Alterations in the levels of metallothionein and metals in the liver, and unique serum liver enzyme response in metallothionein knock-out mice after burn injury

Kiho Cho, Lee Adamson, Jayoung Jeong, Tajia VanHook, Robert Rucker, David G Greenhalgh

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Objectives: Metallothionein (MT) is a small cysteine-rich protein that sequesters and distributes metal ions. Its overexpression stimulates cell proliferation and inhibits apoptosis. We investigated the effects of burn injury on MT expression and metal localization. We also sought to determine roles of MT in the pathophysiologic alterations in the liver after injury. Methods: Mice (C57BLKS/J, MT-I/II knock-out, KO, and wild-type control mice) were subjected to an 18% burn. Liver tissues harvested after injury were analyzed for the MT expression and the levels of zinc, copper, manganese, and iron. Levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase were measured in serum samples from MT-I/MT-II KO mice and controls after injury. Results: Transient induction of MT-I and MT-II mRNAs was observed 3-6 h after injury, while MT-I/MT-II protein peaked on day 1. The induction was localized to hepatocytic nuclei. The intrahepatic levels of zinc, copper, and iron were transiently elevated on day 1, when a down-regulation of manganese was evident. Interestingly, only the serum levels of aspartate aminotransferase were significantly augmented in MT-I/MT-II KO mice compared to controls after injury. Conclusions: These data suggest that MT and metals may participate in the pathogenesis of the liver after burn injury.

Original languageEnglish (US)
Pages (from-to)223-230
Number of pages8
JournalPathobiology
Volume71
Issue number4
DOIs
StatePublished - 2004

Fingerprint

Metallothionein
Knockout Mice
Liver
Metals
Wounds and Injuries
Enzymes
Serum
Manganese
Aspartate Aminotransferases
Zinc
Copper
Iron
Cell proliferation
Alanine Transaminase
Metal ions
Cysteine
Alkaline Phosphatase
Proteins

Keywords

  • Burn injury
  • Liver
  • Metallothionein
  • Metals

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Clinical Biochemistry
  • Immunology and Allergy
  • Cell Biology

Cite this

Alterations in the levels of metallothionein and metals in the liver, and unique serum liver enzyme response in metallothionein knock-out mice after burn injury. / Cho, Kiho; Adamson, Lee; Jeong, Jayoung; VanHook, Tajia; Rucker, Robert; Greenhalgh, David G.

In: Pathobiology, Vol. 71, No. 4, 2004, p. 223-230.

Research output: Contribution to journalArticle

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abstract = "Objectives: Metallothionein (MT) is a small cysteine-rich protein that sequesters and distributes metal ions. Its overexpression stimulates cell proliferation and inhibits apoptosis. We investigated the effects of burn injury on MT expression and metal localization. We also sought to determine roles of MT in the pathophysiologic alterations in the liver after injury. Methods: Mice (C57BLKS/J, MT-I/II knock-out, KO, and wild-type control mice) were subjected to an 18{\%} burn. Liver tissues harvested after injury were analyzed for the MT expression and the levels of zinc, copper, manganese, and iron. Levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase were measured in serum samples from MT-I/MT-II KO mice and controls after injury. Results: Transient induction of MT-I and MT-II mRNAs was observed 3-6 h after injury, while MT-I/MT-II protein peaked on day 1. The induction was localized to hepatocytic nuclei. The intrahepatic levels of zinc, copper, and iron were transiently elevated on day 1, when a down-regulation of manganese was evident. Interestingly, only the serum levels of aspartate aminotransferase were significantly augmented in MT-I/MT-II KO mice compared to controls after injury. Conclusions: These data suggest that MT and metals may participate in the pathogenesis of the liver after burn injury.",
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AB - Objectives: Metallothionein (MT) is a small cysteine-rich protein that sequesters and distributes metal ions. Its overexpression stimulates cell proliferation and inhibits apoptosis. We investigated the effects of burn injury on MT expression and metal localization. We also sought to determine roles of MT in the pathophysiologic alterations in the liver after injury. Methods: Mice (C57BLKS/J, MT-I/II knock-out, KO, and wild-type control mice) were subjected to an 18% burn. Liver tissues harvested after injury were analyzed for the MT expression and the levels of zinc, copper, manganese, and iron. Levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase were measured in serum samples from MT-I/MT-II KO mice and controls after injury. Results: Transient induction of MT-I and MT-II mRNAs was observed 3-6 h after injury, while MT-I/MT-II protein peaked on day 1. The induction was localized to hepatocytic nuclei. The intrahepatic levels of zinc, copper, and iron were transiently elevated on day 1, when a down-regulation of manganese was evident. Interestingly, only the serum levels of aspartate aminotransferase were significantly augmented in MT-I/MT-II KO mice compared to controls after injury. Conclusions: These data suggest that MT and metals may participate in the pathogenesis of the liver after burn injury.

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