Doerrier 2015 Thesis
|Doerrier C (2015) Estudio bioenergetica mitochondrial en la sepsis experimental y efecto protector de la Melatonina. Doctoral Thesis p154.|
Abstract: Sepsis, a systemic inflammatory response of the organism against an infection, represents the major cause of death in the intensive care units of developed countries. For this reason, sepsis is a disease with relevant economic and healthy costs that should be treated. Previous studies demonstrated that septic process courses with an oxidative and nitrosative stress able to damage cellular structures (such as proteins, including respiratory complexes, DNA and membrane lipids). A substantial body of evidence supports a mitochondrial dysfunction associated with sepsis. In this regard, the inflammatory response and the ROS/RNS increase during sepsis trigger mitochondrial dysfunction. Mitochondria play an important role in the energetic metabolism, but also in other processes in physiological and pathological conditions. Therefore, the analysis of mitochondrial function is crucial to understand a specific pathology such as sepsis. Moreover, an exhaustive knowledge on mitochondrial bioenergetics allows to find specifics targets evaluating an effective treatment. Melatonin (N-acetyl-5-methoxytryptamine) is an amphipathic indoleamine, present in all cellular compartments including mitochondria. Melatonin acts as a potent antioxidant and anti-inflammatory molecule with other important actions. Several works have been demonstrated the beneficial effects of melatonin in sepsis. Melatonin prevents septic shock and multiple organ failure reducing, iNOS expression and ROS generation, restoring ETC activity and ATP production.
According with this background, the present work was focused in the study of mitochondrial function during sepsis. Moreover, was evaluated the properties of melatonin against mitochondrial failure during sepsis.
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Medicine, Pharmacology;toxicology, mt-Awareness Pathology: Sepsis Stress:Oxidative stress;RONS Organism: Mouse Tissue;cell: Heart, Liver Preparation: Permeabilized tissue, Isolated mitochondria Enzyme: Marker enzyme, Supercomplex Regulation: Substrate Coupling state: LEAK, OXPHOS, ET Pathway: N, S, NS HRR: Oxygraph-2k