Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice.

Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice. Research Abstract Details 

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Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice. Abstract Text:

Linda E Hammond,Craig D Albright,Lihua He,Ivan Rusyn,Steven M Watkins,Scott D Doughman,John J Lemasters,Rosalind A Coleman,

The absence of mouse mitochondrial glycerol-3-phosphate acyltransferase-1 (Gpat1-/-) increases the amount of arachidonate in liver phospholipids and increases beta-hydroxybutyrate and acyl-carnitines, suggesting an elevated rate of liver fatty acid oxidation. We asked whether these alterations might increase reactive oxygen species (ROS), apoptosis, or hepatocyte proliferation. Compared to wildtype controls, liver mitochondria from Gpat1-/- mice showed a 20% increase in the rate of ROS production and a markedly increased sensitivity to the induction of the mitochondrial permeability transition. Mitochondrial phosphatidylethanolamine and phosphatidylcholine from Gpat1-/- liver contained 21% and 67% more arachidonate, respectively, than wildtype controls, and higher amounts of 4-hydroxynonenal, a product of arachidonate peroxidation. Oxidative stress was associated with an increase in apoptosis, and with 3-fold and 15-fold higher TUNEL positive cells in liver from young and old Gpat1-/- mice, respectively, compared to age-matched controls. Compared to controls, bromodeoxyuridine labeling was 50% and 7-fold higher in livers from young and old Gpat1-/- mice, respectively, but fewer glutathione-S-transferase positive cells were present. Thus, Gpat1-/- liver exhibits increased oxidative stress and sensitivity of the mitochondrial permeability transition pore, and a balanced increase in apoptosis and proliferation.

Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice. Publishing Authors By Initials

LE Hammond,CD Albright,L He,I Rusyn,SM Watkins,SD Doughman,JJ Lemasters,RA Coleman,

For similar inorganic chemicals: free radicals: reactive oxygen species research abstracts see: inorganic chemicals: free radicals: reactive oxygen species research

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Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Experimental and molecular pathology

VOLUME: 82

Page Numbers: 210-9

Journal Abbreviation: Exp. Mol. Pathol.

ISSN: 0014-4800

DAY: 28

MONTH: 12

YEAR: 2006

Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 370711

Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice. Keywords Mesh Terms:

KEYWORDS: Reactive Oxygen Species

MESH TERMS: metabolism

Chemical & Substance for Abstract: Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice. Information

Substance Name: Glutathione Transferase

Registry Number: EC 2.5.1.18

Grant and Affiliation Information for Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice.

AFFILIATION: Department of Nutrition, CB#7461, 2301 Michael Hooker Research Building, Columbia Street, University of North Carolina, Chapel Hill, NC 27599, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: R01 DK56598

ACRONYM: DK

MEDLINETA: Exp Mol Pathol

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