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Excess iron induces hepatic oxidative stress and transforming growth factor beta1 in genetic hemochromatosis.
- Source :
-
Hepatology (Baltimore, Md.) [Hepatology] 1997 Sep; Vol. 26 (3), pp. 605-10. - Publication Year :
- 1997
-
Abstract
- Genetic hemochromatosis (GH) is associated with excess iron deposition in hepatocytes, which results in progressive hepatic injury. The pathogenesis of hepatic injury in GH is poorly understood. In this study, we found enhanced oxidative stress in patients with GH, as evidenced by hepatic malondialdehyde (MDA)-protein adducts and by increased oxidatively modified serum proteins. MDA-lysine epitopes and oxidatively modified serum proteins, as well as immunoglobulin G autoantibodies against MDA-lysine epitopes, were increased in untreated GH patients and to a lesser extent in GH heterozygotes compared with normal individuals. These markers of ongoing oxidative stress decreased with phlebotomy treatment in GH patients. In addition, TGF-beta1 colocalized with hepatic iron and MDA protein adducts in hepatocytes and sinusoidal cells of hepatic acinar zone 1 and normalized after iron removal. Our data suggest that iron overload increases both lipid peroxidation and TGF-beta1 expression, which together could promote hepatic injury and fibrogenesis.
- Subjects :
- Adult
Aldehydes
Autoantibodies analysis
Biopsy
Female
Hemochromatosis pathology
Heterozygote
Humans
Immunoglobulin G analysis
Ketones
Liver pathology
Male
Malondialdehyde immunology
Retrospective Studies
Transferrin metabolism
Blood Proteins chemistry
Hemochromatosis genetics
Hemochromatosis physiopathology
Iron metabolism
Liver metabolism
Malondialdehyde analysis
Oxidative Stress
Subjects
Details
- Language :
- English
- ISSN :
- 0270-9139
- Volume :
- 26
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Hepatology (Baltimore, Md.)
- Publication Type :
- Academic Journal
- Accession number :
- 9303489
- Full Text :
- https://doi.org/10.1002/hep.510260311