Neuronal nitric oxide synthase controls enzyme activity pattern of mitochondria and lipid metabolism Lorenz Schild * ,1 , Iveta Jaroscakova † , Uwe Lendeckel ‡ , Gerald Wolf † and Gerburg Keilhoff † * Institut für Klinische Chemie und Pathologische Biochemie, Bereich Pathologische Biochemie; † Institut für Medizinische Neurobiologie; and ‡ Institut für Experimentelle Innere Medizin, Medizinische Fakultät der Otto-von-Guericke-Universität Magdeburg, Magdeburg, Germany 1 Correspondence: Institut für Klinische Chemie und Pathologische Biochemie, Bereich Pathologische Biochemie, Medizinische Fakultät der Otto-von-Guericke Universität Magdeburg, Leipziger Str. 44, Magdeburg 39120, Germany. E-mail: lorenz.schild@medizin.uni-magdeburg.de <h3>SPECIFIC AIMS</h3> It is known that nitric oxide (NO) inhibits the electron flow in the mitochondrial respiratory chain, stimulates mitochondrial hydrogen peroxide generation, and promotes the biogenesis of mitochondria. This study aims to extend our knowledge about the effect of NO on mitochondria in the brain, muscle, heart, kidney, and liver. We hypothesize that endogenous NO which originates from the neuronal isoform of NO synthase (nNOS) affects the mitochondrial enzyme activity pattern of these tissues. Comparing mice lacking the nNOS (nNOS-KO) with wild-type animals (WT), we analyzed respiratory chain complex and citrate synthase in the corresponding organs. In analyzing the amount of fatty acid synthase and measuring the lipid
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Neuronal nitric oxide synthase controls enzyme activity pattern of mitochondria and lipid metabolism
Schild, Lorenz; Jaroscakova, Iveta; Lendeckel, Uwe; Wolf, Gerald; Keilhoff, Gerburg
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, Volume 20 (1): 145
Fed of American Socs for Experimental Biology – Jan 1, 2006
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