Showing papers on "Lead acetate published in 1970"

Defects in haem synthesis in mammalian tissues in experimental lead poisoning and experimental porphyria.

Abstract: SUMMARY 1. The biochemical effects of experimental lead poisoning and experimental porphyria induced by allyl-isopropylacetamide have been compared in New Zealand White rabbits. 2. In lead poisoning there was an increase in urinary coproporphyrin excretion within 48 hr of the first dose of lead. Urinary 8-aminolaevulic acid excretion increased about 1 week later and urinary porphobilinogen excretion about 3 weeks later. 3. In lead-poisoned rabbits the activity of the enzyme 8-aminolaevulic acid dehydrase was impaired in the brain, liver, kidney and bone marrow. This inhibition was largely due to interference with the sulphydryl groups of the enzyme. 4. No inhibition of the enzyme haem synthetase could be detected in homogenates prepared from lead poisoned tissues but the addition of lead acetate in concentrations similar to those present in the original unhomogenized tissues produced marked inhibition. 5. There was no increase in either the 8-aminolaevulic acid or the porphobilinogen content of the brain in lead poisoning but the b-aminolaevulic acid content of the liver, kidney and bone marrow, and the porphobilinogen content of the kidney were significantly increased. 6. Inhibition by lead of the enzymes 6-aminolaevulic acid dehydrase and haem synthetase may explain the biochemical abnormalities observed in lead poisoning. 7. In experimental porphyria the main enzyme abnormality found was a large increase in 8-aminolaevulic acid synthetase activity in the liver with increases in baminolaevulic acid dehydrase activity in the liver and kidney. In lead poisoning it is common to find anaemia associated with an increased urinary excretion of coproporphyrin, 8-aminolaevulic acid (ALA) and porphobilinogen (PBG) (de Langen & ten Berg, 1948; Haeger, 1957; de Kretser & Waldron, 1963). Much work has been done on the

Endotoxin studies in chicks: effect of lead acetate.

Abstract: Lead acetate administered intravenously in a mixture with endotoxin preparations potentiates the toxic effect of endotoxin for 14-21 day old meat strain chicks. A dose of 2.8 mg of lead acetate/100 g body weight is more effective with endotoxin than a dose of 2.5 mg; however, a dose of 3.0 mg or greater is toxic alone. The degree of potentiation appears to be at least 1000 fold and permits toxicity determinations using endotoxin levels ranging from 0.125 µg to 250 µg/chick. Endotoxin preparations made using NaCl, TCA or phenol-water extraction procedures, possessed toxic activity for chicks when tested by this method.

Abnormalities of erythrocytes and renal tubules of chicks poisoned with lead.

Abstract: Lead toxicosis was produced in chicks by feeding lead (as lead acetate) at the dose level of 5000 or 10,000 ppm. Signs of toxicosis included ataxia and decrease in body weight gain and feed intake. The lead content of livers of chicks fed the large dose (10,000 ppm) was 82.5 ppm and of controls, 0.5 ppm. In studies by light and electron microscopy various stages of mitosis were observed in the erythrocytes in the peripheral blood of chicks fed either dose. By light microscopy, necrosis of the epithelium of the proximal convoluted tubules of the kidneys was observed, and by electron microscopy, nuclei of these cells were seen to contain irregular-shaped, electron-dense inclusions.