Mitochondrial activity: a possible determinant of anoxic injury in renal medulla.
In brain, heart and kidney, cell work in the absence of oxygen has been thought to precipitate anoxic damage by increasing the rate of depletion of cellular energy stores. In the medullary thick ascending limb of isolated perfused rat kidneys, however, reduction of ATP synthesis by a variety of mitochondrial or metabolic inhibitors caused ATP depletion comparable to that produced by oxygen deprivation but did not reproduce the lesions of anoxia. In these cells, unrestrained mitochondrial activity may be an important source of anoxic injury.
Brezis
M
M
Rosen
S
S
Silva
P
P
Spokes
K
K
Epstein
F H
FH
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000968:Antimycin A / Q000031:analogs & derivatives / Q000494:pharmacology; D003486:Cyanides / Q000494:pharmacology; D003847:Deoxyglucose / Q000494:pharmacology; D004734:Energy Metabolism; D000860:Hypoxia / Q000378:metabolism*; D007679:Kidney Medulla / Q000187:drug effects / Q000378:metabolism*; D008314:Malonates / Q000494:pharmacology; D008928:Mitochondria / Q000378:metabolism*; D009840:Oligomycins / Q000494:pharmacology; D010101:Oxygen Consumption; D051381:Rats; D012402:Rotenone / Q000494:pharmacology
D003486:Cyanides; D008314:Malonates; D009840:Oligomycins; D012402:Rotenone; C032456:antimycin; D000968:Antimycin A; D000255:Adenosine Triphosphate; D003847:Deoxyglucose; C030290:malonic acid