Age‐related difference in bioenergetics of lung and heart mitochondria from rats exposed to ozone

Zychlinski, Lech; Raska-Emery, Patricia; Balis, John U.; Montgomery, Mark R.

doi:10.1002/jbt.2570040408

Cited by 5 publications

(2 citation statements)

References 16 publications

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“…Lower redox status may also affect parameters directly related to vasomotor function, as NAD(P)H is a necessary cofactor for eNOS, cyclooxygenases, cytochromes P‐450, glutathione reductase, and NAD(P)H oxidase. Thus, the low GSH/GSSG ratio and pyridine nucleotide redox ratio evident in scorbutic HAEC are more reflective of oxidative stress conditions (49–51) than would be expected normally.…”

Section: Discussionmentioning

confidence: 95%

Vitamin C matters: increased oxidative stress in cultured human aortic endothelial cells without supplemental ascorbic acid

2002

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Because standard culture media for human aortic endothelial cells (HAEC) do not contain vitamin C, we hypothesized that HAEC may be under significant oxidative insult compared with the situation in vivo. To assess parameters of oxidative stress, intracellular vitamin C, glutathione (GSH), GSH/GSSG, and NAD(P)H/NAD(P)+ ratios, as well as oxidant appearance and oxidative damage, were measured in HAEC with or without vitamin C addition. The effect of vitamin C on eNOS activity was also determined. Results showed that HAEC without vitamin C treatment were essentially scorbutic. On addition of 100 mM vitamin C to the culture media, intracellular vitamin C levels increased and peaked at 6 h. A concomitant increase in the total GSH and the GSH/GSSG ratio was also observed; the NAD(P)H/NAD(P)+ ratio increased more slowly over the 24-h time course. Significantly lower (P <0.05) oxidant appearance and steady-state oxidative damage were also observed following vitamin C repletion. Vitamin C treatment increased eNOS activity by 600%. Thus, HAEC are scorbutic under normal culture conditions and exhibit higher oxidative stress than vitamin C repleted cells. Vitamin C supplementation should be considered when using cultured cells, especially when experimental endpoints are related to cellular redox status and eNOS activity.

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Section: Discussionmentioning

confidence: 95%

Vitamin C matters: increased oxidative stress in cultured human aortic endothelial cells without supplemental ascorbic acid

2002

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“…Subacute ozone exposure (0.8 ppm, for 10–20 days) to adult rats led to increased mitochondrial O 2 consumption in lung homogenates, increased mitochondrial number and mitochondrial respiratory activity in alveolar type II cells in the lung ( 81 ). Acute ozone exposure (3 ppm for 8 h) in both adult (4–6 months) and old rats (24–26 months) decreased mitochondrial respiration and mitochondrial O 2 consumption in isolated lung mitochondria ( 78 ). In young (3 weeks) and adult rats (6 months), a more chronic ozone exposure (0.5 ppm, 12 h, 7 days) did not affect lung mitochondrial O 2 consumption.…”

Section: Effect Of Ozone Exposure On Oxidative Stress and Mitochondrimentioning

confidence: 99%

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

et al. 2020

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Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by cigarette smoke and characterized by chronic inflammation, alveolar destruction (emphysema) and bronchiolar obstruction. Ozone is a gaseous constituent of urban air pollution resulting from photochemical interaction of air pollutants such as nitrogen oxide and organic compounds. While acute exposure to ozone induces airway hyperreactivity and neutrophilic inflammation, chronic ozone exposure in mice causes activation of oxidative pathways resulting in cell death and a chronic bronchial inflammation with emphysema, mimicking cigarette smoke-induced COPD. Therefore, the chronic exposure to ozone has become a model for studying COPD. We review recent data on mechanisms of ozone induced lung disease focusing on pathways causing chronic respiratory epithelial cell injury, cell death, alveolar destruction, and tissue remodeling associated with the development of chronic inflammation and AHR. The initial oxidant insult may result from direct effects on the integrity of membranes and organelles of exposed epithelial cells in the airways causing a stress response with the release of mitochondrial reactive oxygen species (ROS), DNA, and proteases. Mitochondrial ROS and mitochondrial DNA activate NLRP3 inflammasome and the DNA sensors cGAS and STING accelerating cell death pathways including caspases with inflammation enhancing alveolar septa destruction, remodeling, and fibrosis. Inhibitors of mitochondrial ROS, NLRP3 inflammasome, DNA sensor, cell death pathways, and IL-1 represent novel therapeutic targets for chronic airways diseases underlined by oxidative stress.

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Age-Specific Difference in Pulmonary Cellular Injury and Mitochondrial Damage

Tuggle

Fanucchi

2014

Mitochondrial Function in Lung Health and Disease

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Age‐related difference in bioenergetics of lung and heart mitochondria from rats exposed to ozone

Cited by 5 publications

References 16 publications

Vitamin C matters: increased oxidative stress in cultured human aortic endothelial cells without supplemental ascorbic acid

Vitamin C matters: increased oxidative stress in cultured human aortic endothelial cells without supplemental ascorbic acid

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

Age-Specific Difference in Pulmonary Cellular Injury and Mitochondrial Damage

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