Myocardial Mitochondrial Injury Induced by Pulmonary Exposure to Particulate Matter in Rats

Abstract

Exposure to air pollution has been associated with acute myocardial ischemia, impaired myocardrial function, and ST-segment depression. Particulate matter (PM)-associated metals, especially vanadium and nickel, have been implicated in observed cardiovascular impairments. We aimed to assess the effect of single intratracheal pulmonary exposure to vanadium-rich respirable oil combustion PM (HP-10) on the intrinsic myocardial ischemic tolerance and mitochondrial integrity in rats. The authors subjected isolated heart tissue slices derived from saline or PM-exposed rats to low glucose low oxygen induced ischemia followed by oxygenated condition with glucose supplementation. Mitochondrial structural integrity was determined by TEM (transmission electron microscopy) and functionality by the 3-(4, 5 dimethylthiazol-2yl)-2, 5 diphenyltetrazolium bromide (MTT) assay. Rats exposed to PM exhibited no apparent inhibition of mitochondrial dehydrogenase activity in oxygenated conditions at 24 or 48 hr post-PM exposure. However, in conditions of simulated ischemia/reoxygenation, these heart slices showed a delayed but consistent and significant decrease in dehydrogenase activity compared to controls at 48 hr after exposure to PM. Electron microscopy revealed significant myocardial mitochondrial injury upon exposure to PM characterized by mitochondrial swelling and fusion. The authors conclude that exposure to soluble vanadium-rich PM induces mitochondrial functional impairment and structural abnormality, which compromises mitochondrial respiration and results in decreased tolerance to ischemia/reoxygenation in rats.

Ultrafine Particulate Matter Increases Cardiac Ischemia/Reperfusion Injury via Mitochondrial Permeability Transition Pore

“…Given the multiple hypotheses regarding potential mechanisms that drive UFP to exacerbate cardiovascular disease, including inflammation, oxidative stress, autonomic dysfunction, or mitochondrial dysfunction (9), we hypothesized that UFP was able to exacerbate cardiac ischemia/reperfusion injury by promoting the opening of the mPTP. Our study supports previous studies linking detrimental cardiovascular endpoints with exposure to UFP (34, 35), and demonstrates a novel target of UFP toxicity within the mitochondria (20, 36), the mPTP. These findings are important for two reasons: 1) these data demonstrate the ability for UFP to exacerbate cardiac injury in the face of a secondary stressor, i.e .…”

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

“…An inadequate energy supply to heart tissue after exposure to PM 2.5 may be through several feasible mechanisms: (1) an increased demand for energy could be induced by an increased heart rate and arrhythmia triggered by PM 2.5 exposure [97]; (2) insufficient blood perfusion to the heart may result from defective vasomotor regulation [98,99] resulting in ineffective diastole from secondary tachyarrhythmia; and (3) acute damage to the mitochondrial respiratory chain will result in reduced production of adenosine triphosphate [83], which serves as a direct source of energy for heart tissue, resulting in an insufficient energy supply to the heart and a diminished threshold for myocardial ischemia [84,100]. The combined effect of increased consumption and an inadequate supply of energy will promote the onset and development of ACS.…”

Comparative cardiopulmonary toxicity of exhausts from soy-based biofuels and diesel in healthy and hypertensive rats

“…Numerous toxicological studies have examined cardiopulmonary health effects of a variety of ambient gas and particulate pollutants such as ozone, real-time ambient particulate matter (PM) and source-specific pollutants, including power plant combustion collected PM, diesel exhaust (DE), nano materials, asbestos and even biofuel exhausts (Brito et al, 2010; Golomb at al., 2012; Kodavanti et al, 2000, 2005, 2011, 2013; Shannahan et al, 2012; Tong et al, 2009). Pulmonary injury from inhalation of these pollutants could be influenced by chemical composition, physical characteristics, surface reactivity, the level of exposure, the method of exposure, the lung deposition of specific pollutant, longevity of exposure and more importantly the animal species and strain related factors.…”