|
Hemosiderin and Hemosiderosis: click here
Primary Hemochromatosis: click here
Iron: click here
Hemoproteins constitute some of the most
important normal endogenous pigments because they include hemoglobin,
the cytochromes, and a variety of enzymes.
Central to an understanding of disorders
involving these pigments is a knowledge of the uptake, metabolism,
excretion, and storage of iron.
A normal adult male requires
approximately 1 mg of iron per day to balance the average net loss each
day through bile, sweat, minute episodic blood loss in the gut, and cell
turnover in the gastrointestinal tract and skin.
During periods of rapid body growth
(infancy and puberty), menstrual years of women, and the last two
trimesters of pregnancy, daily iron requirements are increased. Iron in
food, which is in the ferric state, is reduced to the ferrous form by
reducing substances present in food and is absorbed across the duodenal
and jejunal mucosa.
The sites of absorption should be
mentioned because of their important function of closely regulating the
uptake of iron into the body.
Clinical and experimental studies
indicate that some of the iron entering the mucosal cell may be
complexed to transferring, a beta-globulin, which is the major iron
transport protein and transferred directly and rapidly (within 8 hours
after ingestion) into the plasma. The remainder of iron is oxidized back
to the ferric form and unites with a beta-globulin called apoferritin to
form ferritin, a compound containing about 17 to 23% iron.
Ferritin is then slowly absorbed onto the
blood, taking several days. Since it is in equilibrium with
ferrous iron in the cell, its slow removal tends to maintain ferrous
iron at a high saturated level.
Such intracellular levels of ferrous iron
inhibit further uptake of iron from the lumen of the intestine and
enhance the movement of ferritin from the cell into the blood.
Iron absorption is also regulated by the
level of plasma iron, being increased when plasma iron is low, as in
individuals with sustained blood loss or anemia.
A variety of dietary factors affect iron
absorption - alcohol, ascorbic acid, and fructose tend to enhance
absorption, where as phytates (plant salts), phosphates, fats, and
calcium impair it.
Conditions such as achlorhydria (very low
levels of gastric acid) and the altered gastric mucosa associated with
it also tend to diminish absorption.
Tissue Iron:
Iron
enters the plasma from tissue stores, from the intestinal mucosa and
from reticuloendothelial cells, which remove and destroy damaged red
cells.
Plasma iron
then enters the bone marrow where it is used for synthesis of
hemoglobin.
Iron is stored
in tissues in essentially two forms - ferritin, which is not apparent
with light microscopy but is visualized with electron microscopy
as a tetrad aggregation of intensely electron-dense particles, and
hemosiderin, which is composed of large irregular aggregates of ferritin
that are insoluble and appear as coarse, brown cytoplasmic granules.
The granules
can be demonstrated to contain ferric iron because they form a deep blue
product, ferric ferrocyanide, on reaction of tissue with an acid
solution of potassium ferrocyanide (Prussian blue reaction).
The equilibrium
between storage and plasma iron depends on the degree of transferrin
saturation by iron.
Low plasma iron
levels and reduced saturation shift the equilibrium so that iron is
mobilized from stores to the plasma. When the converse is true, iron
moves from plasma to tissue stores.
Hemosiderosis: click here

|