Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM<sub>10</sub>) Exposure in Lung Mitochondria

Delgado-Buenrostro, Norma L.; Freyre-Fonseca, Verónica; Cuéllar, Claudia María García; Sánchez-Pérez, Yesennia; Gutiérrez-Cirlos, Emma Berta; Cabellos-Avelar, Tecilli; Orozco-Ibarra, Marisol; Pedraza‐Chaverrí, José; Chirino, Yolanda I.

doi:10.1177/0192623312463784

Cited by 12 publications

(5 citation statements)

References 50 publications

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“…With the extension of exposure time, metabolic activity decreased, especially in cultures treated with the highest concentration of both PM forms, mainly due to increased cell mortality, and thus decreased cell number in the cultures, as detected using CV staining. These changes may be related to PM-induced disruption of mitochondrial structure and function [ 48 ] and increased ROS synthesis and oxidative stress [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Metabolic Response of RAW 264.7 Macrophages to Exposure to Crude Particulate Matter and a Reduced Content of Organic Matter

Jankowska-Kieltyka

Román

Mikrut

et al. 2021

Toxics

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Exposure to air pollution from various airborne particulate matter (PM) is regarded as a potential health risk. Airborne PM penetrates the lungs, where it is taken up by macrophages, what results in macrophage activation and can potentially lead to negative consequences for the organism. In the present study, we assessed the effects of direct exposure of RAW 264.7 macrophages to crude PM (NIST1648a) and to a reduced content of organic matter (LAp120) for up to 72 h on selected parameters of metabolic activity. These included cell viability and apoptosis, metabolic activity and cell number, ROS synthesis, nitric oxide (NO) release, and oxidative burst. The results indicated that both NIST1648a and LAp120 negatively influenced the parameters of cell viability and metabolic activity due to increased ROS synthesis. The negative effect of PM was concentration-dependent; i.e., it was the most pronounced for the highest concentration applied. The impact of PM also depended on the time of exposure, so at respective time points, PM induced different effects. There were also differences in the impact of NIST1648a and LAp120 on almost all parameters tested. The negative effect of LAp120 was more pronounced, what appeared to be associated with an increased content of metals.

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Section: Discussionmentioning

confidence: 99%

Metabolic Response of RAW 264.7 Macrophages to Exposure to Crude Particulate Matter and a Reduced Content of Organic Matter

Jankowska-Kieltyka

Román

Mikrut

et al. 2021

Toxics

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“…Both PM 10 and PM 2.5 can penetrate cells and damage the mitochondria, including disruption of structure and function and altered mtDNA copy number (mtDNAcn) in different tissues. (24)(25)(26)(27) For example, in a study of mice, PM 2.5 exposure induced insulin resistance and decreased mitochondrial count in visceral adipose tissue. (26) On the other hand, individual exposures to PM 10 and coarse particles (PM 10 -PM 1 ) showed higher mtDNAcn (24), which may be a compensatory mechanism against damaged mitochondria upon PM exposure.…”

Section: Introductionmentioning

confidence: 99%

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

Breton

Song

Xiao³

et al. 2019

Mitochondrion

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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.

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“…For example, nitric oxide donors to the mitochondria (mediated by S-nitrosates thiol proteins) during ischemia inhibit O 2 consumption [18]. Abnormal lung bioenergetics has been also reported in smokers (especially in patients with chronic obstructive lung disease and down-regulation of prohibitin-1) and with exposures to particulate matters of aerodynamic diameters of ≤10 μm [19,20]. …”

Section: Discussionmentioning

confidence: 99%

Lung tissue bioenergetics and caspase activity in rodents

et al. 2013

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BackgroundThis study aimed to establish a suitable in vitro system for investigating effects of respiratory pathogens and toxins on lung tissue bioenergetics (cellular respiration and ATP content) and caspase activity. Wistar rats and C57Bl/6 mice were anesthetized by sevoflurane inhalation. Lung fragments were then collected and incubated at 37°C in a continuously gassed (with 95% O2:5% CO2) Minimal Essential Medium (MEM) or Krebs-Henseleit buffer. Phosphorescence O2 analyzer that measured dissolved O2 concentration as a function of time was used to monitor the rate of cellular mitochondrial O2 consumption. Cellular ATP content was measured using the luciferin/luciferase system. The caspase-3 substrate N-acetyl-asp-glu-val-asp-7-amino-4-methylcoumarin (Ac-DEVD-AMC) was used to monitor intracellular caspase activity; cleaved AMC moieties (reflecting caspase activity) were separated on HPLC and detected by fluorescence. Lung histology and immunostaining with anti-cleaved caspase-3 antibody were also performed.ResultsFor Wistar rats, the values of kc and ATP for 0 < t ≤ 7 h (mean ± SD) were 0.15 ± 0.02 μM O2 min-1 mg-1 (n = 18, coefficient of variation, Cv = 13%) and 131 ± 69 pmol mg-1 (n = 16, Cv = 53%), respectively. The AMC peak areas remained relatively small despite a ~5-fold rise over 6 h. Good tissue preservation was evident despite time-dependent increases in apoptotic cells. Lung tissue bioenergetics, caspase activity and structure were deleterious in unoxygenated or intermittently oxygenated solutions. Incubating lung tissue in O2 depleted MEM for 30 min or anesthesia by urethane had no effect on lung bioenergetics, but produced higher caspase activity.ConclusionsLung tissue bioenergetics and structure could be maintained in vitro in oxygenated buffer for several hours and, thus, used as biomarkers for investigating respiratory pathogens or toxins.

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Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM₁₀) Exposure in Lung Mitochondria

Cited by 12 publications

References 50 publications

Metabolic Response of RAW 264.7 Macrophages to Exposure to Crude Particulate Matter and a Reduced Content of Organic Matter

Metabolic Response of RAW 264.7 Macrophages to Exposure to Crude Particulate Matter and a Reduced Content of Organic Matter

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

Lung tissue bioenergetics and caspase activity in rodents

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Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM10) Exposure in Lung Mitochondria

Cited by 12 publications

References 50 publications

Metabolic Response of RAW 264.7 Macrophages to Exposure to Crude Particulate Matter and a Reduced Content of Organic Matter

Metabolic Response of RAW 264.7 Macrophages to Exposure to Crude Particulate Matter and a Reduced Content of Organic Matter

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

Lung tissue bioenergetics and caspase activity in rodents

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Resources

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Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM₁₀) Exposure in Lung Mitochondria