Abstract
The objective of this study was to determine if DNA damage caused by ischemic insult (blood depletion) causes an alteration in the activity of endogenous mouse kidney poly(ADP-ribose) synthetase. The results show that kidneys made nonviable by warm (37 degrees C) in vitro ischemia (organ storage to study the effects of blood loss at normal body temperature) and in vivo ischemia (surgical depletion of the blood supply by arterial clamping) exhibit decreased levels of enzyme activity. Kidneys made nonviable by cold (0 degrees C) storage injury (organ storage as utilized for transplantation), however, possess elevated levels of enzyme activity. The DNA isolated from ischemic kidneys was shown to have a stimulatory effect upon exogenous calf thymus poly(ADP-ribose) synthetase. Also, electron microscopy analysis of DNA from ischemic kidneys showed that cold storage injury leads to the formation of large (average size = 500 bases) single-stranded regions. The results suggest that the activities of both endogenous and exogenous poly(ADP-ribose) synthetase are related to the nature of DNA damage resulting from ischemic insult.
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