Prolonged ischemia potentiates apoptosis formation during reperfusion by increase of caspase 3 activity and free radical generation.
Chien
C T
CT
Department of Clinical Research, National Taiwan University Hospital, Taipei, People's Republic of China.
Hsu
S M
SM
Chen
C F
CF
Lee
P H
PH
Lai
M K
MK
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015415:Biomarkers; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism*; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D007511:Ischemia / Q000473:pathology / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology; D011518:Proto-Oncogene Proteins / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000502:physiology*; D015424:Reperfusion; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology; D051028:bcl-2-Associated X Protein
D015415:Biomarkers; D005609:Free Radicals; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases