[Disturbances of hydrogen electron transport system and free radical reactions after severe spinal cord injury].
Local tissue oxygen consumption, nicotinamide-adenine dinucleotide hydrogenase, coenzyme-Q and alpha-tocopherol were measured and the relationships between damage to the hydrogen electron transport system and free radical reactions were examined in a irreversible rat spinal cord injury model. Damage to the hydrogen electron transport system became apparent in the injured spinal cord segment earlier than expected. Oxygen consumption declined to 26% of the baseline level within five to 30 minutes after injury, by one hour, further declined by 21% and by two hours another 17% and by three to four hours by an additional 13%. This severe disturbance of oxygen metabolism was associated with a marked reduction of adenosine triphosphate. A reduction in coenzyme-Q by 50% was noted within 10 minutes after injury and might be at least partially responsible for these changes since a reduction of coenzyme-Q promotes the semiquinone (.coenzyme-Q) forming reaction and also produces the superoxide radical X O2-. While coenzyme-Q reacts with H+ ion, this superoxide radical X O2-, produce a state of scavenger wastage and hyperoxygenation of nicotinamide-adenine dinucleotide hydrogenase at two hours after injury. Lipid peroxigenation resulted from damage to the hydrogen electron transport system which created a state of energy metabolite disruption and cellular membrane damage and ultimately led to cellular autolysis.
D000818:Animals; D004579:Electron Transport; D004734:Energy Metabolism; D005609:Free Radicals; D006859:Hydrogen / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D009243:NAD / Q000378:metabolism; D010101:Oxygen Consumption; D051381:Rats; D013116:Spinal Cord / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000378:metabolism*; D014451:Ubiquinone / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism
D005609:Free Radicals; D009243:NAD; D014451:Ubiquinone; D014810:Vitamin E; D006859:Hydrogen