Environmental Chemical Exposures and Mitochondrial Dysfunction: a Review of Recent Literature.

Environmental chemicals Heteroplasmy Mitochondrial dysfunction Oxidative stress mtDNA

Journal

Current environmental health reports
ISSN: 2196-5412
Titre abrégé: Curr Environ Health Rep
Pays: Switzerland
ID NLM: 101629387

Informations de publication

Date de publication:
Dec 2022
Historique:
accepted: 20 07 2022
pubmed: 29 7 2022
medline: 15 12 2022
entrez: 28 7 2022
Statut: ppublish

Résumé

Mitochondria play various roles that are important for cell function and survival; therefore, significant mitochondrial dysfunction may have chronic consequences that extend beyond the cell. Mitochondria are already susceptible to damage, which may be exacerbated by environmental exposures. Therefore, the aim of this review is to summarize the recent literature (2012-2022) looking at the effects of six ubiquitous classes of compounds on mitochondrial dysfunction in human populations. The literature suggests that there are a number of biomarkers that are commonly used to identify mitochondrial dysfunction, each with certain advantages and limitations. Classes of environmental toxicants such as polycyclic aromatic hydrocarbons, air pollutants, heavy metals, endocrine-disrupting compounds, pesticides, and nanomaterials can damage the mitochondria in varied ways, with changes in mtDNA copy number and measures of oxidative damage the most commonly measured in human populations. Other significant biomarkers include changes in mitochondrial membrane potential, calcium levels, and ATP levels. This review identifies the biomarkers that are commonly used to characterize mitochondrial dysfunction but suggests that emerging mitochondrial biomarkers, such as cell-free mitochondria and blood cardiolipin levels, may provide greater insight into the impacts of exposures on mitochondrial function. This review identifies that the mtDNA copy number and measures of oxidative damage are commonly used to characterize mitochondrial dysfunction, but suggests using novel approaches in addition to well-characterized ones to create standardized protocols. We identified a dearth of studies on mitochondrial dysfunction in human populations exposed to metals, endocrine-disrupting chemicals, pesticides, and nanoparticles as a gap in knowledge that needs attention.

Identifiants

pubmed: 35902457
doi: 10.1007/s40572-022-00371-7
pii: 10.1007/s40572-022-00371-7
pmc: PMC9729331
mid: NIHMS1851547
doi:

Types de publication

Journal Article Review Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

631-649

Subventions

Organisme : NIEHS NIH HHS
ID : R00 ES030749
Pays : United States

Informations de copyright

© 2022. The Author(s).

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Auteurs

Aalekhya Reddam (A)

Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th St, New York, NY, 10032, USA.

Sarah McLarnan (S)

Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th St, New York, NY, 10032, USA.

Allison Kupsco (A)

Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th St, New York, NY, 10032, USA. ak4181@cumc.columbia.edu.

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