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Showing papers on "Lead acetate published in 1978"


Journal ArticleDOI
TL;DR: This recovery occurred despite continued high levels of lead in the blood and in the isolated capillary-microvessel fractions, suggesting that, as capillary endothelial cells mature, they are able to adapt to the presence of large amounts of lead.

86 citations


Journal ArticleDOI
TL;DR: Two methods for the determination of lead absorption have been developed using the rat as the test animal and it can be clearly demonstrated that vitamin D markedly enhances lead absorption.
Abstract: Two methods for the determination of lead absorption have been developed using the rat as the test animal. One is an everted intestinal sac method in which the time course of 210Pb transport across intestinal wall can be followed in vitro; and the other, 210Pb absorption from the intestine following gastric intubation can be followed in vivo. By using these techniques it can be clearly demonstrated that vitamin D markedly enhances lead absorption. Both techniques provide evidence that the distal small intestine is the major site of lead absorption and the site of greatest vitamin D stimulation. Lead acetate is apparently absorbed to the extent of 45% as it passes through the small intestine at a concentration of 0.01 mM.

51 citations


Journal ArticleDOI
TL;DR: The in vivo interaction between Pb concentrations of up to approximately 100 μg/100 ml blood and oxidative hemolytic anemia was due to the ability of lead to inhibit compensatory hematopoiesis after an acute hemolytics episode.

49 citations


Journal ArticleDOI
TL;DR: The results indicate that lead and iron interact at the level of the intestinal iron transport system in iron deficiency and that iron deficiency should be considered in the pathogenesis of lead poisoning.

44 citations


Journal ArticleDOI
TL;DR: In brain mitochondria the NAD-linked dehydrogenases, located in the matrix space, were more sensitive to inhibition by lead than were inner membrane enzymes, and all in vitro lead effects on mitochondrial respiration were comparable in cerebral and cerebellar mitochondria isolated from both immature and adult rats.
Abstract: The effects of lead acetate on respiration in cerebral and cerebellar mitochondria from immature and adult rats were studied polarographically. With all substrates low lead concentrations produced an increase in respiration. Higher concentrations produced an inhibition of both this lead-induced respiration and ADP-dependent (State 3) respiration. Lead-induced respiration required inorganic phosphate and was inhibited by oligomycin, suggesting a coupling to oxidative phosphorylation. Inhibition of respiration was produced by much lower lead concentrations with NAD-linked citric acid cycle substrates than with succinate or α-glycerophosphate. In partially disrupted mitochondria, NAD-linked substrate oxidation was inhibited at lead concentrations which did not affect NADH oxidation. Thus, in brain mitochondria the NAD-linked dehydrogenases, located in the matrix space, were more sensitive to inhibition by lead than were inner membrane enzymes. All in vitro lead effects on mitochondrial respiration were comparable in cerebral and cerebellar mitochondria isolated from both immature and adult rats.

43 citations


Journal ArticleDOI
TL;DR: Pyrimidine 5'-nucleotidase (P5N, EC 3.1.5) appears to be a sensitive index of exposure to low level lead and in children 2 to 5 years old with blood leads of 7 to 80 micrograms/dl there was a negative linear correlation of blood lead and red cell P5N.

42 citations


Journal ArticleDOI
TL;DR: Findings provide direct evidence for an inhibitory effect of lead exposure from birth on central cholinergic function in vivo and may partially be attributed to malnutrition observed in the lead-exposed animals.
Abstract: Rats were exposed to lead acetate from birth, and were killed at the age of 44–51 days for analysis of levels and turnover rates of acetylcholine (ACh). Steady-state levels of ACh were not altered in midbrain, cortex, hippocampus, or striatum of lead-exposed rats. Similarly, no changes in choline (Ch) concentrations were found in cortex, hippocampus, or striatum. In the midbrain, however, a 30% reduction in Ch levels was observed. Changes in specific activity of Ch and ACh were measured as a function of time in selected brain areas of rats infused with a radio-labeled precursor of Ch. Specific activities of ACh were not altered. Ch specific activities were, however, significantly elevated in all brain areas examined, as compared with age-matched control rats. The in vivo ACh turnover rate in cortex, hippocampus, midbrain, and striatum was diminished by 35%, 54%, 51% and 33%, respectively. These findings provide direct evidence for an inhibitory effect of lead exposure from birth on central cholinergic function in vivo. Since a significant reduction of body weight was found in those animals treated with lead acetate, the alteration of central cholinergic function may partially be attributed to malnutrition observed in the lead-exposed animals.

41 citations


Journal ArticleDOI
TL;DR: In vitro neoplastic transformation of Syrian hamster cells by lead acetate and its relevance to environmental carcinogenesis is studied.
Abstract: In vitro neoplastic transformation of Syrian hamster cells by lead acetate and its relevance to environmental carcinogenesis

41 citations


Journal ArticleDOI
TL;DR: Rats fed a semipurified diet that permits normal growth are more susceptible to the toxic effects of lead and can be used more effectively in lead toxicity studies than rats fed Chow.

35 citations


Journal ArticleDOI
TL;DR: The inhibition of δ-aminolevulinic acid dehydratase (ALAD) activity at several blood lead concentrations was confirmed both in vivo and in vitro and was not altered by pretreatment with phenobarbital or benzpyrene.

33 citations


Journal ArticleDOI
TL;DR: The data suggest that for this measure, the lead-reared rat may posses an increased sensitivity to amphetamines, and the potential of this model as an animal analog of minimal brain dysfunction hyperactivity is discussed.
Abstract: The effects of d -amphetamine on several measures of activity and spontaneous alternation were evaluated in rats chronically exposed to a low level of lead acetate via maternal milk

Journal ArticleDOI
TL;DR: Four groups of rats, continuously exposed to one of two lead acetate solutions, ad lib water or a limited amount of water, were tested for three daily 5 min periods on the open field.
Abstract: Four groups of rats, continuously exposed to one of two lead acetate solutions, ad lib water or a limited amount of water, were tested for three daily 5 min periods on the open field. The effects of treatment on activity, relative to animals drinking ad lib water, depended upon the concentration of the lead acetate solution. Animals exposed to a 10 −4 M lead acetate solution showed increased overall activity while animals exposed to a 10 −2 M lead acetate solution showed changes in the relative rate of activity. Activity was not affected by limiting the amount of water consumed. These findings illustrate the importance of recording activity in a manner which allows assessment of changes in activity as well as absolute level.

Journal Article
TL;DR: Airborne fallout from a nearby lead smelter was proposed as the primary mode of pasture contamination and increased urine lead concentration after chelation therapy was the most conclusive laboratory finding.
Abstract: Lead acetate was fed to 4 groups of 2 horses each to study chronic lead intoxication. A 5th group of 3 horses was maintained as controls. The leas was fed in capsules, with the minimum dosage of 6.25 mg/kg/day of lead as lead acetate (group I). The dose was increased from group I through group IV in an approximate geometric series, with each group being given about 125% of the dose given the previous group. These doses were given for 105 days, a period designated as phase 1. Since clinical signs were not observed after 105 days, the doses were increased and fed for an additional 190 days (days 106 to 295). This period was designated phase 2. The smallest daily dose in phase 2 was set at about 125% of the largest daily dose in phase 1. The doses in each group was increased by about 125% of that of the previous group, as was done in phase 1. Seven horses died or were euthanatized after 18 to 190 days of phase 2 (123 to 295 days after the 1st dose). One horse in group I did not develop any clinical signs of intoxication. Dose-related responses were unnoticed with doses larger than 15.3 mg/kg/day. All horses given lead had increased blood lead and serum iron concentrations. During phase 2, the hematocrit (erythrocyte volume) and hemoglobin contents were depressed. The lead concentration in kidney, liver, spleen, pancreas, brain, bone, and heart was increased in the treated horses. The dose level required to produce lead intoxication was greater than that reported for cattle and that estimated in epizootiologic studies of horses.

Journal ArticleDOI
TL;DR: The effects of lead acetate and aging on temporally-spaced responding (differential reinforcement of low rate or DRL-20 seconds) were studied and lead-treated animals exhibited a more variable response to d-amphetamine and a more pronounced number of IRTs in the first class interval.
Abstract: The effects of lead acetate and aging on temporally-spaced responding (differential reinforcement of low rate or DRL-20 seconds) were studied. Three groups of animals were considered along with their respective controls. Neonate-treated Long-Evans

Patent
10 Oct 1978
TL;DR: In this paper, an efficient and inexpensive method for producing lead monoxide from impure lead sulfate bearing materials such as recycled battery mud is provided comprising: (a) reacting said material with an ammonium carbonate solution to convert lead sulfates to lead carbonate; (b) decomposing the lead carbonates to produce impure led monoxide; (c) reacting the impure monoxide with an acidic ammonium acetate solution, and (d) reacting ammonium hydroxide with the lead acetate to form lead hydroxides; and (e) dehyd
Abstract: TITLE: PRODUCTION OF LEAD MONOXIDE FROM LEAD SULFATE WITH ACIDICAMMONIUM ACETATE ABSTRACT: An efficient and inexpensive method for producing lead monoxide from impure lead sulfate bearing materials such as recycled battery mud is provided comprising: (a) reacting said material with an ammonium carbonate solution to convert lead sulfate to lead carbonate; (b) decomposing the lead carbonate to produce impure lead monoxide; (c) reacting said impure lead monoxide with an acidic ammonium acetate solution to form a lead acetate solution; (d) reacting ammonium hydroxide with the lead acetate solution to form lead hydroxide; and (e) dehydrating the lead hydroxide to produce lead monoxide.

Journal ArticleDOI
TL;DR: The apparent, high tolerance of Tetrahymena pyriformis towards lead is believed to be due in part to the low ionic concentration of lead under the present conditions and inpart to a “detoxication mechanism” consisting of retention of lead within the digestive vacuoles and perhaps of accumulation of leads within the small, refractile granules.
Abstract: The ciliateTetrahymena pyriformis was exposed to lead acetate. Cell proliferation in the presence of 0.1% lead salt (with or without EDTA) equaled, after a variable lag period, that of the control cells. The lead (550 ppm) forms a “fluffy” precipitate with the organic growth medium; this was in part prevented by addition of EDTA. The cells primarily ingested the “fluffy” precipitate whereby they became exposed to large amounts of lead. Within the digestive vacuole, the “fluffy” precipitate became converted into refractile structures (3 μm in diameter) which were egested and accumulated at the bottom of the culture flask. The lead content of these defecation balls was higher than that of the “fluffy” precipitate. In addition to the lead-containing vacuoles, the cells contained small, refractile granules. The apparent, high tolerance ofTetrahymena towards lead is believed to be due in part to the low ionic concentration of lead under the present conditions and in part to a “detoxication mechanism” consisting of retention of lead within the digestive vacuoles and perhaps of accumulation of lead within the small, refractile granules.

Journal Article
TL;DR: A significant correlation between Cd and MT concentrations of the hepatic and the renal tissues was observed and lead and possibly some other metals, but not lead, may be determinants of concentration of metal binding protein in tissues.
Abstract: Dairy cows, growing swine, and laying chickens were given supplemental cadmium (Cd) at concentrations of approximately 2 and 10 ppm in feed as cadmium chloride and were given lead at concentrations of 5 and 25 ppm in feed as lead acetate for 12 to 24 weeks. Metallothionein (MT) and Cd concentrations increased more in renal than in hepatic tissues of the Cd-treated animals. The hepatic MT values in pigs and chickens and the renal MT values in all species continued to increase for several weeks after Cd feeding was stopped. A significant correlation between Cd and MT concentrations of the hepatic and the renal tissues was observed, except in bovine liver. The feeding of lead did not have any effect on the hepatic or the renal MT concentrations in cows, pigs, and chickens. Dietary Cd and possibly some other metals, but not lead, may be determinants of concentration of metal binding protein in tissues.

Journal ArticleDOI
TL;DR: A single intracardiac dose of lead acetate induced a 25‐fold increase in mitosis of mouse hepatocytes 5 hr after injection, as determined by autoradiography, suggesting that the mitotic cells were derived from a hepatocyte sub‐population arrested in the G2 phase.
Abstract: A single intracardiac dose of lead acetate (40 microgram lead/g body weight) induced a 25-fold increase in mitosis of mouse hepatocytes 5 hr after injection, as determined by autoradiography. The prompt appearance of a mitotic wave and the relatively large number of mitoses suggest that the mitotic cells were derived from a hepatocyte sub-population arrested in the G2 phase. The injection of lead also stimulated a small increase in labeled hepatocytes within 6 hr. Analysis of grain counts gave no evidence for unscheduled DNA synthesis. The incremental labeled cells may have originated from a small fraction of the G1 population that was ready to enter the S phase without the usual pre-synthetic delay.

Book ChapterDOI
01 Jul 1978
TL;DR: It appears that in the use of lead acetate hair dyes, some lead is absorbed systemically from the scalp in adults and children from a pica clinic.

Journal ArticleDOI
TL;DR: Acetylcholine concentration, when measured in whole brain, returned to normal levels at the end of a GO-day exposure in all the treated groups.
Abstract: To expose pups to lead, a concentration of 0.258, 0.5% and 1%lead acetate was administered through drinking water to Sprague-Dawley, ICR, lactating dams. After weaning, the pups were given the lead acetate in the drinking water. A significant decrease of 43%, 48% and 54% i n whole brain acetylcholine occurred after 21'days of treatment with 0.25%, 0.5% and 1.0% lead acetate, respectively. Similar treatment for 30 days caused a significant but lesser diminution at time of sacrifice of 37%, 38% and 34% i n whole brain acetylcholine content. Acetylcholine concentration, when measured in whole brain, returned to normal levels at the end of a GO-day exposure in all the treated groups. Treatment with 0.25% and 0.5% lead acetate solution did not have any adverse effect on the body weight of the growing mice, but treatment with 1%lead acetate in drinking water caused a significant decrease in body weight of mice. When mice were treated with 0.25%, 0.5% and 1%ead acetate for 30 days, the most pronounced de...

Journal Article
TL;DR: In this article, the authors used axillary and pubic hair analyses to confirm application of a hair dye containing 2% lead acetate for a period of 90 days and found that hair lead levels ranged from less than 6 to 41 ppm at the start and rose to 27 to 466 ppm by the end of the test period.
Abstract: Two experiments were conducted. In the first, 9 adult male subjects applied a marketed hair dye containing 2% lead acetate according to prescribed directions daily for a period of 90 days. Scalp, axillary and pubic hair were monitored for lead content before and at the end of the test period. Scalp hair analyses were used to confirm application of the hair dye; axillary and pubic hair were analyzed as biologic indicators of systemic lead absorption, i.e., metabolic incorporation of lead in hair growing at sites different from the dyed site. The axillary and pubic hair lead levels ranged from less than 6 to 41 ppm at the start and rose to 27 to 466 ppm at the conclusion of the experiment. Using 80 ppm hair lead as a measure of significant systemic absorption, 7 of 9 subjects showed this effect according to uptake by axillary hair and 4 of 9 according to pubic hair uptake. In the second experiment, blood and hair lead levels and blood erythroporphyrin were measured in 11 children from a pica clinic. Blood lead and hair lead levels were significantly correlated, i.e., r = +0.84. A regression formula was constructed relating these two parameters and blood lead values were predicted for the data of experiment 1, using observed hair lead values. The technique has important limitations; nevertheless, within these limitations, 1 of 9 subjects might be expected to have sustained an elevated blood lead level, i.e., in excess of 50 microgram/100 ml. It therefore appears that in the use of lead acetate hair dyes, some lead is absorbed systemically from the scalp.

Journal ArticleDOI
TL;DR: It is concluded that although lead attaches to bone surfaces, the hypercalcemia and hyperphosphatemia are caused by the direct interaction of lead with calcium and phosphate in solution in plasma.
Abstract: The effect of intravenous (i.v.) injection of lead acetate (15 or 30 mg/kg) was studied in young adult male rats. The reaction of lead with rat plasma to produce colloidal material containing both calcium and phosphate was demonstrated both in vitro and in vivo. This material could be centrifuged down at 25,000 ×g from plasma aliquots to which lead had been added or from plasma samples obtained as early as 5 min after i.v. lead injection. The hypercalcemia and hyperphosphatemia reached their peak rapidly after lead injection, and even at the higher dose level these lasted less than 6 h.45Ca and32P were injected at times varying from 1 to 8 days prior to lead administration. Plasma radioactivity levels rose with their stable counterparts without affecting plasma nuclide specific activity. Lead uptake on bone surfaces could be detected within 5 min of injection, and continued to accumulate for at least 6 h. It is concluded that although lead attaches to bone surfaces, the hypercalcemia and hyperphosphatemia are caused by the direct interaction of lead with calcium and phosphate in solution in plasma. The formation of the colloidal material lowers ionic calcium and phosphate. In vivo, calcium and phosphate are immediately withdrawn from extravascular sources returning plasma concentrations to their initial value. The source of at least the calcium is believed to be bone. The attachment of lead to bone surfaces does not in itself release significant amounts of calcium and phosphate into blood.

Journal Article
TL;DR: The present study suggests that repeated treatment of rats with EDTA during continuous exposure to lead reduces renal lead concentration but does not significantly influence the progression of lead induced nephropathy.
Abstract: The renal effects of repeated administration of EDTA were studied in rats given 0.5% lead as lead acetate in drinking water for 24 weeks. Repeated treatment of lead toxic rats with EDTA during continuous exposure to lead reduced blood lead levels and brain and bone lead but not to a statistically significant level (p greater than 0.05). Liver lead concentration in the EDTA treated, lead exposed rats changed only slightly upward, but kidney lead levels decreased greatly when compared to lead exposed, non-EDTA treated rats, (group IV vs. group III), (p less than 0.05). Light and electron microscopy of kidneys of lead treated rats showed evidence of an early interstitial nephropathy characterized by peritubular fibrosis and variation in size of tubular cells. Nuclei of renal tubular cells of lead exposed rats had inclusion bodies, but these were not present in lead exposed, EDTA treated rats. The present study suggests that repeated treatment of rats with EDTA during continuous exposure to lead reduces renal lead concentration but does not significantly influence the progression of lead induced nephropathy.

Journal ArticleDOI
TL;DR: Based on the lead concentrations found in selected tissues, the results indicate that the bioavailability of phospholipid-bound lead is similar to that of lead acetate at the 300 ppm level.
Abstract: Two different forms of lead, lead acetate and phospholipidbound lead, were fed to young and adult male rats for 10 weeks at the 300 ppm dietary level. Based on the lead concentrations found in selected tissues, our results indicate that the bioavailability of phospholipid-bound lead is similar to that of lead acetate at the 300 ppm level. Young rats had higher concentrations of lead in tissues than did adult rats.

Journal ArticleDOI
TL;DR: An acute dose of inorganic lead acetate prolonged rat methohexital-induced narcosis while doses of 1.5 and 2.0 mg kg i.p. did not.

Journal Article
TL;DR: In the monkey, the action of four renal toxics : lead acetate, sodium maleate, cadmium chloride and sodium chromate was compared and monkey and human beta2m have the same molecular weight and are antigenically similar, however, they differed in electrophoretic mobility.


Journal Article
TL;DR: Results indicated that lead caused stone formation in the bladder and calcification of both bladder and prostate; cadmium caused reduction in size and weight of prostate, and histological observation showed marked atrophy of the gland, cuboidal epithelium, and squamous metaplasia in the acini of the prostate.
Abstract: Forty male rats were divided into four groups. Group I served as control. Group II received 1 mg lead injected into the prostate; Group III received 1 mg cadmium chloride; and Group IV received 0.5 mg lead acetate and 0.5 mg cadmium chloride. The lead caused stone formation in the bladder and calcification of both bladder and prostate; cadmium caused reduction in size and weight of prostate, and histological observation showed marked atrophy of the gland, cuboidal epithelium, and squamous metaplasia in the acini of the prostate; there was no synergistic effect of lead acetate and cadmium chloride when combined at the level administered to Group IV.

Journal Article
TL;DR: The method of SCE was used as an indicator of the possible mutagenic activity of lead acetate in in vitro cultures of human lymphocytes, and the negative results obtained led us to examine other parameters, in particular the classical cytogenetic aberrations.
Abstract: The method of SCE was used as an indicator of the possible mutagenic activity of lead acetate in in vitro cultures of human lymphocytes. After determining the optimal concentration of BUdR, the cultures were treated with increasing doses of the metal. The negative results obtained with this method led us to examine other parameters, in particular the classical cytogenetic aberrations.

Journal ArticleDOI
TL;DR: The principle involved in the quantification of methanethiol in the presence of hydrogen sulfide is based on the efficient separation of hydrogen sulphide from methanetiol.
Abstract: The principle involved in the quantification of methanethiol in the presence of hydrogen sulfide is based on the efficient separation of hydrogen sulfide from methanethiol. The removal of hydrogen sulfide from a mixture containing methanethiol is dependent upon the selective reaction of hydrogen sulfide with crystalline lead acetate under dry conditions. It was found that crystalline lead acetate is not as selective as it was previously thought. It was also concluded that methanethiol either reacted or was absorbed by the crystalline lead acetate under dry conditions.