Pathogenesis of hepatic fibrosis in experimental iron overload

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Abstract
Significant increases in prolyl hydroxylase activity, a key enzyme in the collagen biosynthetic pathway, were noted in the hepatic homogenate of Fe loaded [rats] as compared to controls. The increase in prolyl hydroxylase activity was seen without any light microscopic histologic evidence of cell necrosis or accumulation of collagen in the livers from the Fe-loaded animals. Utilizing EM, collagen fibrils were demonstrated immediately adjacent to the hepatocytes in the Fe-loaded animals but not the controls. No fibroblasts or inflammatory cells were noted in this area. There was no evidence of damage to the subcellular organelles of the Fe-loaded hepatocytes. The hyroxyproline content of the Fe-loaded livers was also shown to be increased. These experimental studies in conjuction with clinical observations described below suggest that in vivo Fe overload may have a primary effect on stimulating collagen synthesis by hepatocytes.