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Steatosis of liver and mitochondrial dysfunction
Páleníčková, Eliška ; Novák, František (advisor) ; Balková, Patricie (referee)
Aim: To determine the effect of diet-induced steatosis in the development of mitochondrial dysfunction in the liver and hepatic sensitivity to the partial ischemia. Methods: Male Wistar rats (361 ± 8.8 g) were fed standard (SD) or high-fat diet (HFD). Partial ischemia was induced by short-term clamp (20 min) of vein porta two days before the end of the experiment. Results: Ten-week HFD administration lead due to increased ketogenesis the altered glucose tolerance elevated serum NEFA. We demonstrated the inhibitory effect of HFD on the respiratory capacity of mitochondria in vitro. HFD negatively affected the activity of antioxidant systems and stimulated the formation of lipoperoxides. Partial ischemia had no efect on the mitochondrial oxidative capacity but significantly elevated the oxidative stress. Conclusion: HFD administration lead to the development of fatty liver that was still not accompanied by biochemical markers of liver injury. Nevertheless, we proved the impairment of to mitochondrial respiratory capacity, signs of structural damage of mitochondria and the increased sensitivity to oxidative damage of the liver. Subject words: biochemistry, physiology Keywords: mitochondria, HFD, ischemia, respiratory chain, antioxidant systém, ROS
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The role of lipids and ROS in cardioprotective mechanism of chronic hypoxia
Balková, Patricie
The role of lipids and ROS in cardioprotective mechanism of chronic hypoxia Cardiovascular diseases, mainly ischemic heart disease is one of the most frequently cause of morbidity and mortality in developed countries. Therefore effective protection of the heart against ischemia and reperfusion injury is the crucial aim of experimental and clinical cardiology. One of the main streams of cardiovascular research is looking for possibilities of natural heart resistance augmentation. Adaptation to chronic hypoxia is one possibility how to protect the heart against ischemia-reperfusion injury. Chronic hypoxia increases resistance of the myocardium to acute deficiency of oxygen leading to vetricular arrythmias, postischemic contractile dysfunction and necrotic changes in the tissue. Recently, it has been shown that reactive oxygen species (ROS) play an important role in the cardioprotective mechanism of chronic hypoxia. It is known that oxidative stress has a harmful effect in acute ischemia-reperfusion however ROS generated during the adaptation to hypobaric intermittent chronic hypoxia play a role in the induction of cardioprotection. In this study, we demonstrated that adaptation of adult rats to chronic hypoxia increased the activity and protein abundance of manganese superoxide dismutase (MnSOD) in the...
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The role of lipids and ROS in cardioprotective mechanism of chronic hypoxia
Balková, Patricie
The role of lipids and ROS in cardioprotective mechanism of chronic hypoxia Cardiovascular diseases, mainly ischemic heart disease is one of the most frequently cause of morbidity and mortality in developed countries. Therefore effective protection of the heart against ischemia and reperfusion injury is the crucial aim of experimental and clinical cardiology. One of the main streams of cardiovascular research is looking for possibilities of natural heart resistance augmentation. Adaptation to chronic hypoxia is one possibility how to protect the heart against ischemia-reperfusion injury. Chronic hypoxia increases resistance of the myocardium to acute deficiency of oxygen leading to vetricular arrythmias, postischemic contractile dysfunction and necrotic changes in the tissue. Recently, it has been shown that reactive oxygen species (ROS) play an important role in the cardioprotective mechanism of chronic hypoxia. It is known that oxidative stress has a harmful effect in acute ischemia-reperfusion however ROS generated during the adaptation to hypobaric intermittent chronic hypoxia play a role in the induction of cardioprotection. In this study, we demonstrated that adaptation of adult rats to chronic hypoxia increased the activity and protein abundance of manganese superoxide dismutase (MnSOD) in the...
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The role of lipids and ROS in cardioprotective mechanism of chronic hypoxia
Balková, Patricie ; Nováková, Olga (advisor) ; Drahota, Zdeněk (referee) ; Šmíd, František (referee)
The role of lipids and ROS in cardioprotective mechanism of chronic hypoxia Cardiovascular diseases, mainly ischemic heart disease is one of the most frequently cause of morbidity and mortality in developed countries. Therefore effective protection of the heart against ischemia and reperfusion injury is the crucial aim of experimental and clinical cardiology. One of the main streams of cardiovascular research is looking for possibilities of natural heart resistance augmentation. Adaptation to chronic hypoxia is one possibility how to protect the heart against ischemia-reperfusion injury. Chronic hypoxia increases resistance of the myocardium to acute deficiency of oxygen leading to vetricular arrythmias, postischemic contractile dysfunction and necrotic changes in the tissue. Recently, it has been shown that reactive oxygen species (ROS) play an important role in the cardioprotective mechanism of chronic hypoxia. It is known that oxidative stress has a harmful effect in acute ischemia-reperfusion however ROS generated during the adaptation to hypobaric intermittent chronic hypoxia play a role in the induction of cardioprotection. In this study, we demonstrated that adaptation of adult rats to chronic hypoxia increased the activity and protein abundance of manganese superoxide dismutase (MnSOD) in the...
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Steatosis of liver and mitochondrial dysfunction
Páleníčková, Eliška ; Balková, Patricie (referee) ; Novák, František (advisor)
Aim: To determine the effect of diet-induced steatosis in the development of mitochondrial dysfunction in the liver and hepatic sensitivity to the partial ischemia. Methods: Male Wistar rats (361 ± 8.8 g) were fed standard (SD) or high-fat diet (HFD). Partial ischemia was induced by short-term clamp (20 min) of vein porta two days before the end of the experiment. Results: Ten-week HFD administration lead due to increased ketogenesis the altered glucose tolerance elevated serum NEFA. We demonstrated the inhibitory effect of HFD on the respiratory capacity of mitochondria in vitro. HFD negatively affected the activity of antioxidant systems and stimulated the formation of lipoperoxides. Partial ischemia had no efect on the mitochondrial oxidative capacity but significantly elevated the oxidative stress. Conclusion: HFD administration lead to the development of fatty liver that was still not accompanied by biochemical markers of liver injury. Nevertheless, we proved the impairment of to mitochondrial respiratory capacity, signs of structural damage of mitochondria and the increased sensitivity to oxidative damage of the liver. Subject words: biochemistry, physiology Keywords: mitochondria, HFD, ischemia, respiratory chain, antioxidant systém, ROS
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