Effects of air pollution on mitochondrial function, mitochondrial DNA methylation, and mitochondrial peptide expression.

Autor: Breton CV; Department of Preventive Medicine, Keck School of Medicine USC, 2001 N Soto St., Los Angeles, CA 90032, United States of America. Electronic address: breton@usc.edu., Song AY; Department of Preventive Medicine, Keck School of Medicine USC, 2001 N Soto St., Los Angeles, CA 90032, United States of America., Xiao J; USC Leonard School of Gerontology, 3715 McClintock Ave, Los Angeles, CA 90089, United States of America., Kim SJ; USC Leonard School of Gerontology, 3715 McClintock Ave, Los Angeles, CA 90089, United States of America., Mehta HH; USC Leonard School of Gerontology, 3715 McClintock Ave, Los Angeles, CA 90089, United States of America., Wan J; USC Leonard School of Gerontology, 3715 McClintock Ave, Los Angeles, CA 90089, United States of America., Yen K; USC Leonard School of Gerontology, 3715 McClintock Ave, Los Angeles, CA 90089, United States of America., Sioutas C; USC Viterbi School of Engineering, 3620 South Vermont Ave, Los Angeles, CA 90089, United States of America., Lurmann F; Sonoma Technology, 1450 N. McDowell Blvd., Suite 200, Petaluma, CA 94954, United States of America., Xue S; Department of Preventive Medicine, Keck School of Medicine USC, 2001 N Soto St., Los Angeles, CA 90032, United States of America., Morgan TE; USC Leonard School of Gerontology, 3715 McClintock Ave, Los Angeles, CA 90089, United States of America., Zhang J; Nicholas School of the Enviroment, Duke University, 308 Research Drive LSRC, Durham, NC 27708, United States of America., Cohen P; USC Leonard School of Gerontology, 3715 McClintock Ave, Los Angeles, CA 90089, United States of America.
Jazyk: angličtina
Zdroj: Mitochondrion [Mitochondrion] 2019 May; Vol. 46, pp. 22-29. Date of Electronic Publication: 2019 Apr 10.
DOI: 10.1016/j.mito.2019.04.001
Abstrakt: Mitochondrial DNA is sensitive to damage by exogenous reactive oxygen sources, including traffic-related air pollution (TRAP). Given the important role for mitochondria in human disease, we hypothesized that prenatal air pollution exposure may be associated with mitochondrial dysfunction and that mitochondrial-derived peptides (MDPs) might protect against these effects. In in vitro studies, 24-hour exposure to nanoparticulate matter (nPM) increased oxidation of mtDNA, decreased mitochondrial consumption rate (OCR), and decreased mtDNAcn in SH-SY5Y cells. Addition of MDPs rescued these effects to varying degrees. Liver tissue taken from C57Bl/6 males exposed for 10 weeks to nPM had lower OCR, lower mtDNAcn and higher MDP levels, similar to in vitro studies. In newborn cord blood, MDP levels were positively associated with prenatal TRAP exposures. Moreover, DNA methylation of two distinct regions of the D-Loop in the mitochondria genome was associated with levels of several MDPs. Our in vitro and in vivo data indicate that TRAP can directly affect mitochondrial respiratory function and mtDNAcn. Treatment of cells with MDPs can counteract TRAP induced-effects. Lastly, we present evidence that suggests MDPs may be regulated in part by mitochondrial DNA methylation in humans.
(Copyright © 2019 Elsevier B.V. and Mitochondria Research Society. All rights reserved.)
Databáze: MEDLINE
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