Search PubMed⌕ Search

Biomedical subjects

A Bomford

Publications and source records attributed to A Bomford.

67 records · Page 4Linked to original sources
PubMed1981

Effect of excess dietary zinc on tissue storage of iron in rats.

Earlier investigators observed that addition of large amounts of zinc to the diet or rats can retard growth, lower their hemoglobin levels and reduce storage of iron. In the present studies, addition of 0.75% zinc to a synthetic diet confirmed the reduced storage of iron in the livers and spleens of growing rats, but failed to show an effect on growth rate or hemoglobin levels. The adverse effects of zinc excess on growth and hemoglobin level could, however be reproduced by replacing the Rogers-Harper salt mixture used in the present studies with the Wesson salt mixture use in the earlier studies. Rats fed excess zinc along with the Wesson salt mixture grew less well, had anemia and also had low level in copper in their livers. It is suggested that addition of zinc to the low copper Wesson salt mixture reduced copper absorption sufficiently it deplete liver copper to a level at which mobilization of liver iron stores by a copper-dependent mechanism became impaired, thus depriving red cell production and tissue enzymes of stored iron. The mechanism by which iron stores are depleted by addition of zinc to the better balanced Rogers-Harper salt mixture remains unexplained It is not due to interference by zinc with iron adsorption from the diet nor with cellular uptake of iron from circulating transferrin, and the capacity of tissues to store iron as ferritin is not impaired.

Absorption↗
PubMed1980

A biochemical comparison of normal human liver and hepatocellular carcinoma ferritins.

1. The iron contents, gel migration rates and isoelectric-focusing patterns of normal liver and hepatocellular carcinoma ferritins from the same patients were compared. 2. Sucrose-density-gradient centrifugation showed that the number of iron atoms per ferritin molecule was decreased to approximately half in carcinoma tissue when compared with normal liver. 3. On electrophoresis, hepatocellular carcinoma ferritin migrates faster and is therefore more negatively charged than normal liver ferritin, thus refuting the general view that the more negatively charged a ferritin molecule the greater its iron content. 4. Comparison of tumour and normal liver ferritin subunit compositions on acid/urea/polyacrylamide gels showed hepatocellular carcinoma ferritin to contain an additional, more negatively charged, subunit to normal liver ferritin. 5. Isoelectric focusing showed that hepatocellular carcinoma tissue contains isoferritins with isoelectric points intermediate between the ranges of normal liver and normal heart isoferritins.

Adult↗
PubMed1979

Haemochromatosis.

Explore the source record for details and available documents.

Hemochromatosis↗
PubMed1978

Plasma immunoreactive beta-melanocyte-stimulating hormone in chronic liver disease and fulminant hepatic failure.

Hyperpigmentation believed to be due to melanin, is a feature of chronic liver disease, especially primary biliary cirrhosis and hemochromatosis. Normal plasma concentrations of immunoreactive beta-melanocyte-stimulating hormone (beta-MSH) have been found in both these conditions; thus elevation of plasma beta-MSH plays no role in the pathogenesis of hepatic pigmentation. Normal levels are also found in hepatocellular failure, which supports the hypothesis that the kidney and not the liver is the site of metabolism of this hormone.

Chronic Disease↗
PubMed1977

Variation in the distribution of two human heart ferritin species. Isoferritin profile and subunit composition in normal and iron-overloaded subjects.

On polyacrylamide slab electrophoresis two ferritin species, termed fast and slow, were present in three control and four iron-loaded human hearts. The ratio of the fast to slow species varied between hearts and correlated with the distribution of isoferritins, which had pI values ranging from 4.8 to 5.6. The acidic isoferritins were prominent in all hearts, but one control and the four iron-loaded hearts contained, in addition, basic isoferritins. All ferritins were composed of two subunits, an acidic H type and a more basic HL type, which was the main subunit in normal liver. Hearts with the highest proportions of acidic isoferritin contained the highest proportion of the H subunit.

Adult↗
PubMed1977

Histocompatibility antigens as markers of abnormal iron metabolism in patients with idiopathic haemochromatosis and their relatives.

HLA-A3 was significantly more common in 35 unrelated patients with idiopathic haemochromatosis (69%) than in 95 controls (31%). Further studies in two families suggest that 2 genes are involved in the pathogenesis of the disease, each associated with a separate metabolic defect. Whereas minor abnormalities, namely raised serum-iron and some increase in storage iron, were found in relatives with an HLA A11, B27, CW2 haplotype, those with the A3, B14, CW5 haplotype had no detectable abnormalities. When both these haplotypes were found together, as in the propositus and one sibling in the first family investigated, all the signs of the fully developed disease were apparent. It is suggested that one of the genes is in linkage disequilibrium with HLA-A3 and could be responsible for a kinetic abnormality, possibly increased plasma to storage iron exchange. The other gene, also carried on the sixth chromosome and, in the first family, marked by the HLA A11, B27, CW2 haplotype might result in an increased absorption of dietary iron. The concomitant inheritance of these two genes and the metabolic defects they determine are required for the full development of the disease

Adult↗
PubMed1976

Long term results of venesection therapy in idiopathic haemochromatosis.

Observations on the clinical effects of venesection therapy in 85 treated, as compared with 26 untreated, patients with idiopathic haemochromatosis showed decreased pigmentation and hepatomegaly together with a return to normal tests of liver function in half the patients who had abnormal tests at presentation. Control improved in 28 per cent of those patients with diabetes mellitus, although some patients developed it during the period of observation, despite venesection. Portal hypertension, testicular atrophy and arthropathy were not improved. In only 12 patients was there sufficient reaccumulation of iron after the initial course of venesection to merit further treatment. Rates of iron accumulation in these patients varied between 1-4 mg and 4-8 mg per day and chelatable iron levels were noted to be inappropriately high in relation to body iron stores during the early stages of the reaccumulation period. Life table data shows that the percentage survival five and ten years after diagnosis was 66 and 32 per cent respectively for the treated patients, and 18 and 6 per cent respectively for the untreated patients, both statistically highly significant differences (p less than 0-01). Possible clinical differences such as age of presentation, the presence of diabetes mellitus, cirrhosis, clinical hepatic failure and hepatoma between the treated and untreated groups that might otherwise have weighted survival in favour of the treated group were corrected by the use of covariant analysis. This gave mean log survival values of 4-15 and 2-88 for the treated and untreated patients respectively, equivalent to 63-4 months and 17-8 months, a highly significant difference (p less than 0-01). Ten patients, all of whom had cirrhosis at the time of diagnosis, died of malignant hepatoma between three and 15 years after completing venesection therapy. There was also a high rate of death from neoplasms in a variety of other sites--22 per cent in the venesected group, strikingly higher than that rate predicted for a similarly aged population using national cancer mortality rates.

Adult↗