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'Oxygen Radicals' in keywords Facet   Publication Year 1998  [X]
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1Author    H. Nohl, L. GilleRequires cookie*
 Title    Evaluation of the Antioxidant Capacity of Ubiquinol and Dihydrolipoic Acid  
 Abstract    Ubiquinone and a-lipoic acid are natural constitutents which are involved in mitochondrial energy metabolism. Their bioenergetic activities require redox-cycling. In the case o f a-lipoic acid redox-cycling leads to dihydrolipoic acid which occurs in multienzyme com plexes in­ volved in the citric acid cycle while U Q recycles through semi-and divalently reduced ubiqui­ nones in the respiratory chain. We have proved the validity of the concept about the antioxi­ dant function o f these natural compounds in their reduced form. Ubiquinol was found to interfere with lipid peroxidation o f liposomal membranes being itself degradated by two consecutive oxidation steps. Dihydrolipoic acid was found to totally recycle ubiquinone to the antioxidant active divalently reduced form. In contrast to the antioxidative derived reaction products of ubiquinols which in turn promoted lipid peroxidation, the antioxidant derived reaction product o f dihydrolipoic acid was the unreactive two electron oxidation product a-lipoic acid. Our experim ents demonstrate the existence of an dihydrolipoic acid driven recycl­ ing of U Q to the antioxidative-a c tiv e U Q H 2. The efficiency o f the antioxidative capacity of the latter was found to be diminished through prooxidant activities of the antioxidant-derived metabolites. 
  Reference    Z. Naturforsch. 53c, 250 (1998); received D ecem ber 19 1997/February 3 1998 
  Published    1998 
  Keywords    Ubiquinol, Coenzyme Q, Dihydrolipoic Acid, Lipid Peroxidation, Oxygen Radicals 
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 TEI-XML for    default:Reihe_C/53/ZNC-1998-53c-0250.pdf 
 Identifier    ZNC-1998-53c-0250 
 Volume    53 
2Author    H. Nohl, L. Gille, K. StaniekRequires cookie*
 Title    The Exogenous NADH Dehydrogenase of Heart Mitochondria Is the Key Enzyme Responsible for Selective Cardiotoxicity of Anthracyclines  
 Abstract    The molecular mechanism of the anthracycline-dependent developm ent of cardiotoxicity is still far from being clear. However, it is generally accepted, that mitochondria play a significant role in triggering this organ specific injury. The results presented in this study demonstrate that, in contrast to liver mitochondria, isolated heart mitochondria shuttle single electrons to adriamycin, giving rise to oxygen radical formation via autoxidation of adria­ mycin semiquinones. This one electron reduction of anthracyclines is catalyzed by the exoge­ nous N A D H dehydrogenase associated with complex I o f heart mitochondria, an enzyme which is lacking in liver mitochondria. U pon addition of N A D H heart mitochondria generate significant amounts of adriamycin sem iquinones while liver mitochondria were ineffective. Adriamycin semiquinones undergo both autoxidation leading to superoxide radical release and complex reactions under formation of adriamycin aglycone. Due to the high lipophilicity adriamycin aglycones accumulate in the inner mitochondrial membrane where they interfere with electron carriers of the respiratory chain. Adriamycin aglycone sem iquinones emerging from an interaction with com plex I were found to trigger homolytic cleavage of H20 2 which results in the formation of hydroxyl radicals. A s demonstrated in this study the activation of adriamycin by the exogenous N A D H dehydrogenase of cardiac mitochondria initiates a cas­ cade of reaction steps leading to the establishment o f oxidative stress. Our experiments sug­ gest the exogenous N A D H dehydrogenase o f heart mitochondria to play a key role in the cardiotoxicity of adriamycin. This organ-specific enzyme initiates a sequence of one electron transfer reactions ending up in the establishment of oxidative stress. 
  Reference    Z. Naturforsch. 53c, 279—5 (1998); received D ecem ber 19 1997/February 3 1998 
  Published    1998 
  Keywords    Anthracyclines, Adriamycin, Rat Heart M itochondria, Rat Liver Mitochondria, Oxygen Radicals 
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 TEI-XML for    default:Reihe_C/53/ZNC-1998-53c-0279.pdf 
 Identifier    ZNC-1998-53c-0279 
 Volume    53 
3Author    M. Stohrer3, A. Ndrea Eichinger3, M. Schlachter5, M. Stangassinger3, F. Hoffmann, -La Roche LtdRequires cookie*
 Title    Protective Effect of Vitamin E in a Rat Model of Focal Cerebral Ischemia  
 Abstract    Under certain pathological conditions such as cerebral ischemia and reperfusion the occur­ rence of free radicals is remarkably increased. However, only very little information is avail­ able on their quantitative relevance for the pathophysiology and final outcom e of diseases. The aim of the present study was to evaluate the contribution o f oxygen radicals in the pathogenesis of a stroke. For this purpose a rat model for stroke was used. Two of three vitamin E deficient groups were repleted with different dosages of DL-a-tocopherylacetate. N o signs of vitamin E deficiency could be observed. However, the weight gain during reple­ tion was increased in the vitamin E repleted groups. Brain infarction was created by occlusion o f the right middle cerebral artery (M CAO) for two hours. After 24 hours the measurements o f infarct volum es were taken. The infarct volume of the group with the highest repletion dosage was significantly reduced by 81%. This was also expressed in a higher rate of gait disturbances after MCAO o f the deficient animals. The control of vitamin E status exhibited a similar repletion-dependent level in plasma and brain. These results strongly support the hypothesis that the generation of oxygen radicals occurring during reperfusion is an impor­ tant aspect of the pathophysiological mechanism in brain infarction. 
  Reference    Z. Naturforsch. 53c, 273—2 (1998); received D ecem ber 19 1997/January 22 1998 
  Published    1998 
  Keywords    Vitamin E, Middle Cerebral Artery Occlusion, Rat, Brain Infarct Volume, Oxygen Radicals 
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 TEI-XML for    default:Reihe_C/53/ZNC-1998-53c-0273.pdf 
 Identifier    ZNC-1998-53c-0273 
 Volume    53