Showing papers on "Lead acetate published in 1979"
Journal Article•
TL;DR: Results indicate that chronic low-level lead exposure causes suppression of cell-mediated immune function in rats and resulted in suppression of responsiveness of lymphocytes to mitogen stimulation and in reduced delayed hypersensitivity responsiveness.
Abstract: Studies were performed to investigate the effects of chronic, low level pre- and post-natal lead exposure on cell-mediated immune function in rats. Weanling female rats were exposed to lead (as lead acetate) in their drinking water at 0, 25, and 50 ppm for 7 weeks. At the end of 7 weeks they were mated with untreated males and continued on the same dosage throughout gestation and lactation. The offspring of these females were weaned at 21 days of age and continued on the same lead exposure regimen as their mothers. These offspring were used in immune surveillance procedures between 35 and 45 days of age. Lead exposure at the levels employed had no statistically significant effect on growth and did not result in overt signs of toxicity. Thymic weights were significantly decreased in both males and females of the two lead dosage groups. Furthermore, lead exposure resulted in suppression of responsiveness of lymphocytes to mitogen stimulation and in reduced delayed hypersensitivity responsiveness. Results indicate that chronic low-level lead exposure causes suppression of cell-mediated immune function.
119 citations
TL;DR: Tri-n-butyl lead acetate at concentrations as low as 10/sup -6/ M severely inhibited the sodium-dependent, energy-requiring uptake of a variety of putative neurotransmitters, including dopamine, which was especially strongly affected by covalently bound lead.
88 citations
TL;DR: Behavioral effects produced by exposure to 50 and 300 ppm lead were similar in magnitude but varied in time to onset and decline, suggesting time-dependent, rather than concentration-dependent effects of lead.
84 citations
TL;DR: Lead and cadmium did not significantly affect the response of lymphocyte proliferation by Con A and lipopolysaccharide as well as purified protein derivative (PPD), and group variation and interpretation of data are discussed.
55 citations
TL;DR: It was concluded that the higher blood and tissue lead concentrations in the young were due to increased gastrointestinal absorption, and the consistently higher brain lead concentration in the suckling rats were caused by the increased blood lead concentrations and by the fact that lead is not easily removed from the brain.
51 citations
TL;DR: The possible mechanism for the synergistic action on genetic effects of the lack of calcium and intoxication by heavy metals are discussed, and it is recommended that routine attention be given to the state of calcium metabolism in heavy-metal intoxication.
Abstract: Mice kept on a normal (1.1% calcium) or low-calcium (0.03%) diet were exposed for one month to zinc chloride (0.5% Zn), lead acetate (0.5% Pb) or cadmium chloride (0.06% Cd) or to a mixture of these salts at half the above concentrations. These concentrations, given in a poor calcium diet, represent an LD 50/30 days. After the mice were killed bone-marrow cells were assayed for chromosomal aberrations, and serum calcium was determined. Chromosomal aberrations were detected in the mice maintained on a low-calcium diet and exposed to lead, zinc or a mixture of lead, zinc and cadmium. The possible mechanism for the synergistic action on genetic effects of the lack of calcium and intoxication by heavy metals are discussed, and it is recommended that routine attention be given to the state of calcium metabolism in heavy-metal intoxication.
49 citations
Journal Article•
TL;DR: Monkeys were dosed orally with 500 microgram/kg/day of lead as lead acetate from day 1 of life and tested on a two-choice non-spatial form discrimination using a WGTA apparatus; there was no difference between the groups in the effect of a series of "overtraining" trials introduced between reversals.
Abstract: Monkeys were dosed orally with 500 microgram/kg/day of lead as lead acetate from day 1 of life. No overt signs of lead toxicity were observed. At 2--3 years of age they were tested on a two-choice non-spatial form discrimination using a WGTA apparatus. Treated monkeys showed deficits compared to controls on a series of 20 discrimination reversals; there was no difference between the groups in the effect of a series of "overtraining" trials introduced between reversals.
39 citations
TL;DR: Male White Carneaux pigeons trained to peck three illuminated response keys in a predetermined four-step position sequence are suggested to be more sensitive to the effects of lead than the less stable error rates maintained under the acquisition schedule.
28 citations
TL;DR: The study has revealed that lead enters Tetrahymena through the membrane of digestive vacuoles and through the cell surface, and a mechanism is activated for removal of lead into membrane-bound spaces.
Abstract: Lead acetate (0.1–0.2%) forms a precipitate with the organic growth medium. The Tetrahymena cells ingest this lead-containing precipitate and cell growth is resumed after a variable lag period. Ingested lead is observed as electron-dense material in food vacuoles. Soon after exposure, cytoplasmic lead (preserved with certain fixation only) is revealed as electron-dense particles in cilia and in a halo around digestive vacuoles. Later the lead particles pervade the entire cell but after the lag period they are confined to membrane-bound spaces. In dilute growth medium, high concentrations of lead inhibit food-vacuole formation and cell growth. Under these conditions lead is deposited in alveoli of the pellicle and is also found in autophagic vacuoles and other membrane-limited structures. The study has revealed that lead enters Tetrahymena through the membrane of digestive vacuoles and through the cell surface. The change in distribution of lead during the lag period indicates that a mechanism is activated for removal of lead into membrane-bound spaces. The final storage of lead seems to be in lysosomes.
27 citations
01 Jan 1979
TL;DR: It is suggested that early lead exposure can affect certain behavioral processes and that the effects may persist even after the rat has reached maturity, as well as the ability of high lead-exposed rats to acquire a simultaneous visual discrimination task conducted in an operant chamber.
Abstract: Rats exposed to lead via the maternal milk were tested at maturity on three different visual discrimination tasks. Starting at parturition the dams were given either tap water, 0.20% sodium acetate, 0.02% lead acetate, or 0.20% lead acetate in the drinking water. At weaning, the pups from all the groups were placed on normal chow and tap water. At 20 days of age, the concentration of lead in the blood and brain of the high lead-exposed offspring was approximately 6 times that of controls (11 microgram% vs 66 microgram%). A significant deficit was found in the ability of the high lead-exposed group to acquire a simultaneous visual discrimination task conducted in an operant chamber. No significant differences were observed in the ability of lead-exposed rats to acquire either a successive visual discrimination task or a cued go/no-go discrimination. Thee results suggest that early lead exposure can affect certain behavioral processes and that the effects may persist even after the rat has reached maturity.
27 citations
Journal Article•
TL;DR: Female mice of the C57B1 strain were mated and given from the first day of the pregnancy a normal diet, or a calcium-deficient one, containing 0.2% of calcium, which increases the postimplantation mortality and the rate of skeletal anomalies among the fetuses and diminishes the blood calcium levels in the pregnant females.
Abstract: Female mice of the C57B1 strain were mated and given from the first day of the pregnancy a normal diet, containing 1.1% of calcium, or a calcium-deficient one, containing 0.2% of calcium. Animals of the 2 groups were injected intra-peritoneally with 15 or 35 mg of lead acetate/kg at different times of the fetal organogenesis (8th, 9th, 10th or 12th day of the pregnancy). In the normal diet group, injection of lead increases the postimplantation mortality and the rate of skeletal anomalies among the fetuses. The anomalies are restricted to the anterior part of the axial skeleton and consist essentially in the fusion of 2 or more cervical vertebrae. In addition, lead diminishes the blood calcium levels in the pregnant females. In the calcium deficient group, all these effects of lead are considerably increased and fetuses suffer a loss of weight and delayed ossification. In the animals given such a diet but non lead-injected, the fetal weight is already diminished. However, the ossification and the rate of skeletal anomalies are not affected, and the blood calcium levels of the mothers are similar to those of the control females given a normal diet.
TL;DR: Lead acetate was shown to stimulate a striking leukocytosis in young adult female mice and was due primarily to the elevated levels of neutrophils as suggested by a decrease in the ratios of peripheral agranulocytes to granulocytes.
Abstract: Lead acetate was shown to stimulate a striking leukocytosis in young adult female mice. The effect was manifest 4 days after lead injection and continued throughout the following 4 days. At the higher treatment level, lead induced an increase of 300% for both monocytes and neutrophils. The leukocytosis was due primarily to the elevated levels of neutrophils as suggested by a decrease in the ratios of peripheral agranulocytes to granulocytes. No differences from normal leukocyte cytology were observed in blood samples collected from animals receiving lead.
TL;DR: Tri- n -butyl lead acetate at concentrations of 5.10 −5 -10 −7 M was effective in inhibiting high affinity uptake and in stimulating release of accumulated radioactive putative neurotransmitters by mouse brain homogenates, suggesting that dopaminergic synapses are especially susceptible to such toxicity.
Journal Article•
TL;DR: The studies confirm the greater susceptibility of some active transport mechanisms of the small intestinal mucosa to lead toxicity, compared to those of the kidney, as well as the reduction in the in vivo intestinal absorption of glucose.
TL;DR: The results show that the central nervous system toxicity of Pb in neonatal rats is not associated with accelerated in vitro lipid peroxidation of brain tissue.
Abstract: Neonatal rats were given aqueous lead acetate intragastrically from d 2--20 of life at doses of 0, 25, 75, and 225 mg Pb/kg.d. Blood Pb concentrations on d 21 were (mean +/- SE) 27 +/- 4 (control), 150 +/- 26, 263 +/- 63, and 518 +/- 97 microgram/100 ml, respectively. Growth was significantly depressed only in animals given the highest dose of Pb (225 mg/kg.d). Hematocrits were significantly decreased by d21 at all doses of Pb. Malondialdehyde (MDA) formation in 750 x g (10 min) brain supernatants induced spontaneously by aerobic incubation at 37 degrees C was not altered by Pb on d 7 and 14, but a slight decrease was observed on d 21. The extent of MDA formation induced by enzymatically generated superoxide anion was not altered by Pb toxicity during the first 21 d of life. Addition of Pb to 750 x g (10 min) brain supernatants in vitro significantly decreased MDA formation at Pb concentrations of 10(-5) M and higher. These results show that the central nervous system toxicity of Pb in neonatal rats is not associated with accelerated in vitro lipid peroxidation of brain tissue.
TL;DR: Growing, mongrel dogs were fed high fat, low calcium, semipurified and purified diets with and without 77 ppm lead as lead acetate to experimentally induce the seizures and lead encephalopathy historically associated with accidental canine lead toxicity.
Abstract: Growing, mongrel dogs were fed high fat (22%), low calcium (.1%) semipurified and purified diets with and without 77 ppm lead as lead acetate to experimentally induce the seizures and lead encephalopathy historically associated with accidental canine lead toxicity. Seizures were observed in 44% of the lead toxic dogs and microscopic encephalopathy was observed in 89% of the lead toxic dogs. The encephalopathy was characterized by bilaterally symmetrical areas of vacuole formation involving the neuropile especially in a laminar pattern at the tips of the gyri of the cerebral cortex. The spongy state was accompanied by capillary activation and gliosis. These lesions are similar to those reported in accidental lead toxicoses in other species but previous efforts to experimentally induce these lesions in young dogs fed low-calcium, normal-fat (16%) purified diets have been unsuccessful.
TL;DR: While effects on the vagus nerve participate in the lead-induced sensitivity to norepinephrine, direct cardiac effects are also involved and the arrhythmogenic effect of methoxamine observed in lead-exposed animals could be completely prevented by bilateral vagotomy.
TL;DR: The results indicate that Pb toxicity in neonatal rats is not associated with accelerated in vivo lipid peroxidation in the brain, but that certain oxidant defense mechanisms in thebrain are stimulated by Pb.
Abstract: Neonatal rats were given aqueous lead acetate intragastrically from d 2 to 20 of life at doses of 0, 10, 50, and 225 mg Pb/kg.d. Blood Pb concentrations on d 21 were (mean +- SE) 23 +- 3 (control), 63 +- 19, 246 +- 55, and 994 +- 223 ..mu..g/100 ml, and brain Pb concentrations were 14 +- 2, 60 +- 5, 114 +- 15, and 275 +- 26 ..mu..g/100 g, respectively. Growth was significantly depressed only in rats given the highest dose of Pb (225 mg/kg.d). Solvent-extractable lipofuscin pigment concentration of brain tissue progressively decreased over the 21-d duration of the experiment but was not significantly altered at any dose of Pb. Brain glutathione peroxidase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase activities were stimulated on d 20 at the maximal dose of Pb, but the activities of brain superoxide dismutases and catalase were not altered by Pb exposure. Locomotor activity was significantly increased in the male animals on d 20, but only at the highest dose of Pb. These results indicate that Pb toxicity in neonatal rats is not associated with accelerated in vivo lipid peroxication in the brain, but that certain oxidant defense mechanisms in the brain are stimulatedmore » by Pb.« less
TL;DR: Learning deficits can be produced in the weanling rat at levels of exposure similar to those which cause encephalopathy in the developing neonate.
Abstract: At 23 days of age, three groups of male albino Sprague-Dawley rats were exposed to lead at concentrations of 0, 25, or 50 ppm, provided ad lib, in the acetate form, for 35 days in the drinking water. When tested on the problems of the Hebb-Williams closed-field maze learning task, the subjects receiving both 50 ppm lead acetate and 25 ppm lead acetate displayed significantly impaired learning ability when compared to water-fed controls in the total number of error zones entered over the 12 test problems. The time taken to traverse the maze enclosure, however, was significantly reduced only in the group receiving 50 ppm lead acetate. None of the overt manifestations characteristic of lead poisoning were observed. Learning deficits can be produced in the weanling rat at levels of exposure similar to those which cause encephalopathy in the developing neonate.
TL;DR: The data indicate that subacute lead ingestion results in the stimulation of renal 25-hydroxyvitamin D 3 -1-hydroxylase activity in four-week-old female Japanese quail.
TL;DR: It is suggested that VER latencies may be a sensitive index of subclinical effects of lead on brain, long after discontinuation of lead exposure and when blood levels are normal.
Abstract: Visual evoked responses were studied in the offspring of mother rats exposed to lead acetate. All measurements were taken by experimenters uninformed regarding treatment assignment. The latency of the P2 component was significantly shorter for the lead-exposed animals than for the control animals. It is suggested that VER latencies may be a sensitive index of subclinical effects of lead on brain, long after discontinuation of lead exposure and when blood levels are normal.
TL;DR: It is demonstrated that lead is specific among the metals tested in forming a complex with δ-aminolevulinic acid, which may be important in the mechanism of lead toxicity on the heme biosynthetic pathway.
TL;DR: Pb uptake was almost doubled in the spinal cord of rats having EAE while no significant changes occurred in blood or brain Pb levels.
TL;DR: In this article, the authors presented data for densities, electrical conductances and viscosities of the system lead dodecanoate/lead acetate and showed that the activation energies for viscous flow in the mixtures are similar to that of pure lead dodecaate.
TL;DR: The increase in hepatic GT and GGTP activities in lead treated animals appears to be a response to lead induced cellular damage or may result from interference with regulatory mechanisms responsible for production of these enzymes and not related to hepatic enzyme induction.
Abstract: Summary: Seven-day-old rats were fed 1% lead acetate tetrahydrate solution for 2,4, or 7 days. Adult rats were fed the same lead solution for 6–8 wk. In the newborn rats, hepatic UDP-bilirubin glucuronyl transferase (GT) and gamma glutamyl transpeptidase (GGTP) activities were markedly increased. GT activity was increased after 4 days as compared to the controls (6.3 ± 0.3 vs. 4.3 ± 0.3, P < 0.001), and was maximal after 7 days of treatment (7.5 ± 0.4 vs. 4.6 ± 0.4, P < 0.001). GGTP activity was already maximally increased after 2 days of lead treatment (1.4 ± 0.2 vs. 0.4 ± 0.1, P < 0.001). Hepatic GT and GGTP activities were similarly increased in adult rats (7.9 ± 0.3 vs. 5.1 ± 0.1, P < 0.001, and 0.7 ± 0.1 vs. 0.4 ± 0.1, P < 0.005, respectively). In vitro studies adding lead citrate to liver homogenates did not produce any direct effect on GT and GGTP activities. Speculation: The increase in hepatic GT and GGTP activities in lead treated animals appears to be a response to lead induced cellular damage or may result from interference with regulatory mechanisms responsible for production of these enzymes and not related to hepatic enzyme induction. The hepatic metabolism of drugs ingested by children with an increased lead burden may, therefore, be significantly altered.
TL;DR: The lead content of the adrenal glands, spleen, and bone marrow from lead-fed rats housed at 33°C was significantly increased over that of 23°C maintained animals, suggesting that the effects of the two agents were additive.
TL;DR: Observations that under certain experimental conditions there is stimulated hepatic meicrosomal enzyme activity in rats fed lead acetate are contained.
Abstract: Lead-containing compounds usually inhibit enzymic and metabolic processes. This inhibition is presumed to be the mechanism of intoxication by these compounds. Inhibition of detoxication activities of liver microsomal enzymes could be particularly detrimental because the toxicity of many different substances would be increased. Exposure of experimental animals to lead compounds in several studies has been associated with depressed activity of hepatic microsomal enzymes, reduced levels of hepatic cytochrome P-450, reduced levels of hepatic microsomal protein, and prolonged hexobarbital sleep times. The present report contains observations that under certain experimental conditions there is stimulated hepatic meicrosomal enzyme activity in rats fed lead acetate.
Journal Article•
TL;DR: It cannot be discounted that the exposure of these animals to Na3NTA for a longer period of time would not have had a more adverse effect on haversian bone remodelling activity.
Abstract: This study reports the changes observed in bone-formation dynamics at the cell, tissue and organ level in cortical bone in four standardization research colony-raised male Beagles that were exposed to 0.7 mg of lead acetate per day for 6 months, followed by a 6-month period when no lead acetate was given. Four similar age-sex matched Beagles of the same origin served as controls. Tissue and blood lead levels were measured. Biochemical and hematological analysis were carried out on a monthly basis. Plasma levels of immunoreactive parathyroid hormone were measured. In the absence of any alteration of the dogs' internal milieu, following 6-months exposure to lead there was a decrease in bone formation at the cell (70 percent), tissue (66 percent) and organ (66 percent) levels. Six months after the lead exposure was interrupted, bone formation returned to normal (93 percent at tissue and 100 percent at organ levels), but there was still some depression of activity at the cell level (70 percent). It is not known whether that cell-level depression of activity is due to persistent enzymatic inhibition following the 6-months exposure or whether it is due to the fact that the cell continued to operate in a micro-environment in which tissue levels of lead are elevated, or both.
Journal Article•
TL;DR: Inhibition of red blood cell delta-aminolevulinic acid dehydratase (RBC-ALAD) activity occurred in birds consuming as little as 14.8 ppm lead, which is suitable for investigating high lead foods.
Abstract: A rapid bioassay of lead was established in young japanese quail. Each group of 10 day-old birds received deionized water and a purified diet ad libitum for 2 wk. The diet contained 0.2 microgram lead/g. Lead acetate was added to give 14.8, 34.4, 51.2, 74.4, 234, 563, or 1223 microgram total lead/g by analysis. The duodenum, kidneys, liver and tibias were assayed for lead. Consumption of a diet containing either 563 or 1223 ppm lead caused a decrease (P less than or equal to 0.05) in body weight after 1 wk and an increase in free erythrocyte protoporphyrin after 2wk. Inhibition of red blood cell delta-aminolevulinic acid dehydratase (RBC-ALAD) activity occurred in birds consuming as little as 14.8 ppm lead. Packed cell volumes and hemoglobin concentrations were not affected by the dietary treatments. Lead concentrations in tissues from birds fed the lowest level of added lead were greater than those found in the corresponding tissues of control birds. The concentration of lead in the tibia showed the most distinguishable group means and the most nearly linear response; the highest slope was between 14.8 and 110 ppm dietary lead, using log-log transformations. The rapid bioassay is suitable for investigating high lead foods.
TL;DR: The results suggest that lead affects red cells at multiple metabolic loci, and lead-induced red cell P5N deficiency appears to be one of several pathogenic mechanisms in chronic lead exposure associated with the accumulation of lead in bone marrow.
Abstract: Intravenous administration of lead acetate to rabbits for 10 weeks at 2 week intervals resulted in significantly elevated blood lead levels, slight anemia with marked microspherocytosis and moderate basophilic stippling, and marked depression of red cellδ-aminolevulinic acid (ALA) dehydratase activity. However the decrease in red cell pyrimidine 5′-nucleotidase (P5N) activity was slight when compared to the red cell P5N activity of comparable reticulocyte-rich blood, and intracellular accumulation of pyrimidine nucleotides could not be demonstrated. In the in vitro inhibition test the same degree of inhibition of red cell P5N activity seen in hereditary red cell P5N deficiency was obtained by using a lead concentration 200–400 times higher than the lead levels detected in human plumbism. Most importantly, there were no differences in the lead-induced inhibition of human and rabbit red cell P5N.