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Recognition and management of children with increased lead absorption.
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HLA system and side effects of gold salts and D-penicillamine treatment of rheumatoid arthritis.
Among 67 patients with rheumatoid arthritis treated with gold salts (aurothiopropanol sulphonate) a significant correlation (p less than 10(-2)) was noted between gold toxic reactions, whatever their type, and the HLA antigens A1, B8, Cw7, and DR3. Forty-two patients were genotyped, and a correlation was observed between gold side effects and the haplotype A1 Cw7 B8 DR3 (p less than 10(-2), RR = 8.0). In addition 3 out of 4 cases of renal intolerance to D-penicillamine were observed in patients possessing the Cw7 B8 DR3 haplotype.
HLA antigens and toxic reactions to sodium aurothiopropanol sulphonate and D-penicillamine in patients with rheumatoid arthritis.
One hundred and forty-one patients with rheumatoid arthritis treated with aurothiopropanol sulphonate or D-penicillamine, or both were examined for HLA antigens to investigate the genetic influence on the occurrence of different adverse reactions during therapy. All 13 patients possessing HLA-DR3 had toxic reactions. The relative risk for DR3 positives of developing skin eruptions or proteinuria was calculated to be 10.5 times and seven times respectively that of DR3 negatives. The incidence of DR7 antigen in 94 patients with toxic reactions was significantly decreased (11% compared with 28% in controls) suggesting a protective role for this antigen.
The effects of 2.3-dimercaptopropanol (BAL) on gold reactions.
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Optic neuritis caused by arsenicals; treatment with B.A.L.
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Peripheral mercury embolization occurring during arterial blood sampling.
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Treatment of bismuth stomatitis with BAL.
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Mercuric chloride poisoning in a 23 month old child.
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Unithiol in Wilson's disease.
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Unithiol in Wilson's disease.
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Effect of 2,3-dimercaptopropanol (BAL) on urinary excretion and brain content of mercury.
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The effect of 2-3 dimercapto-propanol (BAL) on experimental nickel carbonyl poisoning.
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The effects of BAL on the metabolism of lead and on the symptomatology in lead intoxication.
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Icterus and amaurosis caused by lead poisoning in a cynomolgus monkey (Macaca fascicularis).
The diagnosis and treatment of a case of lead poisoning in a cynomolgus monkey (Macaca fascicularis) are described. The clinical signs were jaundice and amaurosis. Clinicopathological findings suggested cholestasis. A tentative diagnosis of lead poisoning was made when basophilic stippling of erythrocytes was observed in a peripheral blood smear. The diagnosis was confirmed by finding a lead concentration of 2280 micrograms/litre in a venous blood sample. Cage bars painted with red lead appeared to be the source of the poison. The lead was chelated by the intramuscular administration of 2,3 dimercapto-1-propanol (BAL) and calcium disodium edetate for seven days, followed by oral D-penicillamine for five weeks. The encephalopathy was treated with dexamethasone sodium phosphate. Recovery from the blindness was noted after 10 days and marked improvement of the general well being of the animal was observed after one month.
Dihydrolipoamide dehydrogenase from the halophilic archaebacterium Haloferax volcanii: characterization and N-terminal sequence.
Dihydrolipoamide dehydrogenase, a flavin disulfide reductase, has been purified and characterized from Haloferax volcanii. The enzyme is a dimer of relative mass 128,000, with an optimal activity at pH 9.0 in 1 M NaCl. Following reduction with its substrate, dihydrolipoamide, the enzyme is inactivated through covalent bond formation with the trivalent arsenical p-aminophenyl arsenoxide. The amino acid composition and the amino acid sequence of the first 49 residues of the N-terminus have been determined.
DMSA and DMPS--water soluble antidotes for heavy metal poisoning.
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Phenylarsine oxide inhibits heat shock protein 70 induction in cultured guinea pig gastric mucosal cells.
Phenylarsine oxide (PAO) forms a stable ring complex with vicinal dithiols that can be reversed with 2,3-dimercaptopropanol (DMP) but not by dithiothreitol (DTT) or 2-mercaptoethanol (2-ME). PAO at 2 microM or higher inhibited heat shock protein 70 (HSP70) induction within minutes in cultured guinea pig gastric mucosal cells exposed to heat (43 degrees C) for 30 min. PAO did not affect the nuclear translocation and phosphorylation of heat shock factor 1 (HSF1) induced by heat stress, but it completely blocked the binding activity of HSF1 to the heat shock element (HSE), leading to the block of expression of HSP70 mRNA and accumulation of HSP70 in the cells. These inhibitions were completely reversed with 2 microM DMP but not with 0.1 mM DTT or 1 mM 2-ME, suggesting specific interactions between PAO and vicinal dithiol-containing molecules. Thioredoxin (Trx) reversed the inhibition of the binding activity of HSF1 in whole cell extracts prepared from PAO-treated, heat-stressed cells. Our results suggest that PAO may react with vicinal-containing molecules including Trx and specifically block the interaction between HSF1 and HSE.