Showing papers on "Lead acetate published in 1968"

An analysis of the growth of the cranial vault in rabbits by vital staining with lead acetate

Abstract: The mode and the rate of formation of individual bones in the cranium were studied by vital staining with lead acetate in 13 New Zealand white rabbits beginning at 35 days of age. These evaluations were compared with45Ca uptake at bilaterally comparable sites.

Effect of sulfhydryl compound on the lead acetate-induced endotoxin hypersensitivity of rats.

Abstract: Earlier study has shown that a single, normally well-tolerated, intravenous injection of lead acetate increases the sensitivity of the rat to the endotoxins of various gram-negative bacteria about 100,000 times above normal (H. Selye, B. Tuchweber and L. Bertok, J. Bacteriol. 91:884, 1966). This species is otherwise comparatively resistant to endotoxins (I. Berczi, L. Bertok, and T. Bereznai, Can. J. Microbiol. 12:1070,1966). The mechanism of the lead action in this phenomenon is unknown. It seems likely that the inactivation of SH groups (maybe in enzymes) plays an important role in lead action. In this paper, I report the results of an experiment conducted to investigate this possibility. Female Wistar rats with a mean body weight of 100 g (90 to 110 g) were subdivided into equal groups of 20 animals each and were treated as indicated in Table 1. The following compounds were used: Escherichia coli 089 lipopolysaccharide Westphal-type endotoxin, prepared in this laboratory by the warm phenol-water method (0. Westphal and 0. Lann, Methods Carbohydrate Chem. 5:83, 1965), lead acetate (Fisher Scientific Co., Fair Lawn, N.J.), cysteine hydrochloride (Fisher Scientific Co.), glutathione (Reanal, Budapest, Hungary), DL-methionine (Reanal), and DL-ethionine (Light and Co. L., Colnbrook, England). Each of these materials (in 1 ml of water) was injected into rats, intravenously. The blood pH values of the various treated animals were determined by use of Radiometer TT-1 Anstrup micrometer (Radiometer Co., Copenhagen, Denmark). The experiment was terminated 24 hr after the injections, by killing the survivors. As shown in Table 1, the endotoxin, lead acetate, or any tested sulfhydryl compound (doses were calculated on the basis of their molarity but are expressed more practically in milligrams, as indicated in the footnotes to Table 1) in themselves did not produce any mortality. The various combinations of endotoxin and sulfhydryl compounds and lead acetate also had no visible biological effect, and there were no significant changes in bloodpH value. However, lead acetate and endotoxin together always produce about 100% mortality, as described previously. Cysteine

Lead acetate as a vital marker for the analysis of bone growth.

Abstract: The use of lead acetate as a vital stain adds another method for the study of periodic appositional patterns of hard tissues. The distinct advantage of this technique is that these tissues can be decalcified and examined histologically without loss of the marker. The following method was used in preparation of the sections shown in the text. The rats received an intravenous injection of 4 mg lead acetate/kg body weight. After sacrifice, the tissues were decalcified in 1% HCL through which H2S was constantly bubbled. The action of the H2S gas is to convert the lead at sites of calcification to insoluble lead sulfide. Upon completion of decalcification the sections were embedded in 30% gelatin, and frozen sections at 15–20 μ were cut. The sections were then placed in a 0.1% solution of gold chloride for ten minutes. Next, they were placed in a 5% solution of sodium bisulphate for ten minutes. Subsequently they were washed in distilled water for 30 minutes and finally fixed in a 5% solution of sodium thiosulphate. No additional staining was used. The sections were then mounted with glycerine jelly. The resulting lead lines are sharp and therefore conducive to quantitative measurements. Because of the relatively thin sections cut, histologic details can be observed.

Calcergy inhibited by calciphylactic challengers

Abstract: The subcutaneous calcification effected in the rat at sites directly treated with calcergens, such as lead acetate, CeCl(3), CaCl(2), and KMnO(4), is inhibited by simultaneous local application of various calciphylactic challengers, but not by many other compounds.

Effect of endotoxin tolerance on the lead acetate-induced endotoxin hypersensitivity of rats.

Abstract: As is well known, the parenteral (intravenous or intraperitoneal) administration of a rather small dose of endotoxin renders animals, for a certain time, tolerant to a lethal endotoxin dose and also increases their natural resistance, i.e., elicits a so-called endotoxin resistance to a lethal dose of living bacteria (1, 2, 4, 5). According to our experience, a single small dose of intravenously or intraperitoneally administered endotoxin duly developed resistance in 24 hr (which then lasted for 14 to 16 days) against lethal doses of endotoxins or living bacteria (Bertok and Berczi, unpublished data). On the other hand, the endotoxin sensitivity of rats is known to be increased 10,000to 100,000-fold by the previous administration of a normally well-tolerated dose of lead acetate (3, 5). The experiment reported here was designed to reveal whether endotoxin hypersensitivity may still be induced by lead acetate in rats rendered tolerant to endotoxin or whether such animals are also resistant to the lead acetate-induced endotoxin hypersensitivity. Two hundred rats of Wistar origin (90 to 110 g each) were used. The animals were subdivided into four equal groups and treated as indicated in Table 1. The following compounds were used: Escherichia coli 089 lipopolysaccharide Westphaltype endotoxin, prepared in this laboratory by the warm phenol-water method (6), and lead acetate, obtained from Fisher Scientific Co., Fair Lawn, N.J. As shown in Table 1, a single intravenous injection of 50 ,ug of endotoxin protected 90% of the animals against a lethal dose of endotoxin administered 24 hr later and resulted in 80% protection also against lead acetate-induced endotoxin hypersensitivity. The experimental results suggest that, in the majority (80%) of rats rendered tolerant to endotoxin, lead acetate fails to induce endotoxin hypersensitivity. However, it seems more probable that lead acetate does induce TABLE 1. Effect of enzdotoxin tolerance on lead acetate-induced endotoxin hypersensitivity in rats

Action of thyroxine and calcitonin on experimental soft-tissue calcification.

Abstract: Experiments on rats indicate that pretreatment with thyroxine or calcitonin inhibits the soft-tissue calcification and the osteitis fibrosa induced by parathyroid extract overdosage. When the hormones are administered concurrently there is a summation of their actions. Calcitonin but not thyroxine inhibitits the skin calcification (calcergy) induced by an intravenous injection of lead acetate followed by topical administration of polymyxin. Moreover, calcitonin diminishes the hypercalcemia produced by a single injection of lead acetate, whereas thyroxine is ineffective in this respect. The mechanism of action of both hormones is briefly discussed.

Lead as a reducing agent in the preparation of bibenzyls and aromatic azoxy-compounds

Abstract: Lead powder is a convenient reagent for the reduction of aromatic nitro-compounds to the corresponding azoxy-derivatives. Both commercial lead powder and pyrophoric lead prepared from lead acetate and sodium borohydride solutions were effective. Reaction occurs under reflux in dimethylformamide or moist ethanol. Sixteen azoxy-compounds with alkyl, aryl, methoxy-, and halogeno-substituents have been prepared by use of this reagent. The two 2,6-dimethyl-substituted nitrobenzenes examined were reduced to the corresponding anilines. Lead converted benzyl chloride into bibenzyl but none of our specimens of lead were active for the conversion of iodo-benzene into biphenyl which Meszares has effected with another type of pyrophoric lead.

Pulmonary calcergy induced by inhalation of irritating gases.

Abstract: Experiments of the rat indicate that selective calcification in the pulmonary hilus region can be produced by the inhalation of formaldehyde-containing air following calcergic sensitization with intravenously administered lead acetate. The technique reveals otherwise latent degrees of pulmonary irritation by air contaminants.