AJP - Gastrointestinal and Liver Physiology, Vol 270, Issue 2 376-G384, Copyright © 1996 by American Physiological Society
Vitamin E decreases hepatic levels of aldehyde-derived peroxidation products in rats with iron overload
S. Parkkila, O. Niemela, R. S. Britton, K. E. Brown, S. Yla-Herttuala, R. O'Neill and B. R. Bacon
Department of Anatomy, University of Oulu, Finland.
Hepatic iron overload can cause lipid peroxidation with the formation of
aldehydic products, hepatocellular injury, and fibrosis. Vitamin E
(alpha-tocopherol) may prevent peroxidation-induced hepatic damage. We used
confocal laser scanning microscopy, digital image analysis, and
immunohistochemical methods to quantitate aldehyde-derived peroxidation
products in the liver of rats with experimental iron overload with or
without supplemental vitamin E. A strong autofluorescent reaction
colocalizing with iron deposits was present in the livers of iron-loaded
rats. Fluorescent granules were unevenly distributed in the cytosol of both
hepatocytes and Kupffer cells in the periportal regions.
Immunohistochemical studies revealed the presence of malon-dialdehyde
adducts in the periportal regions of the ironloaded rats. Vitamin E
supplementation markedly reduced the fluorescence intensity and the amount
of aldehyde-derived peroxidation products and changed the distribution of
stainable iron and iron-associated peroxidation products such that their
levels were much decreased in Kupffer cells. These results indicate that
aldehyde-derived covalent chemical addition products are formed in the
liver in iron overload. Vitamin E supplementation markedly reduces the
amount of these compounds and changes their cellular distribution. These
findings should be implicated in the role of antioxidant therapy in
conditions causing iron overload and lipid peroxidation.
