About: Iron-rich air pollution nanoparticles: an unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress

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About: Iron-rich air pollution nanoparticles: an unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Iron-rich air pollution nanoparticles: an unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress
Creator	Ma, Calderón-Garcidueñas, L Calderón-Garcidueñas, Lilian González-Maciel, A Ma, L Maher, Barbara Reynoso-Robles, R Torres-Jardón, R
Source	Elsevier; Medline; PMC
abstract	Exposure to particulate air pollution is a major environmental risk factor for cardiovascular mortality and morbidity, on a global scale. Both acute and chronic cardiovascular impacts have so far been attributed to particulate-mediated oxidative stress in the lung and/or via ‘secondary’ pathways, including endothelial dysfunction, and inflammation. However, increasing evidence indicates the translocation of inhaled nanoparticles to major organs via the circulation. It is essential to identify the composition and intracellular targets of such particles, since these are likely to determine their toxicity and consequent health impacts. Of potential major concern is the abundant presence of iron-rich air pollution nanoparticles, emitted from a range of industry and traffic-related sources. Bioreactive iron can catalyse formation of damaging reactive oxygen species, leading to oxidative stress and cell damage or death. Here, we identify for the first time, in situ, that exogenous nanoparticles (∼15 – 40 nm diameter) within myocardial mitochondria of young, highly-exposed subjects are dominantly iron-rich, and co-associated with other reactive metals including aluminium and titanium. These rounded, electrodense nanoparticles (up to ∼ 10 x more abundant than in lower-pollution controls) are located within abnormal myocardial mitochondria (e.g. deformed cristae; ruptured membranes). Measurements of an oxidative stress marker, PrP(C) and an endoplasmic reticulum stress marker, GRP78, identify significant ventricular up-regulation in the highly-exposed vs lower-pollution controls. In shape/size/composition, the within-mitochondrial particles are indistinguishable from the iron-rich, combustion- and friction-derived nanoparticles prolific in roadside/urban environments, emitted from traffic/industrial sources. Incursion of myocardial mitochondria by inhaled iron-rich air pollution nanoparticles thus appears associated with mitochondrial dysfunction, and excess formation of reactive oxygen species through the iron-catalyzed Fenton reaction. Ventricular oxidative stress, as indicated by PrP(C) and GRP78 up-regulation, is evident even in children/young adults with minimal risk factors and no co-morbidities. These new findings indicate that myocardial iron overload resulting from inhalation of airborne, metal-rich nanoparticles is a plausible and modifiable environmental risk factor for cardiac oxidative stress and cardiovascular disease, on an international scale.
has issue date	2020-06-21(xsd:dateTime)
bibo:doi	10.1016/j.envres.2020.109816
bibo:pmid	32593898
has license	no-cc
sha1sum (hex)	aa2611c40c11d7b50b87222eaa4cfbc29a8b0301
schema:url	https://doi.org/10.1016/j.envres.2020.109816
resource representing a document's title	Iron-rich air pollution nanoparticles: an unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress
has PubMed Central identifier	PMC7306213
has PubMed identifier	32593898
schema:publication	Environ Res
resource representing a document's body	covid:aa2611c40c11d7b50b87222eaa4cfbc29a8b0301#body_text
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