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Previous human studies have shown that drinking tea during meals significantly inhibits the absorption of both food iron and medicinal iron. This study provides evidence from experiments with rats that the tannins in the tea are responsible for the inhibition, probably by forming non-absorbable complexes with the iron within the intestinal lumen. The molar ratio of tannin: iron is dependent on the pH, being 1:1 at pH 2,0 2:1 at pH 5,5 and 3:1 at pH 8,0. Since tannins are present in many vegetable foods the formation of such complexes may be a factor in the poor availability for absorption of much food iron.

The absorption of radioactive iron from a solution of ferrous ascorbate, and from a standard meal containing intrinsically labelled haemoglobin and wheat, was measured in 12 Indian housewives, 18 white hospital patients and 12 subjects with idiopathic haemochromatosis. Eight of the latter had been fully treated by multiple venesections, so that their serum ferritin concentrations were below 25 mug/1. Since the serum ferritin concentrations of the housewives and the hospital patients were comparable, their body iron stores were considered to be depleted to a similar degree. There were no significant differences between the absorptions of ferrous ascorbate or of the haem iron in the standard meal by each group, but the housewives and the hospital patients absorbed significantly less of the non-haem food iron. The mean non-haem food iron absorptions were 36.4%, 5.8% and 18.9% for the treated haemochromatotic subjects, the Indian housewives and the white hospital patients respectively. The discrepancies between the absorptions of the different forms of food iron were highlighted by calculating the ratios between them. The mean non-haem: haem food iron absorption ratio for the group of treated haemochromatotic subjects was 0.98, and for the Indian housewives only 0.18. The white hospital patients did not form a homogenous population: the ratios of the five males and three of the females were greater than 1.0, whereas those of the remaining 10 females were less than 0.5. The results of this study suggest that mal-absorption of non-haem iron from a meal containing bread, presumably due to a defect at the luminal level, may be an important factor in the pathogenesis of iron deficiency in some subjects. The abnormality appears to be particularly prevalent among Indian women living in Durban.

In Bantu subjects with iron overload iron is visible in skeletal muscle cells and in the tissue histiocytes which lie between these cells. In the present study the concentrations of ;muscle' iron were measured chemically in subjects with varying hepatic storage iron concentrations. The results indicate that the concentrations of storage iron in ;muscle' are much lower than those in the liver. However, the muscle mass is so large that the total amount of iron present is at least equal to that in the liver in subjects with normal body stores. The concentrations of iron in ;muscle' are raised in subjects with iron overload but the degree to which they rise is far less than occurs in the liver; a thirtyfold increase in hepatic iron concentrations is associated with only a sixfold increase in ;muscle' iron. Experiments in rats revealed that storage iron in ;muscle' represents a relatively non-miscible pool which responds very little to acute changes in the iron environment.

Studies of the ascorbic acid status in two subjects with idiopathic haemochromatosis and in 12 with transfusional siderosis showed that all had decreased levels of white cell ascorbic acid. The urinary excretion of ascorbic acid was also diminished in those subjects in whom such measurements were made. The administration of ascorbic acid was followed by only a small rise in the urinary ascorbic acid output, while the oxalic acid levels (measured in two subjects) showed a significant rise. These findings resemble those described in siderotic Bantu, and support the thesis that increased iron stores lead to irreversible oxidation of some of the available ascorbic acid.