[The role of the mitochondria generating reactive oxygen species and nitric oxide in postischemic functional disturbance of the kidney].
Experiments on 10 rats and 10 rabbits were made to investigate metabolic aftereffects of 40-minute heat ischemia and subsequent reperfusion. It was found that mitochondrial function deteriorated significantly in an early postischemic period. The disorder manifested with a relative prevalence of cell ATP consumption over its synthesis. This is accompanied with intensive production by mitochondria of nitric oxide and oxygen free radicals. Fluorescent probes and confocal microscopy of vital renal sections showed that mitochondria are responsible for excessive generation of nitric oxide and oxygen radicals in the kidney in an early reperfusion period. The discussion concerns the role of nitric oxide in reperfusion renal damage and participation of mitochondria in formation of its anti-ischemic resistance.
Kirpatovskiĭ
V I
VI
Plotnikov
E Iu
EIu
Kazachenko
A V
AV
Golovanov
S A
SA
Syromiatnikova
E V
EV
Vysokikh
M Iu
MIu
Zorov
D B
DB
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D005260:Female; D005456:Fluorescent Dyes; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D018613:Microscopy, Confocal; D008928:Mitochondria / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D011817:Rabbits; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
D005456:Fluorescent Dyes; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D000255:Adenosine Triphosphate