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Biomedical subjects

C D Thomson

Publications and source records attributed to C D Thomson.

49 records · Page 3Linked to original sources
PubMed1978

On supplementing the selenium intake of New Zealanders. 1. Short experiments with large doses of selenite or selenomethionine.

1. Urinary and faecal excretion of single oral doses of 1 mg selenium or 0.1 mg Se as selenomethionine (Semet-Se) in solution were studied in two women. Most of the Se was absorbed and little was eliminated in the urine (0.05-0.22 dose). 2. The results have been compared with those from an earlier study (Thomson, 1974) on the same two women after similarly sized doses of sodium selenite (selenite-Se) in solution. Although selenite-Se was almost as well absorbed as Semet-Se more was excreted in the urine (0.41-0.85 dose). 3. Repeated dosing with 1 mg selenite-Se on five consecutive days in one of the women indicated that 1.1 mg had been retained. 4. Twenty patients with muscular complaints from Tapanui (South Otago, New Zealand), a low-Se soil area, ingested 0.5 mg selenite-Se daily for 20 d. Blood Se increased rapidly to almost twice the initial concentration but reached a plateau well below most values reported for residents outside New Zealand. No difference in blood Se concentration was found between those who did or did not report improvement. 5. Spasmodic medication with selenite-Se by some residents near Lincoln (Christchurch, New Zealand) for periods of up to 10 years or more had increased the blood Se somewhat.

Adult↗
PubMed1978

On supplementing the selenium intake of New Zealanders. 2. Prolonged metabolic experiments with daily supplements of selenomethionine, selenite and fish.

1. The daily intake of selenium by three subjects was supplemented with 100 microgram Se as selenomethionine (Semet-Se) or sodium selenite (selenite-Se)/d for 10-11 weeks, or with 65 microgram Se as in mackerel (Scomber japonicus) (fish-Se)/d for 4 weeks. 2. Urinary and faecal excretion of Se was measured and also Se concentration in whole blood, plasma and erythrocytes. Measurements on blood were made at intervals after supplementation had ceased. 3. Selenite-Se was not as well absorbed (0.46 of the intake) during the first 4 weeks as Semet-Se (0.75 of the intake) and fish Se (0.66 of the intake). 4. Blood Se increased steadily with Semet-Se, from 0.08 to 0.18 microgram Se/ml, but more slowly with selenite-Se, reaching a plateau in 7-8 weeks at 0.11 microgram Se/ml. Plasma Se increased more rapidly with Semet-Se than with selenite-Se, so that initially with Semet-Se plasma Se was greater than erythrocyte Se. 5. Daily urinary excretion increased with all forms of supplement, with initially a greater proportion of absorbed selenite-Se being excreted than Semet-Se or fish-Se. A close relationship was found between plasma Se and 24 h urinary excretion. The findings suggested that there was a rapid initial excretion of presumably unbound Se then a slower excretion of residual unbound, loosely bound or bound Se. 6. Total retentions of 3.5 mg selenite-Se and 4.5 mg Semet-Se were large when compared with an estimate of body content of 6 mg Se, derived in another paper (Stewart, Griffiths, Thomson & Robinson, 1978). Retention of Semet-Se and fish-Se appeared to be reflected in blood Se, whereas for selenite-Se, blood Se reflected retention for only a short period after which Se appeared to be retained without altering the blood Se. This suggested that Semet-Se and selenite-Se were metabolized differently. 7. A double blind-dosing trail with 100 microgram Semet-Se was carried out for 12 weeks on twenty-four patients with muscular complaints in Tapanui, a low-Se-soil area. Blood Se increased in the experimental group (from 0.067 to 0.143 microgrm Se/ml); clinical findings were not conclusive and will be presented elsewhere. 8. Bood Se was measured in New Zealand residents before travelling to Europe or to North America. On return their blood Se was increased, and depending upon the period of time spent outside New Zealand some values reached concentrations found in visitors and new settlers to New Zealand. 9. The results from these studies and the earlier studies of single and multiple dosing have been used to look at the various criteria in use for assessing Se status of subjects. It is suggested that plasma Se be used in preference to 24 h urinary excretion, and in addition to whole blood Se and glutathione peroxidase (EC 1.11.1.9) activity.

Adolescent↗
PubMed1978

Quantitative selenium metabolism in normal New Zealand women.

1. Quantitative selenium metabolism has been studied in normal young New Zealand women by measuring total Se intake and urinary and faecal Se output, and by using values for absorption, excretion and turnover of 75Se determined after administration of[75Se]selenomethionine or [75Se]selenite. 2. In a period of 14 d when a normal ad lib. diet was being consumed, mean dietary Se for four women was 24.2 microgram/d, mean urinary Se was 13.1 microgram/d and mean faecal Se was 10.8 microgram/d; mean Se balance during this time was + 0.3 microgram/d. 3. Intestinal absorption of food Se was 0.76--0.83 of intake (mean 0.79). 4. Whole-body Se was calculated in three different ways; (a) using the specific activity of urinary Se and retained whole-body 75Se; (b) using plasma Se and the occupancy of 75Se in whole-body and plasma; (c) using absorbed food Se and the occupancy of absorbed 75Se in whole-body. 5. Whole-body Se calculated from measurements obtained following the administration of [75Se]selenomethionine was 4.7--10.0 mg (mean 6.9) using method (a), 4.1--7.2 mg (mean 5.2) using method (b) and 4.3--8.9 mg (mean 6.2) using method (c). 6. Whole-body Se calculated from results obtained after giving [75Se]selenite was 2.7--3.4 mg (mean 2.9) using method (a), 2.3--5.0 mg (mean 3.5) using method (b) and 2.1--3.0 mg (mean 2.6) using method (c). 7. The results of this study indicate that the minimum dietary requirement of Se for the maintenance of normal human health is probably not more than 20 microgram/d.

Adult↗
PubMed1978

Selenium concentration and glutathione peroxidase activity in blood of New Zealand infants and children.

The blood selenium (Se) concentrations of New Zealand children were lower than those reported for children living in other countries. This low blood Se was primarily determined by the low dietary intake of the children which, in turn, reflects the low Se content of New Zealand soils. Blood Se also varied geographically, with age, and with differences in quantities and types of food eaten. Children with phenylketonuria and maple syrup urine disease on synthetic diets had low Se intakes and blood Se concentrations compared with children on normal diets, and blood Se was seen to decrease with the length of time on these diets. A strong correlation (r = 0.62, P less than 0.001) was found between the blood Se levels and glutathione peroxidase activities for 107 children. Glutathione peroxidase activities of the children were lower than activities observed in New Zealand adults, refelecting their lower blood Se concentrations.

Adolescent↗
PubMed1977

Selenium concentrations and glutathione peroxidase activities in whole blood of New Zealand residents.

1. A relationship was found between selenium concentrations and glutathione peroxidase (EC 1.11.1.9) activities in whole blood of 264 New Zealand residents (r 0-71, P less than 0-001). 2. New Zealand residents returning from visits overseas of 7 months to 3 years had elevated blood Se, but normal GSH-Px activities, whereas for some new settlers in New Zealand both Se and GSH-Px activities were high.

Adolescent↗
PubMed1975

Metabolic studies of [75Se]selenocystine and [75Se]selenomethionine in the rat.

1. The long-term fate in rats of an oral dose of [75Se]selenocystine was compared with that of an oral dose of [75Se]selenomethionine. 2. Urinary and faecal radioactivities were measured during the 1st week and whole-body radioactivity was determined for 10 weeks. Rats were killed at weekly intervals for 4 weeks and at weeks 6 and 10 for analysis of tissue distribution of 75Se. 3. Intestinal absorption of [75Se]selenocystine was 81% of the administered dose; that of [75Se]selenomethionine was 86%. Urinary excretion of absorbed [75Se]selenocystine was 13-9% and that of [75Se]selenomethionine was 5-8% in the 1st week. 4. Whole-body retention of 75Se was greater for [75Se]selenomethionine than for [75Se]selenocystine but after the 1st week it decreased at a similar rate in both groups. Tissue distribution of retained 75Se was also similar in both groups. 5. The initial utilization of [75Se]selenocystine was different from that of [75Se]selenomethionine. However, after the 1st week 75Se from both sources appeared to be metabolized similarly, suggesting that dietary Se of both forms is ultimately incorporated into the same metabolic pool. 6. When these findings were compared with those of earlier studies with [75Se]selenite and 75Se incorporated in vivo into rabbit kidney (RK-64Se) (Thomson, Stewart & Robinson, 1975) the metabolism of [75Se]selenocystine resembled that of [75Se]selenite and RK-75Se, rather than that of [75Se]selenomethionine.

Amino Acids, Sulfur↗
PubMed1975

Metabolic studies in rats of (75-Se)selenomethionine and of 75-Se incorporated in vivo into rabbit kidney.

1. [75-Se]selenomethionine was administered to four rabbits and after 4 d their kidneys were removed and homogenized. The long-term fate in rats of an oral dose of this kidney homogenate (RK-75-Se) was compared with that of an oral dose of ]75-Se]selenomethionine mixed with unlabelled rabbit kidney homogenate. 2. Urinary adn faecal radioactivities were measured during the 1st week and whole-body radioactivity was determined for 10 weeks. Rats were killed at weekly intervals for 4 weeks for analysis of tissue distribution of 75-Se. 3. Intestinal absorption of RK-75-Se was 87%; that of [75-Se]selenomethionine was 91%. Urinary excretion of absorbed RK-75-Se was 13-3% and that of [75-Se]selenomethionine was 7-6%, in the 1st week. 4. Whole-body retention of 75-Se was greater for [75-Se]selenomethionine than for RK-75-Se but after the 1st week decreased at a similar rate in both groups. Tissue distribution of retained 75-Se was also similar in both groups. 5. The initial utilization of 75-Se in rabbit kidney is different from that of [75-Se]selenomethionine. However, after the 1st week 75-Se from these sources appears to be metabolized similarly, suggesting that Se from both is ultimately incorporated into the same metabolic pool.

Animals↗
PubMedDate not supplied

Selenium and total parenteral nutrition.

Despite the increasing recognition of selenium (Se) as an essential trace element in man, little is known about its metabolism during total parenteral nutrition (TPN) and the possible development of Se deficiency in high risk patients. From a general population known by its geographical location to have low Se blood levels, we studied a group of 23 surgical patients receiving TPN for at least one week. Whole blood Se levels were less than in the normal general population and, being some of the lowest observed in adult man, approached levels observed in animals with Se-responsive syndromes. Se continued to be lost predominantly in the urine although the Se content of the TPN fluids was very low (less than 0.6 micrograms/24 hr). Patients with excessive volumes of gastrointestinal excretion lost more Se. Se supplementation may be required in some patients receiving TPN.

Humans↗
PubMedDate not supplied

Selenium supplementation in total parenteral nutrition.

Four adult patients with very low plasma selenium (Se) levels ( less than or equal to 1.5 microgram/100 ml) were given Se supplements while receiving total parenteral nutrition. A comparison was made using the compounds selenomethionine and sodium selenite given either intravenously or by mouth. Urinary excretion and Se plasma responses differed, and indicated that selenomethionine retention was greater. However, the incorporation of Se into the erythrocyte and its enzyme glutathione peroxidase was unpredictable and delayed and was not a good indicator of supplement response. No deleterious effects of supplements were observed. Se supplements are indicated especially in patients with a high risk of developing low Se levels and are best monitored by plasma Se levels.

Administration, Oral↗