Showing papers on "Lead acetate published in 1986"
TL;DR: It appears likely that the observed decrease in SOD in young rats is caused indirectly by a lead-induced copper deficiency rather than by a direct inhibitory effect of lead.
287 citations
TL;DR: It is strongly suggested that lead acetate induces the synthesis of Pb-MT as well as Zn-MT in rat liver.
Abstract: Administration of a sublethal dose of lead acetate to rats induced the simultaneous synthesis of a Pb-metallothionein (Pb-MT)-like protein (Pb-BP) and Zn-thionein (Zn-BP) in the liver. The Pb-BP had an apparent molecule mass of 6900 Da and seemed to bind preferentially to lead in the liver cytosol. The Zn-BP was identified by comparison of the Mr, elution profiles from Sephadex G-75 and DEAE-Sephadex A-25 columns, and polyacrylamide-gel-electrophoretic mobility, with those of rat liver Zn-MT-II. The Pb-BP accumulated in the liver to a maximum 6 h after the intraperitoneal injection of lead acetate and accounted for about 60% of the lead in the liver cytosol at this stage. However, after that, it gradually decreased in the liver, until it was close to the basal amount 24 h after the induction. In contrast, the amount of Zn-MT increased gradually, reached a maximum 12 h after the administration of lead acetate and maintained a constant value until at least 24 h after the induction. Amino acid analysis of the Pb-BP indicated that it contained about 28% half-cysteine. These results strongly suggest that lead acetate induces the synthesis of Pb-MT as well as Zn-MT in rat liver.
53 citations
TL;DR: The differential sensitivity of open field activity and select hippocampal theta frequencies to the timing of lead administration suggests that the identification of toxic consequences depends on the function assessed and the developmental stage during which lead exposure occurred.
39 citations
Journal Article•
TL;DR: It is concluded that the effects of lead in cognitive tasks are not secondary to changes of general activity level, whereas true cognitive deficits are likely to underly the impairment of learning set formation seen in the low lead group.
Abstract: Rhesus monkeys were pre- and postnatally exposed to 0, 350, or 600 ppm lead acetate in the diet. Blood lead levels of the mothers were less than 1, 24.4, and 37.4 micrograms/100 g blood, respectively, while those of the offspring were substantially higher, at least in the early stages of development. At the age of 12-15 months the animals were tested for group activity levels in an unfamiliar environment. No substantial lead-related alterations of activity occurred neither for group activity nor for the activity of individual animals. There were, however significant dose-related impairments of pattern discrimination learning set formation, while in simple discrimination learning during the early training phases deficits were seen in the high lead group only. Emotional alterations of these animals may account for this result, whereas true cognitive deficits are likely to underly the impairment of learning set formation seen in the low lead group. It is concluded that the effects of lead in cognitive tasks are not secondary to changes of general activity level.
39 citations
Journal Article•
TL;DR: Evidence is provided that Hg++ and Pb++ can directly induce active tension by action on processes which rely on extracellular Ca++ and segments exposed to these analogues lost their ability to respond to other agonists.
Abstract: Mercuric chloride and lead acetate caused contraction of rabbit aortic segments in vitro. Mercuric chloride was added to a Krebs Henseleit solution; lead acetate was added to a Tris-buffered medium to avoid any precipitation of lead. Cadmium (Cd++) acetate, in either medium, had no direct effect. The Hg++- and Pb++-induced contractions were significantly reduced when Ca++ was omitted from the physiological buffer or when pH decreased. The alkylated analogues of Hg++ and Pb++ salts had little direct contractile effect. However, segments exposed to these analogues lost their ability to respond to other agonists. This report provides evidence that Hg++ and Pb++ can directly induce active tension by action on processes which rely on extracellular Ca++.
29 citations
TL;DR: The results indicate that lead-treated rats, as compared to controls, have augmented and prolonged pressor responses to epinephrine and norepinephrine; less pronounced depression of arterial pressure in response to epinphrine and isoproterenol; and more pronounced tachycardia in response in the lead- treated rats.
28 citations
Journal Article•
TL;DR: Quantitative histological examination and Golgi analysis of the cerebellum revealed a number of alterations in the lead treated rats, including a reduction in the dendritic arborization of Purkinje cells in the treated rats at 30 days of age.
Abstract: Long-Evans hooded rat pups were given 600 mg/kg body weight lead acetate every 24 hours via stomach intubation beginning one day after birth until an accumulative dose of 2400 mg/kg was administered. The body weights of the lead treated rat pups at 10 and 30 days of age were not significantly decreased when compared to controls. The brain weights at 10 and 30 days of age in the lead exposed rats was significantly greater than those of the control rats. Blood lead levels averaged 526.35 micrograms/dl at 10 days of age in lead treated rats and 0.079 microgram/dl in controls. Quantitative histological examination and Golgi analysis of the cerebellum revealed a number of alterations in the lead treated rats. Lead exposure resulted in a significant decrease in the molecular layer width (72%). The granule cell density was depressed in the lead exposed rats, despite the observation that the granule cell layer width did not differ significantly in the two groups. This suggests that the granule cell packing in this layer was decreased. The Golgi study revealed a reduction in the dendritic arborization of these cells in the treated rats at 30 days of age. There was a 20% reduction in height and a 14% reduction in width in the Purkinje cells dendrites of the lead exposed rats when compared to Purkinje cells of age matched controls. Estimation of the amount of dendritic material by the Scholl method revealed a 40% decrease in the dendritic arborization of Purkinje cells following lead exposure.
25 citations
TL;DR: The hypothesis that lead acetate may inhibit spermatogenesis by a disturbance of the metabolic activities of the Sertoli cells is supported.
Abstract: The effects of lead acetate on protein synthesis and lactate production by cultures of rat Sertoli cells in vitro were studied. Sertoli cell cultures prepared from 20 day old Sprague-Dawley rats were exposed to 0.01, 0.05 and 0.10 mM lead acetate. Lactate production was significantly elevated by all concentrations of lead after 3, 6, 9 and 12 hours of exposure. Protein biosynthesis as measured by [3H]-leucine incorporation was significantly depressed by 0.05 and 0.10 mM lead acetate after 2 hours of exposure. These results support the hypothesis that lead acetate may inhibit spermatogenesis by a disturbance of the metabolic activities of the Sertoli cells.
25 citations
TL;DR: Data indicate that lead is readily exchangeable from osteoclastic bone cells and, as in soft tissues (hepatocytes), the bulk of cellular lead is associated with mitochondria.
24 citations
Journal Article•
TL;DR: Comparison of these data to previous studies from this laboratory of FI performance, suggests that FR response rates are less sensitive than FI to disruption by lead.
Abstract: Male rats were chronically treated via drinking water with 50 or 500 ppm sodium acetate or 50 or 500 ppm lead acetate from weaning. Behavioral testing on a fixed-ratio (FR) schedule of reinforcement began at 55 days of age. A series of increasing ratio values was studied. The lower exposure level was without effect at any ratio value. The 500 ppm concentration decreased response rates over the first 15-20 sessions of FR5 and FR25, after which rates reached control levels. Changes in response rate derived primarily from longer interresponse times (IRTs) and decreased running rates. Differences in performance were not evident at FR values of 50 and 100. The 50 ppm concentration produced blood lead (PbB) values averaging 30.3 micrograms/dl; the 500 ppm concentration produced PbBs of 58-94 micrograms/dl. Zinc protoporphyrin levels resulting from 500 ppm exposure differed from controls even after one month of exposure, and continued to increase over eight months of exposure, to 72 micrograms/dl. Comparison of these data to previous studies from this laboratory of FI performance in which the identical exposure protocol was employed, suggests that FR response rates are less sensitive than FI to disruption by lead.
22 citations
Journal Article•
TL;DR: Significant increase in blood and testis of lead levels along with decrease of ALA-D levels were observed and other details concerned with the damage of the testicular tissue are discussed.
Abstract: The experiments were performed on mature male rats divided in five groups, one control and four experimental in which the animals received 1 mg, 2 mg, 4 mg and 6 mg/kg body weight lead acetate intraperitoneally respectively, over a period of 30 days. ALA-D and lead was estimated in the blood by the use of atomic absorption spectrophotometer and ATP-ase, AMP-ase, Alk-ase were histochemically localized. Significant increase in blood and testis of lead levels along with decrease of ALA-D levels were observed. Changes in the testicular tissue were encountered. Other details concerned with the damage of the testicular tissue are discussed.
TL;DR: The behaviour of the treated offspring in social encounters was shown by ethological procedures to differ from that of controls and the behavioural effects of lead differed between males and females and were different in juveniles from those seen in adulthood.
TL;DR: The intestinal mucosal epithelium is affected which leads to malabsorption, while in the kidney proximal tubular cells degenerate causing secretion of essential materials such as glucose, amino acids, etc., in the urine.
TL;DR: It is suggested that disulfiram potentiates the adverse effects of lead on growth rates and on cerebellar Purkinje neuron function by facilitating the accumulation of lead in brain tissue.
TL;DR: It is suggested that future work directed at mechanism(s) underlying lead-induced alterations in agonistic behavior of male Binghamton Heterogeneous stock mice should consider life span changes in biobehavioral profiles.
TL;DR: The results suggest that lead acetate (10 mM) administered for 8 weeks does not suppress the primary direct humoral immune response to SRBC in inbred and outbred mice of several H-2 haplotypes.
TL;DR: It is concluded that low-level lead exposure is not associated with an impairment of either T-or NK-cell function and splenocytes isolated from exposed animals to mediate native and interferon-activated natural cytotoxicity.
TL;DR: The results indicate that the Pb-BP is cross-reactive with the antibody against rat Zn-thionein II, strongly suggesting that this protein is a species of metallothionein.
TL;DR: The findings imply that the initial target of inorganic lead in the CNS may be the plasma membrane of the capillary endothelial cells, and that lead may act by altering the physiological function of these membranes.
TL;DR: These data provide a more stringent test of the chemical monitor–biological monitor correlation than has previously been possible and despite evidence of a compensation mechanism developing in the enzyme determinations, enzyme activity ratios still correlate reasonably well with blood lead levels.
Abstract: Blood lead levels, together with delta-aminolevulinic acid dehydratase activity determinations have been measured on rats dosed with up to 1000 ppm lead acetate in their drinking water for periods up to 5 weeks. Despite evidence of a compensation mechanism developing in the enzyme determinations, enzyme activity ratios, if properly chosen, still correlate reasonably well (r = 0.87) with blood lead levels. Activity ratios using data on the shoulders of pH-activity profiles (e.g. activity ratios of 6.4 and 7.2), however, give much less satisfactory correlations. These data provide a more stringent test of the chemical monitor-biological monitor correlation than has previously been possible.
TL;DR: In this paper, the electrodeposition of lead was carried out on five substrates: C, Cu, Ag, Au and Pb from aqueous solution of 2.5 M ammonium acetate, 2.4 M acetic acid and 0.11 M lead chloride.
Journal Article•
TL;DR: It is suggested that neonatal lead exposure alters the dendritic development of pyramidal cells of rat motor cortex.
Abstract: Neonatal Long-Evans rat pups were given the standard dose, 600 mg of lead acetate per kg of body weight every 24 hours beginning one day after birth until a cumulative dose of 2400 mg/kg (4 doses) had been administered via stomach intubation. Blood lead levels in lead treated rats averaged 526.35 micrograms/dl at 10 days of age. Blood lead values in age-matched controls averaged 0.079 microgram/dl. The body weights of the lead treated rats were not significantly different than control rats at 30 days of age. The brain weights were significantly greater than those of control rats at 30 days. Camera lucida drawings of pyramidal cells from motor cortex of control rats contained significantly (54%) more secondary and tertiary branches extending laterally from the primary apical dendrite than pyramidal cells of lead treated rats. The dendritic branches were numbered according to their branching point away from the soma. There was a significant reduction in the number of 4, 5, 6, and 7th order branches extending from the apical dendrite and 3 and 4th order branches extending from the basal dendrites in the leaded-rats. The mean dendritic length was reduced by 19% in basal dendrites and by 28% in apical dendrites. Measurements of dendritic material by the Scholl method revealed 17% reduction in the basal dendrites and a 36% reduction in the apical dendritic material in treated rats. These results suggest that neonatal lead exposure alters the dendritic development of pyramidal cells of rat motor cortex.
TL;DR: The decreased response to muscarinic receptor activation by methacholine and to membrane depolarization by KCl could result from the impairment of calcium influx or intracellular function.
TL;DR: Lead acetate, as a 0.025% solution in the drinking fluid, did not adversely affect the reproductive success in breeding mice, weights of pups at birth or cause delays in development, but when encountering females at 30-31 weeks, the treated males showed more immobility than did the controls.
TL;DR: The flow cytometry Coulter volume analysis may be a useful and sensitive technique for the assessment of cellular changes that occur in the bone marrow in response to xenobiotic exposure.
TL;DR: The data suggest that the proximal tubular segment may be the most likely renal target of chronic lead toxicity and the results point also to a much greater retention of Pb by the kidney than by salivary glands.
TL;DR: Although Pb ingestion resulted in decreased concentration of Cu in blood and tissue, additional dietary Cu had no effect on Pb levels and can be assumed to be the direct result of a toxic effect of Pb.
Abstract: The effects of Pb ingestion with and without concurrent dietary Cu supplementation were determined on parameters associated with Cu deficiency in rats fed a nutritionally adequate diet. Groups of weanling male Sprague-Dawley rats were fed a purified (AIN-′76) diet and given Pb (0 or 500 ppm) and Cu (0, 6, or 12 ppm) as the acetate salt in deionized drinking water for 5 wk. A Pb-induced Cu deficiency resulted that was characterized by decreased levels of Cu in tissue and blood, decreased activities of the Cu-dependent enzymes, ceruloplasmin (serum) and Superoxide dismutase (erythocytes), and increased concentration of Fe in liver. These effects of Pb were prevented completely or in part by concurrent Cu supplementation. The Pb-induced decrease in hemoglobin and hematocrit values and the decrease in weight gain were not prevented by Cu supplementation of the diet and can therefore be assumed to be the direct result of a toxic effect of Pb. Although Pb ingestion resulted in decreased concentration of Cu in blood and tissue, additional dietary Cu had no effect on Pb levels.
Journal Article•
TL;DR: It is concluded that if hyperphagocytosis of endotoxin occurs in MDP-pretreated mice, it does not cause additional mortality, and Muramyl dipeptide appeared to be a safe reticuloendothelial stimulant that did not enhance the toxicity of lead or LPS in this experimental model.
Abstract: Muramyl dipeptide (MDP) is a nonspecific immune adjuvant thought to affect the macrophage. MDP had been used safely without immunosuppressive or toxic side effects in our laboratory and others. Endotoxin, or lipopolysaccharide (LPS), is thought to be responsible for many of the systemic toxic effects of gram-negative infection. Lead acetate potentiates the lethal effects of endotoxin, an effect attributed to increased hepatotoxicity involving both hepatocytes and Kupffer macrophages. This study was undertaken to examine putative mechanism of action of MDP relating to the reticuloendothelial system. Endotoxin was given intraperitoneally to susceptible mice that were pretreated with MDP, lead acetate, or both, and to unmodified controls. Lead acetate significantly enhanced lethality due to LPS, but pretreatment with MDP did not alter mortality. Carbon clearance was measured in mice treated with MDP, lead, or both. There was no difference in the phagocytic index of control mice and those mice treated with lead acetate at various times prior to the injection. Carbon clearance increased significantly in mice pretreated with MDP but was unaltered by the addition of lead acetate. We conclude that if hyperphagocytosis of endotoxin occurs in MDP-pretreated mice, it does not cause additional mortality. Muramyl dipeptide appeared to be a safe reticuloendothelial stimulant that did not enhance the toxicity of lead or LPS in this experimental model.
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TL;DR: The methionine status of the animals seems to be an important factor in determining the liver glutathione level of pair-fed rats treated with lead + lindane.
Abstract: The effects of dietary methionine on lead and lindane toxicities in rats were studied in two experiments. Rats were fed methionine-deficient (60% of requirement) or methionine-sufficient soy protein-based diets with lead acetate added (10,000 mg/kg Pb) and treated with a single dose of lindane (25% of LD50 or 88 mg/kg, p.o.) in both experiments. In experiment I, all rats were fed ad libitum. In experiment II, rats fed the methionine-sufficient diet were pair-fed to rats fed the methionine-deficient diet. In experiments I and II, the methionine-sufficient and the methionine-deficient rats had decreased final body weights, increased liver weights, decreased hematocrits, and no changes in glutathione S-transferase activity when compared to a control group. Lead + lindane treatments increased liver glutathione levels in the methionine-sufficient and methionine-deficient rats in both experiments. However, in experiment II (pair-feeding), the methionine-sufficient rats had a much greater level of liver glutathione than the methionine-deficient rats. The methionine status of the animals seems to be an important factor in determining the liver glutathione level of pair-fed rats treated with lead + lindane.
TL;DR: Effects of administration of lead acetate on Sidman avoidance behavior were assessed in juvenile and adult rats which were obtained by continued selective breeding and which have a high level avoidance ability and small individual differences (THA rat: Tokai high avoider rat).
Abstract: Effects of administration of lead acetate on Sidman avoidance behavior were assessed in juvenile and adult rats which were obtained by continued selective breeding and which have a high level avoidance ability and small individual differences (THA rat: Tokai high avoider rat). THA rats were administered lead acetate solution at 200-300 mg/kg/day as Pb until 7 wk of age through maternal milk before weaning from mothers which had been administered lead acetate from the 13th day of gestation and per os by gastric tube after weaning. Three series of Sidman avoidance behavior tests were conducted from 49th, 100th and 150th day after birth each for 10 d, 1 h every day. In the first series, a significant delay of shock avoidance acquisition was observed in lead-administered male rats compared with the control subjects, while no acquisition delay was seen in female rats. The lead administered male rats could be divided into two groups with different response patterns; a low susceptible group (LSG) which exhibited as good acquisition rate from the beginning similar to the control rats and a high susceptible group (HSG) which showed a significant delay and individual differences. In the 2nd test series, very high avoidance rates were obtained in all the test groups except in male HSG, but in the 3rd test series, male HSG also attained a final acquisition of high avoidance rate. There was no developmental variation between the groups nor difference in lead contents of the organs of the exposed group. Useful characteristics of THA rats for behavioral toxicology are discussed.