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[Determination of lipase catalytic activity with 2,3-dimercapto-1-propanol-tributyrate as substrate].

The two point test for the determination of lipase by Kurooka et al. (J. Biochem. Tokyo 81, 361-369 (1977)) was studied in detail. This procedure uses 2,3-dimercapto-1-propanol-tributyrate as substrate and Ellman's reagent as an acceptor for the released thiol groups. The time course of the enzymic hydrolysis of the substrate showed a pronounced lag phase, which can be influenced by sodium glycocholate. There is no proportionality between the quantity of added serum and the concentration of released thiol groups. Preincubation of the sample with the esterase inhibitor, phenylmethylsulphonylfluoride, as recommended by the authors, does not completely inhibit the serum esterase activity. The action of sodium dodecyl sulphate, which is included in the system, is not explained; in the continuous titrimetric test with triolein as substrate, it acts as a powerful lipase inhibitor. Using 104 serum samples, significant differences were found between the results from this method and those obtained by the titrimetric determination of lipase. Possible fundamental improvements of this test system, using thioesters as substrate, are discussed.

Dimercaprol↗

Fetal uptake and distribution of metallic mercury vapor in the mouse: influence of ethanol and aminotriazole.

The placental transport of mercury in pregnant mice and its localization in the embryo and fetus from early organogenesis through the whole fetal period was studied by whole-body autoradiography and gamma counting. Metallic mercury (203Hg0) (after inhalation) was compared to inorganic 203HgCl2 (after i.v. injection). Hg0 appears to be oxidized to Hg2+ in the fetal tissues and Hg0 inhalation results in about 4-fold higher fetal mercury concentration than Hg2+ injection (9.9 versus 2.4% gram dose per gram tissue). Preadmission to the dams with ethanol or aminotriazole resulted in higher fetal concentrations (especially in the liver) of mercury after inhalation of Hg0 but not after injection of Hg2+. A high placental concentration and accumulation in the corpora lutea of mercury after Hg0 inhalation should be also noted.

Amitrole↗

[Concentration of gold in macrophages of the bone marrow in rheumatic diseases subjected to chrysotherapy].

Ultrastructural investigation of bone marrow cells of histiocytic lineage to determine the presence of microcrystals containing gold was carried out in 12 patients. Eleven patients had classical or definite rheumatoid arthritis and one had palindromic rheumatism; the duration of these diseases ranged from 6 months to 10 years. Two patients had never received chrysotherapy and therefore served as controls. The remaining 10 patients had been treated with sodium aurothiopropanolsulfonate for periods ranging from 1 week to 4 years and 4 months without any clinical signs of laboratory findings--hematological changes in particular--of drug intolerance. No crystalline structures could be found in the 2 controls or in the patient who had just begun treatment. Conversely, in the 9 other patients, the lysozymes of bone marrow macrophages contained needle-like microcrystals containing one atom of gold for two atoms of sulfur, i.e. identical in proportion to the injected product. For equivalent total doses, deposits appeared to be equally numerous regardless of the time span between the last injection and the sampling (2-21 months). These crystals were present in the bone marrow several years after the beginning of chrysotherapy. The actual mechanism of their precipitation remains unknown at present.

Adult↗

Chelation of cadmium from metallothionein in vivo and its excretion in rats repeatedly injected with cadmium chloride.

Chelation and removal of cadmium from rats which were exposed to cadmium by multiple injections were studied in vivo after injection of two different compounds, 2,3-dimercaptopropanol (BAL) and diethylenetriamine pentaacetic acid (DTPA). Rats were injected i.p. with 1 mg of Cd/kg as 109CdCl2 daily for 4 days and 3 days after the last injection, they were treated with the chelating agents alone or in combination 5 days in a week for 2 weeks. BAL (50 mg/kg) alone or in combination with DTPA (50 mg/kg) was effective in removing cadmium from the body without increasing the level of cadmium in the kidney, the critical organ in cadmium toxicity. After treatment with BAL alone and BAL-DTPA, cadmium was excreted mainly in the feces with marked decrease in hepatic and renal concentrations of both cadmium and metallothionein. Injection of DTPA alone increased the urinary excretion of cadmium without any significant change in tissue cadmium. Although the urinary excretion of zinc was increased after injection of DTPA and also BAL-DTPA, there was no change in the tissue levels of zinc and copper. The results of this study suggest the potential use of BAL or BAL-DTPA combination as a mode of chelation of cadmium from the body under proper experimental conditions in chronic cadmium poisoning. It may be possible to prevent tubular damage in the kidney, the critical organ in cadmium toxicity by this treatment.

Animals↗

[Acute delirium in bismuth poisoning].

Typical clinical signs and symptoms of bismuth intoxication are illustrated in a cases of a 45-year-old woman. Initially psychasthenia appears followed by acute delirium with ataxia, myoclonic jerks and occasionally coma. If patients survive the acute phase they recover only gradually following discontinuation of bismuth medication. In cases of extreme intoxication, permanent memory deficits may occur. Etiology, pathogenesis, laboratory findings, differential diagnosis and therapy of this rare iatrogenic encephalopathy are discussed.

Bismuth↗

[Acute self-poisoning with arsenic and treatment with BAL (author's transl)].

A case of attempted suicide by ingestion of 4.8 g As2O3 (more than 20 times the estimated lethal dose) is reported. Absorption of arsenic caused elevated urinary levels over 5 days BAL treatment was started within three hours after arsenic ingestion. The patient did not develop any signs of polyneuropathy or other clinical changes.

Arsenic Poisoning↗