Effect of Artificial Cells on Hepatic Function After Ischemia–Reperfusion Injury in Liver
- E.J. Chang; S.H. Lee; K.C. Mun; S.I. Suh; J.H. Bae; S.P. Kim; H.J. Choi; K.B. Cho; J.S. Hwang
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- Background: The liver suffers from ischemia/reperfusion injury during transplantation.
Reactive oxygen species generated by xanthine oxidase during reperfusion of the ischemic
liver may be partially responsible for the hepatic injury. Oxygen free radicals are removed
by antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione
peroxidase. Using glutaraldehyde and lysine we constructed crosslinked hemoglobin,
containing SOD and catalase, and assessed its ability to protect against ischemia/
reperfusion injury during transplantation.
Methods: In contrast to the sham-operated control groups, blood was exchanged using
crosslinked hemoglobin (polyHb) a PolyHb–SOD–catalase (PSC) group. After ischemia/
reperfusion injury, several parameters of hepatic damage and oxygen free radicals were
measured as well as microscopic examination.
Results: Alanine aminotransferase, aspartate aminotransferase, superoxide produc-
tion, hydrogen peroxide, and malondialdehyde levels were higher among the PolyHb
group than sham-operated controls. The PolyHb group revealed a few apoptotic
bodies, some acute inﬂammatory inﬁltrates in the sinusoids, nuclear fragmentations,
cell shrinkage, and chromatin clumping with formation of apoptotic bodies in the
apoptotic cells under microscopic examination. Alanine aminotransferase, aspartate
aminotransferase, superoxide production, and hydrogen peroxide levels were lower in
the PSC than the PolyHb group. Hepatic structures were well preserved in the PSC
Conclusions: Reactive oxygen species contribute to hepatic dysfunction with morpho-
logic changes. PSC is effective to reduce hepatic damage by lowering oxygen free
radical–mediated injury after ischemia/reperfusion in the liver.
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