Alterations of energetic metabolite levels by free radicals during optic nerve ischemia.
An experimental model of optic nerve ischemia was designed in the rabbit to determine early biochemical alterations, i.e.--changes of high energy phosphate metabolites (ATP and phosphocreatine)--in occlusive and peri-occlusive areas. Vascular occlusion provoked a rapid fall of ATP and phosphocreatine in the optic nerve. Free radicals scavengers, superoxide dismutase plus catalase or dimethylthiourea were able to counteract the drop of phosphate metabolites in the peri-occlusive area. These results show that hypoxia leads to oxygen-derived free radical generation which can be responsible for cell damage and emphasize the role of free radicals in the pathogenesis of ocular diseases related to vascular dysfunction.
Vériac
S
S
Laboratoire de Physiologie Cellulaire, Université Montpellier, France.
Tissié
G
G
Bonne
C
C
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002374:Catalase; D004195:Disease Models, Animal; D016166:Free Radical Scavengers; D005609:Free Radicals; D007511:Ischemia / Q000378:metabolism*; D009900:Optic Nerve / Q000098:blood supply*; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism*; D011817:Rabbits; D013482:Superoxide Dismutase; D013890:Thiourea / Q000031:analogs & derivatives
D016166:Free Radical Scavengers; D005609:Free Radicals; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; C038983:1,3-dimethylthiourea; D002374:Catalase; D013482:Superoxide Dismutase; D013890:Thiourea