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oapen-20.500.12657-491992021-11-23T13:57:12Z 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 bic Book Industry Communication::M Medicine::MJ Clinical & 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. 2021-06-02T10:09:15Z 2021-06-02T10:09:15Z 2017 chapter ONIX_20210602_10.5772/65364_313 https://library.oapen.org/handle/20.500.12657/49199 eng application/pdf n/a 52468.pdf InTechOpen 10.5772/65364 10.5772/65364 09f6769d-48ed-467d-b150-4cf2680656a1 FP7-PEOPLE-2012-ITN 315760 open access
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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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