2026-10-01T20:49:43Zhttps://phdtheses.ekt.gr/eadd_oai/request

oai:10442/14912024-07-13T18:08:32Zhdl_10442_2

Different species of animals (rats, mice and hamsters) were exposed to high oxygen concentrations (40, 60, 85, 100%) for prolonged period (2-14 days). Survival time and changes in lung antioxidant enzyme activity of superoxide dismutase (SOD) in response to hyperoxia were determined. All animal species die after prolonged exposure to 100% oxygen (1Atm). The primary damage is to the lung and the signs are those of progressive respiratory distress syndrome until death. Also all the animal species in hyperoxic environment of 40-60% showed insignificant lung changes and insignificant increase in lung antioxidant enzyme activity of SOD. The same results we had in hyperoxic environment of 85% oxygen for the animal species of mice and hamsters. The animal species of rats after exposure to 85% oxygen for 7 days showed significant lung changes and significant increase 113% in lung antioxidant enzyme activity of SOD especially in mitochondria 187%, and became "tolerant" (survived more than 11 days ) to 100% oxygen. In contrast, control rats without proexposure to 85% oxygen, mice and hamsters after proexposure to 85% oxygen for seven days, died within 70-80 hours in 100% oxygen. The special behaviour of the animal species rats, the stimulation of the biochemical antioxidant enzyme system during the acute stage of oxygen toxicity, the return of enzyme almost to normal levels after prolonged exposure to 85% oxygen , the lung adaptation of animal rats in environment of 85% oxygen and the development of tolerance in environment of 100% oxygen, the accompanying metabolic and histodynamic changes of lung cells in hyperoxic environment , constitute the main conclusions of this study. All these, on one hand, emphasize the important role that superoxide dismutase acts to control the free radical cell injury probably by scavenging the initial reactive products of oxygen, and on the other hand raise a point in relation with the stimulation mechanism of the antioxidant enzyme system probably with many factors activating during the acute respiratory distress and causing the augmentation of antioxidant enzyme.[…] Η παρούσα εργασία είναι μία πειραματική μελέτη της τοξικότητας του οξυγόνου σε πειραματόζωα. Σκοπός της είναι η καλύτερη κατανόηση των αμυντικών μηχανισμών που αναπτύσσονται στον πνεύμονα απέναντι στην τοξική δράση του οξυγόνου όταν αυτό χορηγείται σε υψηλές πυκνότητες. Ιδιαίτερη δε αναφορά γίνεται στο ρόλο της δισμουτάσης του υπεροξειδίου (SOD) και στη σχέση της με την άμυνα του κυττάρου του πνεύμονα έναντι των τοξικών "ελεύθερων ριζών οξυγόνου". […]Προστατευτικοί μηχανισμοί που αναπτύσσονται στον πνεύμονα μετά από εισπνοή τοξικών πυκνοτήτων οξυγόνου: Μελέτη σε πειραματόζωαKapravelos, NikolaosΚαπραβέλος, Νίκος1990greAristotle University Of Thessaloniki (AUTH)Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)Ιατρική και Επιστήμες ΥγείαςΚλινική ΙατρικήMedical and Health SciencesClinical Medicine10.12681/eadd/1491http://hdl.handle.net/10442/hedi/1491PhD Thesis