PubMed Health⌕ Search

Biomedical subjects

M S Clegg

Publications and source records attributed to M S Clegg.

28 records · Page 2Linked to original sources
PubMed1989

Localization of bismuth radiotracer in rat kidney following exposure to bismuth.

It has been proposed that alpha emitting 212Bi (t1/2 = 60 min) coupled to tumor-specific antibodies may be a useful radiotherapeutic agent. However, since Bi can accumulate in the kidney, it is necessary to characterize the factors influencing localization of Bi within this tissue in order to evaluate the potential for radiation damage to the renal system. In this study, the localization of Bi radiotracers was determined in kidneys of rats previously exposed and not exposed to mumole quantities of Bi. Following repeated injection of Bi (4 x 14 mumols (3 mg Bi)/kg bw) the element accumulated mainly in the kidney followed by liver, spleen, pancreas, bone, and brain. Kidney copper and liver zinc concentrations were higher in Bi-exposed rats than in non-exposed rats. Within the cytosol, in Bi-exposed rats, Bi radiotracer in the kidney was associated with a metallothionein-like protein (Mt). In contrast, non-exposed rats contained no detectable metallothionein-like proteins in the kidney and the Bi tracer was associated with the hemoglobin fraction of the cell. Thus, when Bi is administered in tracer quantities such as that incorporated for use as a radiopharmaceutical, no induction of, and association with, metallothionein-like proteins should occur. These results suggest that the potential nephrotic effects of 212Bi will be influenced by the individual's previous exposure to Bi-containing drugs, or other metallothionein-inducing insults.

Animals↗
PubMed1988

A pathologic and toxicologic evaluation of veal calves fed large amounts of zinc.

Tissues were examined from 26 male Holstein veal calves given large amounts of dietary zinc. All calves had been fed 706 micrograms zinc/g of milk replacer for 28 days before the first death occurred. Calves died naturally (14, group A) or were euthanatized (12, group B) after 23 days of feeding a lower concentration of zinc (150 micrograms/g). Average amounts of zinc in liver (wet weight) were 345.72 micrograms/g (group A) and 344.84 micrograms/g (group B). Mean kidney zinc concentrations were 219.0 micrograms/g (group A) and 252.38 micrograms/g (group B). Tissue manganese, copper, and iron levels were normal. Changes at necropsy included pneumonia, fluid digesta, and petechiae and infarcts in liver, kidney, and heart (as a result of bacterial infections). Histological changes that were directly attributed to dietary zinc intake were: marked atrophy and necrosis of pancreatic acinar tissue (group A); multifocal fibrosis of pancreatic acini (group B); multifocal renal cortical fibrosis with necrosis in convoluted tubules and loops of Henle, and with intratubular mineralization (groups A and B). Hepatic midzonal mineralization and fibrosis of the adrenal zona glomerulosa were seen in group B calves.

Animal Feed↗
PubMed1987

An epidemiologic study of mortality in veal calves subsequent to an episode of zinc toxicosis on a California veal calf operation using zinc sulfate-supplemented milk replacer.

Ninety-five 3- to 6-month old male Holstein veal calves were evaluated after an episode of zinc toxicosis, to describe clinical signs and to identify management and/or host-related factors that may have contributed to death. Clinical signs appeared 23 days after feeding of milk replacer commenced. Of 85 calves examined, 64 had pneumonia (75.5%), 62 had ocular signs (72.9%), 46 had diarrhea (54.1%), 34 were anorectic (40.0%), 15 were bloated (17.6%), 8 had cardiac arrhythmias (9.4%), 3 had convulsions (3.5%), and 3 were polydipsic/polyphagic (3.5%). Clinical signs began to appear when calves each were being fed approximately 1.5 to 2.0 g of zinc/day and exposed to a cumulative zinc intake of 42 to 70 g, from a milk replacer containing 706 micrograms of elemental zinc/g of milk replacer. Of 95 calves studied, 1 died before zinc was supplemented, 16 died during the episode, 12 were euthanatized, 1 was lost to follow-up evaluation, 1 was culled, and 64 were slaughtered. Deaths attributable to zinc toxicosis were observed between 25 and 53 days after the milk replacer was supplemented with zinc. Calves died while being exposed cumulatively to 30 to 66 g of zinc. The factors of previous pneumonia severity, age, cumulative daily exposure to zinc, and calf location within a bay were examined for possible associations with mortality, using stepwise logistic regression. Though younger calves tended to have a higher mortality than older calves, neither age category nor severity of pneumonia, before zinc supplementation, accounted for a significant mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1987

Hypertension-induced alterations in copper and zinc metabolism in Dahl rats.

It has been suggested that one risk factor in the development of hypertension and vascular disease may be abnormal copper and zinc metabolism. In the current study we tested the hypothesis that hypertension itself may result in alterations in the metabolism of these essential elements. Dahl salt-sensitive rats were fed diets containing 0.4 or 8.0% NaCl for 32 days. At the conclusion of the study, blood pressure was significantly higher in the rats fed a high NaCl diet than in controls. Liver, kidney, and heart copper concentrations were significantly lower in the rats fed a high NaCl diet compared with controls, while plasma copper levels were higher. In contrast, tissue zinc levels were higher in the rats fed a high NaCl diet than in controls, while plasma zinc levels were lower. It is hypothesized that alterations in copper and zinc metabolism may be one factor underlying tissue damage in these animals.

Animals↗
PubMed1986

Analysis of whole blood manganese by flameless atomic absorption spectrophotometry and its use as an indicator of manganese status in animals.

To investigate the use of whole blood manganese (Mn) as an indicator of total body Mn, we measured Mn in whole blood and liver of rats fed purified diets containing adequate (45 micrograms Mn/g diet) or deficient (1 microgram Mn/g diet) Mn. The mean hepatic Mn concentration was significantly lower (P less than 0.001) in the Mn-deficient group compared to the control group, 0.36, microgram Mn/g and 1.73 micrograms Mn/g, respectively. Furthermore, whole blood Mn was significantly reduced (P less than 0.001) in the deficient group when compared to the control group, 4.0 ng Mn/ml and 8.6 ng Mn/ml, respectively. Hepatic Mn linearly regressed against whole blood Mn yielded a statistically significant (P less than 0.001) correlation coefficient of 0.775. These data suggest that whole blood Mn is a valid indicator of body Mn status and thus may be useful, in addition to the measurements of serum copper and zinc, for the diagnosis and prognosis of diseases in which the metabolism of trace elements is affected. In addition, this paper describes and delineates operational parameters for the measurement of whole blood Mn using the IL 551 atomic absorption spectrophotometer and the IL 555 B flameless atomizer.

Animals↗
PubMed1986

Association of low blood manganese concentrations with epilepsy.

A comparison of hospitalized epileptic patients with matched normals showed that the mean whole blood manganese (Mn) concentration of the epileptic population was significantly lower than the mean of the normal population. The whole blood Mn concentration in the epileptics did not correlate either with seizure frequency or with anticonvulsant therapy. It was observed, however, that patients whose epilepsy was a result of trauma had significantly higher blood Mn concentrations than patients whose history was negative for trauma.

Adolescent↗
PubMed1982

Developmental changes in composition of cats milk: trace elements, minerals, protein, carbohydrate and fat.

The concentrations of iron, copper, zinc, manganese, calcium, magnesium, protein, carbohydrate and fat were analyzed in cats' milk during the course of lactation. Cats' milk is different from most species in that the concentrations of iron, copper, zinc and manganese are lower during the first 2 days of lactation than on days 3-7. After the initial rise in the concentration of these elements, the concentration of iron decreased from 5.9 micrograms/ml to 3.0 micrograms/ml, with most of the decrease occurring between days 8 and 21. Copper concentration declined from 1.6 micrograms/ml to 0.8 microgram/ml, with most of the change occurring between days 8 and 28. Concentration of manganese increased during lactation, from 0.14 microgram/ml of 0.39 microgram/ml. Calcium concentration increased rapidly during the first 3 weeks from 550 micrograms/ml to 1500 micrograms/ml, with little change thereafter. The magnesium concentration (congruent to 100 micrograms/ml) and zinc concentration (congruent 6 micrograms/ml) were not affected by stage of lactation. Protein increased during lactation from 4% to 7%, and fat from 3% to 5%, whereas carbohydrate concentration (congruent 4%) did not change significantly. These data demonstrate that the nutrient intake of the kitten changes markedly during the early neonatal period and that these changes should be taken into account in evaluating studies of suckling cats.

Animals↗
PubMedDate not supplied

Nutritional aspects of manganese from experimental studies.

In experimental animals, dietary manganese deficiency can result in numerous biochemical and structural abnormalities. Deficient animals can be characterized by impaired insulin production, alterations in lipoprotein metabolism, an impaired oxidant defense system, and perturbations in growth factor metabolism. If the deficiency occurs during early development, there can be pronounced skeletal abnormalities and an irreversible ataxia. Several lines of evidence suggest that manganese deficiency may be a problem in some human populations. Manganese toxicity can also pose a significant health risk. In experimental animals, acute manganese toxicity can result in numerous biochemical pathologies. However, the above occurs typically when the manganese is given via injection; most animals show considerable resistance to dietary manganese toxicosis. Similarly, confirmed cases of manganese toxicity in humans are currently restricted to cases of exposure to high levels of airborne manganese, and to cases when manganese excretory pathways are compromised.

Animal Nutritional Physiological Phenomena↗