AJP - Gastrointestinal and Liver Physiology, Vol 268, Issue 3 471-G479, Copyright © 1995 by American Physiological Society
Quantifying oxidative injury in the liver
R. S. Poggetti, E. E. Moore, F. A. Moore, K. Koike, R. Tuder, B. O. Anderson and A. Banerjee
Department of Surgery, Denver General Hospital, Colorado.
Oxidative injury is a mechanism common to both ischemia-reperfusion (IR)
and leukocyte-mediated injury. Reperfused tissue beds and elaborated
mediators can activate a cascade of intercellular and interorgan injuries
that often precipitates multiple organ failure. Initiation of lung injury
by gut IR is a case in point, but concomitant liver injury may have been
overlooked because of the absence of comparably sensitive physiological
markers. In this study, we explore the hypothesis that occurrence of
portally derived oxidant-induced liver dysfunction may be detected with
both sensitivity and specificity. We simulated pure oxidative injury to the
liver and separated the contributions from secondary systemic oxidation.
Both tissue and plasma indicators were evaluated, each reflecting aspects
of oxidation, membrane integrity, and metabolic function. Tissue markers
readily detect oxidative liver injury, but systemic 3-hydroxybutyrate
(3-OHB) concentration and ketone body ratio (KBR) are the most sensitive.
Comparison of 3-OHB concentrations against the corresponding KBR can be
used to distinguish adjustments within a physiological range from the
transition into injury.
