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Biomedical subjects

C F Mills

Publications and source records attributed to C F Mills.

16 recordsLinked to original sources

Trace elements in animals.

Trace element deficiency and toxicity in animals induces a wide variety of clinical effects although few are sufficiently specific to permit diagnosis without supporting investigation of changes in tissue trace element content or of the activity of metabolic processes influenced by trace element supply. Study of such trace element dependent processes has shown that extensive changes often arise before overt signs of disease appear. Some of these subclinical effects have pathological consequences and thus cannot be ignored when seeking correlations between geochemical anomalies and disease incidence. Many past estimates of the quantitative requirements of animals for the essential trace elements are imprecise. Although recent work is providing clearer definition of requirements, many common dietary components have a marked influence upon the efficiency with which such elements can be utilized from the diet. Recent evidence indicates that such antagonists influence both the absorption and the subsequent fate of essential and toxic elements in body tissues and these processes have to be taken into account when investigating the aetiology of disorders believed to be attributable to anomalies in trace element supply. Their existence is not always detectable if attention is confined to the trace element analysis of body tissues or to the nature of clinical lesions. Provided the complexity of soil-plant-animal relations with respect to trace element supply is fully recognized in the interpretation of data, the geochemical approach to the initial recognition of areas associated with a high risk of anomalies in trace element supply to animals and man has considerable potential value. This is already apparent from investigations upon the incidence of trace element problems in animals. As yet, its validity for similar purposes in man is less fully established.

Animals

Increased hepatic copper concentration in Indian childhood cirrhosis.

19 Indian children with liver disease were studied. 5 in whom a clinical and histological diagnosis of Indian Childhood Cirrhosis was made had massive orcein-staining deposits in liver cells. The hepatic copper content in these 5 cases was strikingly high (1389 microgram/g dry tissue, range 1045--2303) the normal range being 15--55 microgram/g. Of the other 14 cases, only 2 had hepatic copper levels above normal (170 and 262 microgram/g.) This high hepatic copper concentration may be caused by excessive copper ingestion or an abnormality of copper metabolism.

Coloring Agents

Cadmium toxicity.

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Animal Feed

Observations on the selenium status of cattle in the north-east of Scotland.

Cattle on 18 of 21 farms in north-east Scotland were found to have low whole blood activities of the selenium-containing enzyme, glutathione peroxidase (less than 5 units per ml whole blood), and a low blood concentration of selenium (less than 0.05 mg per litre). These cattle had all been fed on locally produced feedstuffs without any mineral supplementation. The low selenium status in cattle occurred on farms with soils derived from a range of parent material, no one particular type predominating.

Animals

Biochemical and pathological changes in tissues of Friesian cattle during the experimental induction of copper deficiency.

1. Copper deficiency was induced in five Friesian cattle offered a semi-synthetic diet containing less than 1 mgCu/kg. Changes in blood and liver Cu contents and in the Cu-containing enzymes, ferroxidase I (caeruloplasmin; EC 1.16.3.1) and monoamine oxidase (EC 1.4.3.4) of plasma and cytochrome oxidase (EC 1.9.3.1) of liver and skeletal muscle were monitored during Cu depletion. 2. Rapid decreases in blood and liver Cu and plasma ferroxidase I activity were found at least 80 d before the first appearance of overt clinical signs of deficiency. Plasma monoamine oxidase and liver cytochrome oxidase activities decreased less rapidly and thus may provide useful indices of chronic Cu depletion.

Animals

Protective effect of zinc supplementation against copper toxicosis in sheep.

1. A study has been made of the effects of dietary zinc supplementation on the development of copper toxicosis in three groups each of eight 12-week-old lambs. 2. None of the lambs receiving 420 mg Zn/kg diet developed Cu toxicosis in the 24-week experimental period, compared with three in the control group receiving 43 mg Zn/kg and possibly one in the group receiving 220 mg Zn/kg. 3. Liver Cu concentrations were reduced by up to 40% in the Zn-supplemented animals, with concomitant reductions, especially in the early stages of the experiment, in the extent of liver damage, as assessed by measurement of plasma aspartate aminotransferase (EC 2.6.1.1) and arginase (EC 3.5.3.1) activities. 4. Plasma and liver Zn concentrations were increased only slightly in the lambs receiving the Zn-supplemented diets, and the only indication of possible toxic effects of the Zn supplements was the development of a slight anaemia in those animals receiving 420 mg Zn/kg diet. 5. The results suggest that the incidence of Cu toxicosis in sheep may be controlled by increasing their dietary Zn intake.

Animals

Changes in enterocyte mitochondria associated with deficiency of copper in cattle.

Comparisons were made between specimens of intestinal mucosa from three young Friesian steers, killed when showing clinical signs associated with copper deficiency, and three controls that had received supplementary copper. Copper deficiency was associated with marked depletion of cytochrome oxidase in the epithelium of the duodenum, jejunum and ileum, and with partial villus atrophy in the duodenum and jejunum. Enterocytes from the duodenum, jejunum and ileum showed mitochondrial abnormalities ranging from slight swelling to marked localised dilation. Many of the mitochondria not affected by swelling had a distinctly condensed appearance. These changes are discussed in relation to the copper-responsive diarrhoea that affects a proportion of cattle suffering from copper deficiency.

Animals

Perinatal changes in the absorption of trace elements.

Fetal demands for many of the essential trace elements change markedly during the terminal stages of development. Susceptibility to deficiency during early postnatal life is influenced by the extent of fetal trace element reserves, by inadequacies in the supply of some elements in maternal milk and by postnatal changes in the efficiency of trace element absorption. The efficiency with which essential and some toxic trace elements are absorbed after birth is a function both of age and of diet. Homeostatic mechanisms for the control of iron absorption are poorly developed in the newborn. There are indications that pinocytotic absorption of iron, copper, lead and cadmium may occur at this stage and account for the high efficiency with which these elements are absorbed from a liquid diet. Evidence of developmental changes in the enterohepatic recirculation of such metals is considered and an account is given of our very inadequate understanding of the processes of trace metal absorption in the weaned animal.

Aging