TY - JOUR
T1 - The involvement of the intracellular superoxide production system in hepatic ischemia-reperfusion injuryIn vivo and in vitro experiments using transgenic mice manifesting excessive CuZn-SOD activity
AU - Suzuki, Masanori
AU - Takeuchi, Heigo
AU - Kakita, Tetsuya
AU - Unno, Michiaki
AU - Katayose, Yu
AU - Matsuno, Seiki
PY - 2000/10/15
Y1 - 2000/10/15
N2 - In vivo and in vitro studies were conducted using transgenic mice with 1.8-fold increased SOD activity in the cytoplasmic fraction compared to normal mice in order to evaluate the role of cytoplasmic superoxide dismutase (SOD) in hepatic ischemia-reperfusion injury. In the in vivo study, after inducing 15 min 70% partial hepatic ischemia followed by 45 min reperfusion, we determined the plasma levels of ALT, hyaluronic acid, and phosphatidylcholine hydroperoxide (PCOOH) as the membranous lipoperoxide of the hepatic tissue. In addition, in vitro ischemia-reperfusion studies for cultured hepatocytes were conducted in an anaerobic chamber that could create a hypoxic or oxygen-rich environment in order to clarify the amelioration of reperfusion injuries in the SOD rich hepatocytes. High levels of ALT and PCOOH were found as a result of reperfusion in normal mice, while a suppression of the increase in these levels was noted in the transgenic mice. In both groups, the hyaluronic acid levels were not modified. These results suggest that intracellular superoxide production is involved in the mechanism of hepatic ischemia-reperfusion injury, and that an improvement of the ability to eliminate intracellular superoxide species can contribute to the prevention of reperfusion injury. Copyright (C) 2000 Elsevier Science Inc.
AB - In vivo and in vitro studies were conducted using transgenic mice with 1.8-fold increased SOD activity in the cytoplasmic fraction compared to normal mice in order to evaluate the role of cytoplasmic superoxide dismutase (SOD) in hepatic ischemia-reperfusion injury. In the in vivo study, after inducing 15 min 70% partial hepatic ischemia followed by 45 min reperfusion, we determined the plasma levels of ALT, hyaluronic acid, and phosphatidylcholine hydroperoxide (PCOOH) as the membranous lipoperoxide of the hepatic tissue. In addition, in vitro ischemia-reperfusion studies for cultured hepatocytes were conducted in an anaerobic chamber that could create a hypoxic or oxygen-rich environment in order to clarify the amelioration of reperfusion injuries in the SOD rich hepatocytes. High levels of ALT and PCOOH were found as a result of reperfusion in normal mice, while a suppression of the increase in these levels was noted in the transgenic mice. In both groups, the hyaluronic acid levels were not modified. These results suggest that intracellular superoxide production is involved in the mechanism of hepatic ischemia-reperfusion injury, and that an improvement of the ability to eliminate intracellular superoxide species can contribute to the prevention of reperfusion injury. Copyright (C) 2000 Elsevier Science Inc.
KW - Free radicals
KW - Hepatic ischemia-reperfusion injury
KW - Lipoperoxidization
KW - Superoxide
KW - Superoxide dismutase
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U2 - 10.1016/S0891-5849(00)00369-5
DO - 10.1016/S0891-5849(00)00369-5
M3 - Article
C2 - 11053777
AN - SCOPUS:0034667719
VL - 29
SP - 756
EP - 763
JO - Free Radical Biology and Medicine
JF - Free Radical Biology and Medicine
SN - 0891-5849
IS - 8
ER -