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Biomedical subjects

M R Moore

Publications and source records attributed to M R Moore.

At least 271 records · Page 15Linked to original sources
PubMed1977

The effect of calcium on lead absorption in rats.

The effects of Ca2+ on lead absorption as PbCl2 and 203PbCl2 were studied in rats. 1. Doubling of dietary calcium with Ca3(PO4)2 significantly decreased lead absorption as assessed by 203Pb retention, tissue lead concentration, urinary excretion of delta-aminolaevulinate and increased activities of delta-aminolaevulinate dehydratase and ferrochelatase. 2. Similar effects on lead absorption were shown by the Ca2+ salts, Cl-, CO32-, PO43-, SO42-, gluconate and glycerophosphate. 3. CaCl2 and calcium glycerophosphate were found to be most effective in decreasing lead absorption when administered immediately before lead dosage. 4. A negative exponential relationship was found between CaCl2 concentration and 203Pb absorption at 120h. The result suggest that, above 4 mmol of administered calcium, residual lead absorption is unaffected by increasing gastrointestinal calcium concentrations. 5. Increased systemic calcium had no effect on lead retention. 6. Calcium in the concentrations found in domestic hard-water supplies significantly decreased absorption of a solution of 203Pb dissolved in it compared with absorption of 203Pb dissolved in soft or distilled water. 7. Milk and skimmed milk were found to have no effect on 203Pb absorption in rats.

Animals↗
PubMed1977

A retrospective analysis of blood-lead in mentally retarded children.

Blood-lead concentrations were measured retrospectively in the blood contained on cards used for testing for phenylketonuria in the first two weeks of life. Cards which belonged to 80 of a group of 77 children with mental retardation of unknown aetiology and 77 controls were identified. Of 77 usable cards, 41 were from mentally retarded children and 36 were from controls; 24 mental-retardation/control pairs were found. There was a highly significant trend towards higher blood-lead concentrations in the mentally retarded children. Water-lead concentrations in the maternal home during pregnancy correlated with blood-lead concentrations in the mentally retarded children. These results reinforce the probable association between lead exposure during pregnancy and the development of mental retardation of otherwise unknown aetiology.

Child↗
PubMed1977

Renal insufficiency associated with excessive lead exposure.

Water lead concentrations were measured in 970 households throughout Scotland. Blood lead concentrations were measured in 283 people living in houses with water lead levels of over 0-48 mumol/l (100 mug/l). A highly significant correlation was found between lead concentrations in water and blood. Raised blood lead concentrations were associated with renal insufficiency, reflected in raised serum urea concentrations, and with hyperuricaemia, although there was no evidence of clinical disease in any of the affected people. This is further evidence that excessive lead in domestic water supplies has a harmful effect on the community's health.

Environmental Exposure↗
PubMed1977

Lead in drinking water in soft water areas--health hazards.

Studies have been made of the uptake of lead into drinking water and the association of that with the blood lead of persons resident in houses supplied with such water. Significant regressions were found between water lead and blood lead concentrations. Very high concentrations were found in houses with lead plumbing. There were in addition increased lead concentrations found in houses using copper piping joined with lead soldered joints. These studies have suggested that some health hazards might be expected to be associated with the increased environmental uptake of lead in these situations.

Adolescent↗
PubMed1977

Alterations in the activity of enzymes of haem biosynthesis in lead poisoning and acute hepatic prophyria.

1. The activities of six of the enzymes of haem biosynthesis have been assayed in peripheral blood from patients with lead poisoning, acute intermittent porphyria or hereditary coproprophyria. 2. Compared with normal subjects the lead-poisoned subjects had highly significant depression of delta-aminolaevulinate dehydratase, coproporphyrinogen oxidase and ferrochelatase. 3. Lead-poisoned subjects had highly significant elevation of delta-aminolaevulinate synthase activity. 4. delta-Aminolaevulinate synthase activity was inversely related to the haemoglobin concentration. 5. Increased delta-aminolaevulinate synthase and decreased delta-aminolaevulinate dehydratase activity are also found in acute intermittent porphyria. 6. Increased delta-aminolaevulinate synthase, normal prophobilinogen deaminase and uroporphyrinogen decarboxylase and decreased coproporphyrinogen oxidase are found in both lead poisoning and hereditary coproporphyria. 7. These enzyme changes explain the recognized patterns of porphyrins and prophyrin precurosrs in blood and urine in these conditions.

5-Aminolevulinate Synthetase↗
PubMed1977

The treatment of acute intermittent porphyria with laevulose.

1. The activities of the enzymes of haem biosynthesis were studied in 23 patients with acute intermittent porphyria. The mitochondrial enzymes delta-aminolaevulinate synthase, coproporphyrinogen oxidase and ferrochelatase were measured in leucocytes and the cytosolic enzymes delta-aminolaevulinate dehydratase, porphobilinogen deaminase and uroporphyrinogen decarboxylase in erythrocytes. 2. Leucocyte delta-aminolaevulinate synthase activity was elevated (P less than 0-001), with marked diminution of porphobilinogen deaminase activity (P less than 0-001) and reduction in the activities of delta-aminolaevulinate dehydratase (P less than 0-01) and uroporphyrinogen decarboxylase (P less than 0-005). 3. A therapeutic regimen based on intravenous laevulose infusion was studied. In four patients in acute attack and one in remission laevulose treatment was associated with a fall in delta-aminolaevulinate synthase activity, a rise in porphobilinogen deaminase and uroporphyrinogen decarboxylase activities, and a fall in urinary prophyrin precursor excretion (P less than 0-001). These studies provide a basis for the evaluation of the use of sugars in acute intermittent porphyria.

5-Aminolevulinate Synthetase↗
PubMed1977

Hereditary coproporphyria presenting with photosensitivity induced by the contraceptive pill.

A 26-year-old woman developed photosensitivity and jaundice after starting on an oral contraceptive agent. She was found to have hereditary coproporphyria. Histological examination of two liver biopsies taken during and after the acute attack did not reveal any changes thought to be due to hereditary coproporphyria. Screening of the patient's family revealed a further six latent cases.

Adult↗
PubMed1977

Pregnancy and the acute porphyrias.

An analysis is presented of the obstetric histories of 50 women with acute porphyria, comprising 39 with acute intermittent porphyria, 3 with variegate porphyria and 8 with hereditary coporporphyria. Fifty-four per cent of the women with acute intermittent porphyria had an acute attack of porphyria in pregnancy and/or the puerperium. Only one maternal death was recorded. One patient with variegate prophyria and two with hereditary coproporphyria had an attack related to pregnancy. The total fetal wastage was 13 per cent. The babies born to mothers with acute intermittent porphyria, who experienced an acute attack during pregnancy, were smaller than those in which no such attack occurred (P less than 0.001). In 13 non-porphyric primigravidae there was a rise in urinary excretion of delta-aminolaevulinic acid, porphobilinogen and coproporphyrin up to the 28th week of gestation. It is probable that pregnancy has some deleterious effects in acute prophyria but the prognosis of the porphyric pregnancy is much better than the literature suggests.

Acute Disease↗
PubMed1977

Hereditary coproporphyria and epilepsy.

A 9-year-old boy with mental deterioration and epilepsy suffered an acute attack of hereditary coproporphyria associated with worsening of seizure control. Leucocyte coproporphyrinogen oxidase activity was undetectable in the patient during this attack, and was reduced in his mother, a latent case. The complex relationship between porphyria, epilepsy, and anticonvulsant drugs is discussed.

Aminolevulinic Acid↗