Intrahepatic Delivery of Pegylated Catalase Is Protective in a Rat Ischemia/Reperfusion Injury Model.


Journal

The Journal of surgical research
ISSN: 1095-8673
Titre abrégé: J Surg Res
Pays: United States
ID NLM: 0376340

Informations de publication

Date de publication:
06 2019
Historique:
received: 04 09 2018
revised: 27 11 2018
accepted: 10 01 2019
pubmed: 17 2 2019
medline: 31 1 2020
entrez: 17 2 2019
Statut: ppublish

Résumé

Ischemia/reperfusion injury (IRI) can occur during liver surgery. Endogenous catalase is important to cellular antioxidant defenses and is critical to IRI prevention. Pegylation of catalase (PEG-CAT) improves its therapeutic potential by extending plasma half-life, but systemic administration of exogenous PEG-CAT has been only mildly therapeutic for hepatic IRI. Here, we investigated the protective effects of direct intrahepatic delivery of PEG-CAT during IRI using a rat hilar clamp model. PEG-CAT was tested in vitro and in vivo. In vitro, enriched rat liver cell populations were subjected to oxidative stress injury (H In vitro, PEG-CAT pretreatment of liver cells showed substantial uptake and protection against oxidative stress injury. In vivo, direct intrahepatic, but not systemic, delivery of PEG-CAT during IRI significantly reduced alanine aminotransferase and aspartate aminotransferase in a time-dependent manner (P < 0.01, P < 0.0001, respectively, for all time points) compared to control. Similarly, tissue malondialdehyde (P = 0.0048), adenosine triphosphate (P = 0.019), and GSH (P = 0.0015), and the degree of centrilobular necrosis, were improved by intrahepatic compared to systemic PEG-CAT delivery. Direct intrahepatic administration of PEG-CAT achieved significant protection against IRI by reducing the volume distribution and taking advantage of the substantial hepatic first-pass uptake of this molecule. The mode of delivery was an important factor for protection against hepatic IRI by PEG-CAT.

Sections du résumé

BACKGROUND
Ischemia/reperfusion injury (IRI) can occur during liver surgery. Endogenous catalase is important to cellular antioxidant defenses and is critical to IRI prevention. Pegylation of catalase (PEG-CAT) improves its therapeutic potential by extending plasma half-life, but systemic administration of exogenous PEG-CAT has been only mildly therapeutic for hepatic IRI. Here, we investigated the protective effects of direct intrahepatic delivery of PEG-CAT during IRI using a rat hilar clamp model.
MATERIALS AND METHODS
PEG-CAT was tested in vitro and in vivo. In vitro, enriched rat liver cell populations were subjected to oxidative stress injury (H
RESULTS
In vitro, PEG-CAT pretreatment of liver cells showed substantial uptake and protection against oxidative stress injury. In vivo, direct intrahepatic, but not systemic, delivery of PEG-CAT during IRI significantly reduced alanine aminotransferase and aspartate aminotransferase in a time-dependent manner (P < 0.01, P < 0.0001, respectively, for all time points) compared to control. Similarly, tissue malondialdehyde (P = 0.0048), adenosine triphosphate (P = 0.019), and GSH (P = 0.0015), and the degree of centrilobular necrosis, were improved by intrahepatic compared to systemic PEG-CAT delivery.
CONCLUSIONS
Direct intrahepatic administration of PEG-CAT achieved significant protection against IRI by reducing the volume distribution and taking advantage of the substantial hepatic first-pass uptake of this molecule. The mode of delivery was an important factor for protection against hepatic IRI by PEG-CAT.

Identifiants

pubmed: 30771685
pii: S0022-4804(19)30035-6
doi: 10.1016/j.jss.2019.01.028
pmc: PMC6752955
mid: NIHMS1519413
pii:
doi:

Substances chimiques

catalase-polyethylene glycol 0
Polyethylene Glycols 3WJQ0SDW1A
Hydrogen Peroxide BBX060AN9V
Catalase EC 1.11.1.6
Aspartate Aminotransferases EC 2.6.1.1
Alanine Transaminase EC 2.6.1.2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

152-163

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL131941
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL135648
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI106704
Pays : United States

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

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Auteurs

Clifford Akateh (C)

The COPPER Laboratory, The Ohio State University Wexner Medical Center, Columbus, Ohio; Comprehensive Transplant Center, The Ohio State University Wexner Medical Center, Columbus, Ohio; Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio.

Eliza W Beal (EW)

The COPPER Laboratory, The Ohio State University Wexner Medical Center, Columbus, Ohio; Comprehensive Transplant Center, The Ohio State University Wexner Medical Center, Columbus, Ohio; Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio.

Jung-Lye Kim (JL)

The COPPER Laboratory, The Ohio State University Wexner Medical Center, Columbus, Ohio.

Brenda F Reader (BF)

The COPPER Laboratory, The Ohio State University Wexner Medical Center, Columbus, Ohio; Comprehensive Transplant Center, The Ohio State University Wexner Medical Center, Columbus, Ohio; Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio.

Katelyn Maynard (K)

The COPPER Laboratory, The Ohio State University Wexner Medical Center, Columbus, Ohio.

Jay L Zweier (JL)

Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio.

Bryan A Whitson (BA)

The COPPER Laboratory, The Ohio State University Wexner Medical Center, Columbus, Ohio; Comprehensive Transplant Center, The Ohio State University Wexner Medical Center, Columbus, Ohio; Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio.

Sylvester M Black (SM)

The COPPER Laboratory, The Ohio State University Wexner Medical Center, Columbus, Ohio; Comprehensive Transplant Center, The Ohio State University Wexner Medical Center, Columbus, Ohio; Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio. Electronic address: Sylvester.Black@osumc.edu.

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