Hydroxyl Radical Generation from Environmentally Persistent Free Radicals (EPFRs) in PM<sub>2.5</sub>

Gehling, William; Khachatryan, Lavrent; Dellinger, Barry

doi:10.1021/es401770y

Cited by 202 publications

(138 citation statements)

References 54 publications

(203 reference statements)

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“…PM 2.5 can produce reactive oxygen species (ROS) such as superoxide radical (O 2 -) and hydroxyl radical (-OH) in vitro, and aqueous suspension of ambient PM 2.5 may generate OH (Wu et al, 2012;Gehling et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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-Epidemiological studies have confirmed that ambient fine particulate matter (PM 2.5 ) exposure is associated with cardiovascular disease (CVD). However, the underlying mechanisms in PM 2.5 exposure-induced heart injury are largely unknown. It has been acknowledged that NADPH oxidase (Nox) 4 plays a critical role in CVD development. To investigate the acute effects of PM 2.5 on the mouse heart and the role of Nox4 in PM 2.5 exposure-induced cardiac injury, C57BL/6J mice were instilled with saline or 1.5, 3.0, 6.0 mg/kg BW PM 2.5 suspension for two weeks (five days per week). The levels of malondialdehyde (MDA), super oxide dismutase (SOD), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β in heart supernatants were determined using related kits. The expression of Nox4, p67 phox , p47 phox and p22 phox in heart tissue was evaluated by immunofluorescence staining or Western blotting, respectively. Protein levels of p53, Bax, Bcl-2 and Caspase-3 in the heart were examined using immunohistochemical staining and Western blotting. TUNEL assay was used to measure myocardial apoptosis. PM 2.5 exposure leads to obvious cardiac injury. PM 2.5 exposure increases MDA level and iNOS activity, and decreases activity of SOD in heart supernatants of mice. High levels of TNF-α and IL-1β in heart supernatants of mice with PM 2.5 instillation were determined. Nox4 and Noxassociated subunits such as p67 phox , p47 phox and p22 phox expression levels were increased in heart tissue of mice after PM 2.5 exposure. Additionally, PM 2.5 exposure causes myocardial apoptosis in the mouse heart. This study suggested that Nox4 is involved in PM 2.5 exposure-induced cardiac injury in mice.

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Section: Discussionmentioning

confidence: 99%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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“…and aqueous suspension of ambient PM 2.5 may generate . OH [34,35]. Under stress conditions, activities of anti-oxidative enzymes such as SOD may be inhibited, whereas excessive ROS are easy to attack the cell membrane and form MDA, which is a typical product of lipid peroxidation (LPO).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial damage: An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats

Kou

Geng

et al. 2015

Journal of Hazardous Materials

131

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“…4–7 Recent evidence demonstrates ROS is also generated from the redox cycling of environmentally persistent free radicals (EPFRs) from a model system in addition to EPFRs in PM 2.5 . 8–10 …”

Section: Introductionmentioning

confidence: 99%

Environmentally Persistent Free Radicals and Their Lifetimes in PM_2.5

Gehling

Dellinger²

2013

Environ. Sci. Technol.

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213

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For the first time, an expansive study into the concentration and extended decay behavior of environmentally persistent free radicals in PM2.5 was performed. Results from this study revealed three types of radical decay—a fast decay, slow decay, and no decay—following one of four decay patterns: a relatively fast decay exhibiting a 1/e lifetime of 1–21 days accompanied by a slow decay with a 1/e lifetime of 21–5028 days (47% of samples); a single slow decay including a 1/e lifetime of 4–2083 days (24% of samples); no decay (18% of samples); and a relatively fast decay displaying an average 1/e lifetime of 0.25–21 days followed by no decay (11% of samples). Phenol correlated well with the initial radical concentration and fast decay rate. Other correlations for common atmospheric pollutants (ozone, NOx, SO2, etc.) as well as meteorological conditions suggested photochemical processes impact the initial radical concentration and fast decay rate. The radical signal in PM2.5 was remarkably similar to semiquinones in cigarette smoke. Accordingly, radicals inhaled from PM2.5 were related to the radicals inhaled from smoking cigarettes, expressed as the number of equivalent cigarettes smoked. This calculated to 0.4–0.9 cigarettes per day for nonextreme air quality in the United States.

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Hydroxyl Radical Generation from Environmentally Persistent Free Radicals (EPFRs) in PM_2.5

Cited by 202 publications

References 54 publications

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Mitochondrial damage: An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats

Environmentally Persistent Free Radicals and Their Lifetimes in PM_2.5

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Hydroxyl Radical Generation from Environmentally Persistent Free Radicals (EPFRs) in PM2.5

Cited by 202 publications

References 54 publications

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Mitochondrial damage: An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats

Environmentally Persistent Free Radicals and Their Lifetimes in PM2.5

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Hydroxyl Radical Generation from Environmentally Persistent Free Radicals (EPFRs) in PM_2.5

Environmentally Persistent Free Radicals and Their Lifetimes in PM_2.5