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Updated: May 15, 2026

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Urban PM2.5 activates GAPDH and induces RBC damage in COPD patients
Araceli Montoya-Estrada1, Yessica D Torres-Ramos, Arturo Flores-Pliego
1Departamento de Bioquimica y Biologia Molecular, Instituto Nacional De Perinatologia, Isidro Espinosa de los Reyes (INPerIER), Montes Urales, Mexico.
Abstract:
During Chronic Obstructive Pulmonary Disease (COPD) progression, the intracellular antioxidant defence in RBCs must preserve the integrity of the plasmalemma through NADPH+ generation to obtain a sufficient number of reduced non-protein SH-groups. Here, we studied the activities of enzymes in RBCs that are related to glutathione metabolism under conditions of increasing oxidative stress, which are associated with COPD progression, by increasing cellular damage in vitro with PM2.5, a ROS generator. The study included 43 patients, who were separated according to their GOLD classification into moderate and severe groups, along with 11 healthy volunteers (HV). Blood samples were analysed for G6PD, GAPDH, GPx, and GR. The results showed significant decreases in the oxidation of the G6PD, GR and GPx proteins, resulting in decreased enzymatic activity. By contrast, an increase (p<0.05) in GAPDH was observed, suggesting a pool of ATP on the membrane. However, it is evident that RBCs are damaged during the progression of COPD, although their integrity is preserved, and they retain limited function, thus allowing patient survival without haemolysis.
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