycles at the Boilermaker Union Local 29, located in Quincy, Massachusetts. We measured personal PM 2.5 in the background ambient environment. We measured blood mtDNA methylation in the mtDNA promoter (D‐loop) and genes essential for ATP synthesis (MT‐TF and MT‐RNR1) by bisulfite pyrosequencing. All analyses were adjusted for demographics, type of job, season, welding‐work day, and mtDNA methylation experimental batch effect. The participants’ PM 2.5 exposure was significantly higher after a welding‐work day (mean 0.38 mg/m3) than the background personal level (mean 0.15 mg/m3, P<0.001). Blood mtDNA methylation in the D‐loop promoter was associated with PM 2.5 levels (β=−0.99%, SE=0.41, P=0.02). MT‐TF and MT‐RNR1 methylation was not associated with PM 2.5 exposure (β=0.10%, SE=0.45, P=0.82). Interaction of PM 2.5 exposure levels and D‐loop promoter methylation was significantly associated with markers of heart rate variability.ConclusionsBlood mtDNA methylation levels were negatively associated with PM 2.5 exposure and modified the adverse relationships between PM 2.5 exposure and heart rate variability outcomes.

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Section: Discussionmentioning

confidence: 73%

“…Next, 1 µL of converted DNA was used for polymerase chain reaction (PCR) amplification using GoTaq Hot Start polymerase (Promega). PCR conditions and primer sequences for mitochondrial assays have been described previously 12. Pyrosequencing was performed using the PSQ Q96 MD pyrosequencing system (Qiagen), as described previously.…”

Section: Methodsmentioning

confidence: 99%

Effects of Air Pollution and Blood Mitochondrial DNA Methylation on Markers of Heart Rate Variability

Byun

Colicino

Trevisi

et al. 2016

JAHA

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“…Alterations in mitochondrial DNA methylation have been demonstrated in cardiovascular disease 51 and in response to environmental exposures. 52,53 It has been speculated that such epigenetic changes may give rise to the altered mitochondrial function observed in drug addiction. 14 However, our study did not identify differential methylation of mitochondrial genes in response to morphine induction.…”

Section: Discussionmentioning

confidence: 99%

The effect of morphine upon DNA methylation in ten regions of the rat brain

Barrow

Byun

et al. 2017

Epigenetics

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A and Guo, L (2017) The effect of morphine upon DNA methylation in ten regions of the rat brain. Epigenetics, 12 (12 AbstractMorphine is one of the most effective analgesics in medicine. However, its use is associated with the development of tolerance and dependence. Recent studies demonstrating epigenetic changes in the brain after exposure to opiates have provided insight into mechanisms possibly underlying addiction. In this study, we sought to identify epigenetic changes in ten regions of the rat brain following acute and chronic morphine exposure. We analyzed DNA methylation of six nuclear-encoded genes implicated in brain function (Bdnf, Comt, Il1b, Il6, Nr3c1 and Tnf) and three mitochondrially-encoded genes (Mtco1, Mtco2 and Mtco3), and measured global 5-methylcytosine (5-mc) and 5-hydroxymethylcytosine (5-hmc) levels. We observed differential methylation of Bdnf and Il6 in the pons, Nr3c1 in the cerebellum, and Il1b in the hippocampus in response to acute morphine exposure (all p<0.05). Chronic exposure was associated with differential methylation of Bdnf and Comt in the pons, Nr3c1 in the hippocampus and Il1b in the medulla oblongata (all p<0.05). Global 5-mc levels significantly decreased in the superior colliculus following both acute and chronic morphine exposure, and increased in the hypothalamus following chronic exposure. Chronic exposure was also associated with significantly increased global 5-hmc levels in the cerebral cortex, hippocampus and hypothalamus, but significantly decreased in the midbrain. Our results demonstrate, for the first time, highly localized epigenetic changes in the rat brain following acute and chronic morphine exposure. Further work is required to elucidate the potential role of these changes in the formation of tolerance and dependence.

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“…In recent years, researchers are finding it worthy to investigate potential links between PM 2.5 exposure and adverse birth outcomes (Slama et al, 2008;Dadvand et al, 2013), epigenetic alteration (Baccarelli et al, 2008;Salam et al, 2012;Byun et al, 2013;Hou et al, 2013) infant mortality (Woodruff et al, 1997;Lipfert et al, 2000;Dales et al, 2004;Glinianaia et al, 2004) atherosclerosis (Araujo et al, 2008;Araujo, 2011;Kaufman, 2011), stroke (Brook, 2008;Brook andRajagopalan, 2009, 2012;Maheswaran et al, 2010Maheswaran et al, , 2012, rheumatic autoimmune disease (Zeft et Table 1. Particulate matter and health outcomes for PM 10 , PM 2.5 and ultrafine particles (UFPs).…”

Section: Introductionmentioning

confidence: 99%

Estimating the global abundance of ground level presence of particulate matter (PM2.5)

et al. 2014

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Abstract. With the increasing awareness of the health impacts of particulate matter, there is a growing need to comprehend the spatial and temporal variations of the global abundance of ground level airborne particulate matter with a diameter of 2.5 microns or less (PM 2.5). Here we use a suite of remote sensing and meteorological data products together with groundbased observations of particulate matter from 8,329 measurement sites in 55 countries taken 1997-2014 to train a machinelearning algorithm to estimate the daily distributions of PM 2.5 from 1997 to the present. In this first paper of a series, we present the methodology and global average results from this period and demonstrate that the new PM 2.5 data product can reliably represent global observations of PM 2.5 for epidemiological studies.

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Effects of airborne pollutants on mitochondrial DNA Methylation

Cited by 178 publications

References 37 publications

Effects of Air Pollution and Blood Mitochondrial DNA Methylation on Markers of Heart Rate Variability

Effects of Air Pollution and Blood Mitochondrial DNA Methylation on Markers of Heart Rate Variability

The effect of morphine upon DNA methylation in ten regions of the rat brain

Estimating the global abundance of ground level presence of particulate matter (PM2.5)

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