Hypocapnic Alkalosis Enhances Oxidant-induced Apoptosis of Human Alveolar Epithelial Type II Cells
Autor: | Katsuya Mikawa, Takuyo Misumi, Toshihiro Ando, Kahoru Nishina, Hidefumi Obara |
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Rok vydání: | 2007 |
Předmět: |
medicine.medical_specialty
Alkalosis Metabolic alkalosis Apoptosis 030204 cardiovascular system & hematology Lung injury Biochemistry Cell Line 03 medical and health sciences 0302 clinical medicine Internal medicine Humans Medicine Acidosis A549 cell chemistry.chemical_classification Reactive oxygen species business.industry Biochemistry (medical) Metabolic acidosis Cell Biology General Medicine respiratory system Oxidants medicine.disease Pulmonary Alveoli Endocrinology chemistry 030220 oncology & carcinogenesis Immunology medicine.symptom business |
Zdroj: | Journal of International Medical Research. 35:118-126 |
ISSN: | 1473-2300 0300-0605 |
Popis: | Apoptosis of alveolar epithelial type II (AEC-II) cells induced by reactive oxygen species (ROS) contributes to extensive alveolar damage during acute lung injury. Hypercapnic acidosis and hypocapnic alkalosis are known to modulate ROSmediated lung damage. This study assessed the effects of acid–base balance disturbances on hydrogen peroxide (H2O2)-induced apoptosis of the AEC-II-like human cell line A549, which was cultured under different conditions of pH and CO2 tension (normal pH and CO2, hypercapnic acidosis, metabolic acidosis, hypocapnic alkalosis and metabolic alkalosis). H2O2-induced apoptosis was assessed by a dye-uptake bioassay and induction of caspase activity, which were quantified using analytical digital photomicroscopy. Acidosis or alkalosis of the culture medium alone did not induce A549 cell apoptosis. Hypocapnic alkalosis significantly increased H2O2-induced apoptosis and caspase activation of A549 cells. Metabolic alkalosis non-significantly increased H2O2-induced A549 cell apoptosis and caspase activation. These data suggest that hypocapnic alkalosis intensifies oxidative-induced apoptosis of alveolar epithelial cells. |
Databáze: | OpenAIRE |
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