Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems

Hypoxia-reoxygenation injury is a commonly used in vitro model of ischemia, which is useful to study the recovery processes following the hypoxic period. Hypoxia can be rapidly induced in vitro by replacing the culture atmosphere with hypoxic or anoxic gas mixture. Cellular injury mostly occurs as a...

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Päätekijät: Alves, Célia, Moreno, Teresa, Martins, V., Cruz Minguillón, María, Querol, Xavier, Eleftheriadis Luís Mendes, Konstantinos, de Miguel, Eladio
Aineistotyyppi: Online
Kieli:englanti
Julkaistu: InTechOpen 2021
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Linkit:ONIX_20210602_10.5772/65364_313
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author Alves, Célia
Moreno, Teresa
Martins, V.
Cruz Minguillón, María
Querol, Xavier
Eleftheriadis Luís Mendes, Konstantinos
de Miguel, Eladio
author_browse Alves, Célia
Cruz Minguillón, María
Eleftheriadis Luís Mendes, Konstantinos
Martins, V.
Moreno, Teresa
Querol, Xavier
de Miguel, Eladio
author_facet Alves, Célia
Moreno, Teresa
Martins, V.
Cruz Minguillón, María
Querol, Xavier
Eleftheriadis Luís Mendes, Konstantinos
de Miguel, Eladio
author_sort Alves, Célia
collection Directory of Open Access Books
description Hypoxia-reoxygenation injury is a commonly used in vitro model of ischemia, which is useful to study the recovery processes following the hypoxic period. Hypoxia can be rapidly induced in vitro by replacing the culture atmosphere with hypoxic or anoxic gas mixture. Cellular injury mostly occurs as a result of energetic failure in this model: the lack of oxygen blocks the mitochondrial respiration and anaerobic metabolism becomes the major source of high-energy molecules in the cells. In the absence of glucose, glycolysis and pentose phosphate pathway fail to suffice the cellular energy prerequisite and longer periods of oxygen-glucose deprivation (OGD) can completely deplete the cellular NAD+ and ATP pools. The lack of NAD+ results in severe metabolic suppression and predisposes the cells to other injury types. This includes oxidant-induced damage, since oxidative stress activates poly(ADP-ribose) polymerase (PARP) that further depletes the cellular NAD+ pool and leads to excessive cell death. The impaired mitochondrial respiration also leads to an increase in the mitochondrial membrane potential and augments the mitochondrial superoxide generation leading to oxidative stress. The above processes ultimately lead to necrotic cell death, but in certain cell types, mitochondrial damage can also trigger apoptosis.
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spelling doab-20.500.12854ir-702602024-03-31T22:44:30Z Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems Alves, Célia Moreno, Teresa Martins, V. Cruz Minguillón, María Querol, Xavier Eleftheriadis Luís Mendes, Konstantinos de Miguel, Eladio hypoxia-reoxygenation injury, poly(ADP-ribose) polymerase, energetic failure, mitochondrial dysfunction, oxidative stress thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJL Respiratory medicine Hypoxia-reoxygenation injury is a commonly used in vitro model of ischemia, which is useful to study the recovery processes following the hypoxic period. Hypoxia can be rapidly induced in vitro by replacing the culture atmosphere with hypoxic or anoxic gas mixture. Cellular injury mostly occurs as a result of energetic failure in this model: the lack of oxygen blocks the mitochondrial respiration and anaerobic metabolism becomes the major source of high-energy molecules in the cells. In the absence of glucose, glycolysis and pentose phosphate pathway fail to suffice the cellular energy prerequisite and longer periods of oxygen-glucose deprivation (OGD) can completely deplete the cellular NAD+ and ATP pools. The lack of NAD+ results in severe metabolic suppression and predisposes the cells to other injury types. This includes oxidant-induced damage, since oxidative stress activates poly(ADP-ribose) polymerase (PARP) that further depletes the cellular NAD+ pool and leads to excessive cell death. The impaired mitochondrial respiration also leads to an increase in the mitochondrial membrane potential and augments the mitochondrial superoxide generation leading to oxidative stress. The above processes ultimately lead to necrotic cell death, but in certain cell types, mitochondrial damage can also trigger apoptosis. 2021-02-10T12:58:18Z 2021-06-02T10:09:15Z 2017 chapter ONIX_20210602_10.5772/65364_313 https://library.oapen.org/handle/20.500.12657/49199 https://directory.doabooks.org/handle/20.500.12854/70260 eng open access image/jpeg image/jpeg n/a n/a https://library.oapen.org/bitstream/20.500.12657/49199/1/52468.pdf https://library.oapen.org/bitstream/20.500.12657/49199/1/52468.pdf InTechOpen 10.5772/65364 10.5772/65364 035ecc65-6737-43cf-a13a-6bdf67ce01f4 open access
spellingShingle hypoxia-reoxygenation injury, poly(ADP-ribose) polymerase, energetic failure, mitochondrial dysfunction, oxidative stress
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJL Respiratory medicine
Alves, Célia
Moreno, Teresa
Martins, V.
Cruz Minguillón, María
Querol, Xavier
Eleftheriadis Luís Mendes, Konstantinos
de Miguel, Eladio
Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems
title Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems
title_full Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems
title_fullStr Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems
title_full_unstemmed Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems
title_short Chapter Characterisation of Airborne Particulate Matter in Different European Subway Systems
title_sort chapter characterisation of airborne particulate matter in different european subway systems
topic hypoxia-reoxygenation injury, poly(ADP-ribose) polymerase, energetic failure, mitochondrial dysfunction, oxidative stress
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJL Respiratory medicine
topic_facet hypoxia-reoxygenation injury, poly(ADP-ribose) polymerase, energetic failure, mitochondrial dysfunction, oxidative stress
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJL Respiratory medicine
url ONIX_20210602_10.5772/65364_313
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