Suppression of the inducible form of nitric oxide synthase prior to traumatic brain injury improves cytochrome c oxidase activity and normalizes cellular energy levels

Neuroscience

Volumn 151, Issue 1, 2008, Pages 148-154

  Huttemann M ^a   Lee, I ^a   Kreipke, C W ^a   Petrov, T ^a  

^a WAYNE STATE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

ATP; cytochrome c oxidase; iNOS; mitochondria; nitric oxide; trauma

Indexed keywords

ADENOSINE TRIPHOSPHATE; ANTISENSE OLIGONUCLEOTIDE; CYTOCHROME C OXIDASE; INDUCIBLE NITRIC OXIDE SYNTHASE; NITRIC OXIDE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN CORTEX; BRAIN MICROCIRCULATION; CELL ENERGY; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME INHIBITION; MALE; MITOCHONDRION; NONHUMAN; OXIDATIVE PHOSPHORYLATION; PRIORITY JOURNAL; RAT; TRAUMATIC BRAIN INJURY;

ADENOSINE TRIPHOSPHATE; ANIMALS; BLOTTING, WESTERN; BRAIN; BRAIN INJURIES; ELECTRON TRANSPORT COMPLEX IV; ENERGY METABOLISM; ENZYME INHIBITORS; IN SITU HYBRIDIZATION; MALE; MITOCHONDRIA; NITRIC OXIDE; NITRIC OXIDE SYNTHASE TYPE II; OLIGORIBONUCLEOTIDES, ANTISENSE; RATS; RATS, SPRAGUE-DAWLEY; UP-REGULATION;

EID: 37849028561     PISSN: 03064522     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neuroscience.2007.09.029     Document Type: Article

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