Eine Studie zum hypobaren hypoxischen Stress in Rattenmodellen

Hypoxic stress at high altitude leads to an increased production of reactive oxygen species (ROS), which damage lipids in the cell membrane as well as proteins and DNA within the cell. The cells have a range of antioxidant enzymes and non-enzymatic mechanisms to counteract these damages caused by oxidative stress. This includes protection through reduced glutathione (GSH), glutathione S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPX), and catalase (CAT). Furthermore, a ubiquitous protein known as heme oxygenase I has been shown to significantly influence various stress stimuli. These enzymes play an important role in the plant's adaptation to stress conditions. The effects of severe and acute hypobaric hypoxic insults on biomarkers for oxidative stress were studied in vivo using a rat model. Heme oxygenase I was modulated by metalloporphyrin, which is a known pharmacological upregulator and inhibitor of heme oxygenase (HO). This study sheds light on the role of heme oxygenase modulation in combating oxidative damage induced by hypobaric hypoxia (HH). After pre-treatment with HO modulators, the rats were examined.