Showing papers on "Lead acetate published in 1987"
TL;DR: To identify more specifically the site of lead's toxic actions on the hypothalamic-pituitary-testicular axis, the response of lead-treated male rats as compared to control animals to naloxone, gonadotropin-releasing hormone (GnRH), and LH stimulation was studied.
Abstract: Environmental exposure to toxic levels of lead occurs in a number of industries with potential adverse effects on the reproductive capacity of exposed men. Using a rat model, we previously reported that dietary exposure to lead resulted in suppressed spermatogenesis and testosterone levels without significant changes in luteinizing hormone (LH). In this study, to identify more specifically the site of lead's toxic actions on the hypothalamic-pituitary-testicular axis, the response of lead-treated male rats as compared to control animals to naloxone, gonadotropin-releasing hormone (GnRH), and LH stimulation was studied. Three groups of 52-day-old Wistar rats were allowed access to either deionized distilled water containing no lead acetate or a 0.3% lead acetate solution for 30 days. In each study group, 10 control and 10 lead-treated animals were anesthetized prior to cardiac puncture and collection of serum for the measurement of lead level and baseline LH (Groups I and II) or testosterone levels (Group III). In Group I, 20 min after an i.p. injection of naloxone (1.5 mg/kg/BW), the animals were killed by decapitation, and serum was collected for LH measurement. Thirty minutes after an i.p. injection of GnRH (100 ng/100 gm BW), Group II animals were killed by decapitation, and serum was collected for LH. Sixty minutes after an injection of LH (100 mg/100 mg BW), serum was collected from Group III animals for testosterone measurement. All control animals and lead-treated animals consumed similar volumes of water. Control animals had undetectable levels of lead in their blood. Lead-treated animals had mean blood lead values of 30 micrograms/dl +/- 5 micrograms/dl.(ABSTRACT TRUNCATED AT 250 WORDS)
76 citations
TL;DR: It is concluded that primary cultured brain cells are appropriate in vitro systems for studying the in vivo cellular responses to lead and inhibition of aerobic energy metabolism appears to be closely associated with cell damage.
62 citations
TL;DR: Synergistic or inhibitory effects are not observed after chronic simultaneous administration of lead acetate and N-nitrosodiethylamine, although both carcinogens act in common on P2 and P3C proximal tubule segments.
Abstract: Chronic oral administration of lead acetate and/or N-nitrosodiethylamine to rats produces three different types of renal cell tumors composed of basophilic, chromophobic or oncocytic cells. The most frequent tumor, often visible macroscopically, is made up of basophilic cells and forms tubular, cystic, pseudo-papillary or solid structures; it may show considerable cellular atypia but does not metastasize or invade the surrounding parenchyma. Chromophobic and oncocytic tumors are rare and can only be detected with the microscope; they usually form cystic or solid structures. Basophilic and chromophobic tumors arise from specific segments of the proximal tubules, characteristic for each carcinogen: P2, P3C and P3M for lead acetate; P2 and P3C for N-nitrosodiethylamine. Karyomegalia in proximal tubule cells appears to be irrelevant in renal carcinogenesis. However, the appearance of basophilic and chromophobic cells in P2, P3C and P3M segments is considered to be an early change in tumor development. Oncocytic microadenomas originate from collecting ducts showing focal oncocytic transformation. Synergistic or inhibitory effects are not observed after chronic simultaneous administration of lead acetate and N-nitrosodiethylamine, although both carcinogens act in common on P2 and P3C proximal tubule segments.
36 citations
TL;DR: There was an increase in cholesterol, decrease in ascorbic acid contents and reduction in the glucose-6-phosphate dehydrogenase activity in the testis of lead-treated rats, which suggest that the disturbed steroidogenesis during growing stage may be responsible for altering the germinal function of theTestis at maturity.
Abstract: Summary Daily intraperitoneal administration of lead (8 mg/kg) as lead acetate in male rats from 21 till 120 days of age triggered histopathological and biochemical alterations in the testis. Histopathological examination revealed disturbance in spermatogenesis besides Leydig cells degeneration. There was an increase in cholesterol, decrease in ascorbic acid contents and reduction in the glucose-6-phosphate dehydrogenase activity in the testis of lead-treated rats. These alterations suggest that the disturbed steroidogenesis during growing stage may be responsible for altering the germinal function of the testis at maturity.
31 citations
TL;DR: It is suggested that persistent alterations of the menstrual cycle and perhaps premature menopause resulted from prolonged exposure to lead at levels which produced no obvious signs or symptoms of toxicosis.
29 citations
TL;DR: It is demonstrated that changes in cell surface markers on discrete subpopulations of lymphoid cells present in the spleens of heavy metal exposed mice may not correlate with alterations in the functional activity of these cells, but changes in murine bone marrow surface markers in response to cadmium or lead treatment predicts a shift to immature cell types.
27 citations
Journal Article•
TL;DR: Currents through calcium channels of members of an identified cluster of neurons (B cells) in the pond snail Lymnaea stagnalis were studied under voltage clamp, and the inhibition of barium currents by in vitro lead exposure is irreversible, at least in short-term experiments.
Abstract: Currents through calcium channels of members of an identified cluster of neurons (B cells) in the pond snail Lymnaea stagnalis were studied under voltage clamp. The normal physiological saline was modified to maximize the visibility of voltage-dependent calcium currents and minimize contamination by other currents. Barium was used as the charge carrier for the calcium channels. Depolarizing voltage steps induce an inward current, the magnitude of which varies with the barium concentration. In brains taken from animals not exposed in vivo to lead, in vitro addition of lead acetate to the recording medium (0.25 to 14 microM) inhibits the barium current by 59 +/- 14% (mean +/- s.d.), in a manner that is independent of the lead concentration. The magnitude of the residual current still varies with the barium concentration. The voltage dependence of the current appears to be unaffected by lead. In contrast to some other calcium-channel blockers, such as cobalt, the inhibition of barium currents by in vitro lead exposure is irreversible, at least in short-term experiments. Contrary to expectations based on these in vitro results, barium currents in B cells of animals exposed to 5 microM lead for 6 to 12 weeks in vivo were approximately twice as large as barium currents in B cells from unexposed controls, when both were recorded in lead-free saline. It is possible that chronic in vivo lead exposure causes an increase in the number of calcium channels in these neurons.
27 citations
TL;DR: Lead excretion from the body may be increased by a high intake of nutrients such as thiamine, iron and fiber, that lead excretion in feces via bile may be enhanced by a large intake of vitamins such asThiamine and that accordingly the lead concentration in the blood of the workers is reduced.
23 citations
TL;DR: As lead, nickel and selenium appear to exert complex and possibly opposite effects on antibody response and phagocytosis, it remains to establish which immunotoxic consequences if any, an acute or chronic exposure to these heavy metals is likely to have in man.
Abstract: Previous studies have shown that heavy metals may exert marked immunomodulatory effects, at least in rodents, despite some discrepancies. However, the mechanism of their influence on the immune system is still unclear. As host resistance assays against experimental infections are generally considered as the most relevant criteria when predicting the immunotoxicity of drugs and chemicals, the effects of lead acetate, nickel chloride and sodium selenite on the resistance toward experimental Klebsiella pneumoniae infection was investigated in mice, with particular emphasis on the interference of the time of toxic exposure with the infectious challenge. Interestingly, one single intraperitoneal dose of 24 mg/kg lead or 4 mg/kg nickel enhanced the resistance of mice against Klebsiella pneumoniae when administered 24 hours before the infectious challenge, whereas host resistance proved to be impaired when the same dose was injected 5 hours after the infectious challenge. A 3-day pretreatment with 8 or 1...
21 citations
TL;DR: Lead-treated males, aged 17-18 weeks, showed significantly shorter latencies to aggression towards unfamiliar males than did controls, and animals treated with lead had significantly reduced body weights throughout their lives.
20 citations
TL;DR: In this paper, surface structures and selectivities of lead-poisoned Pd or Pd/graphite catalysts were studied and two types of surface species, adsorbed lead and bulk lead, were identified by XRD or the potential sweep method.
TL;DR: In this paper, the effect of lead nitrate [Pb(NO3)2] and lead acetate [(CH3COO)2Pb] individually and in combination on protonemal spread, time taken for bud initiation, bud number, shoot length, and chlorophyll content in Semibarbula orientalis was investigated.
TL;DR: The results indicate that the delay in acridine orange loss by lysosomes exposed to UV can serve as a sensitive probe to the lead content of the cell milieu and the induced responses.
Abstract: We present here the delayed leakage of lysosome acridine orange in cell cultures exposed to lead acetate. Delayed leakage was accompanied by loss of actin. These responses were not elicited by sodium acetate but could be duplicated by extracts of air sample filters from a high air pollution area but not a cleaner air site.
TL;DR: The authors investigated the effects of lead acetate to the cochlea and the VIII nerve using CM (cochlear microphonics) and AP (action potential) of the guinea pigs and measured the results by MCV of the sciatic nerve with measurement of blood lead concentration.
Abstract: Segmental demyelination and axonal degeneration of motor nerves induced by lead exposure is well known in man, and animals. The effect of lead acetate exposure to man may involve the cranial nerves, since vertigo and sensory neuronal deafness have been reported among lead workers. However, there are few reports concerning the dose-effects of lead acetate both to the peripheral nerve and the cranial VII nerve with measurement of blood lead concentration. The authors investigated the effects of lead acetate to the cochlea and the VIII nerve using CM (cochlear microphonics) and AP (action potential) of the guinea pigs. The effects of lead acetate to the sciatic nerve were measured by MCV of the sciatic nerve with measurement of blood lead concentration.
TL;DR: Female rats were administered intraperitoneal injections of solutions of lead acetate and sodium selenite to assess degrees of protection afforded by sodium Selenite against chromosomal damage caused by lead acetates.
TL;DR: Results suggest that excretion of lead in feces is enhanced by thiamine and that it promotes evacuation of lead from the body.
TL;DR: Lead inclusion bodies are formed in the offspring indirectly exposed to lead via the dams during gestation and lactation and concurrent exposure to disulfiram reduces the incidence of inclusion bodies in renal proximal tubules, probably due to formation of a lead-dithiocarbamate complex.
TL;DR: It is concluded that chronic exposure to these concentrations of lead, when combined with high blood pressure, slightly enhances the susceptibility of the heart to arrhythmias induced by myocardial ischaemia.
Abstract: The aim of this study was to investigate whether chronic (3 months) lead (250 or l000ppm), administered as lead acetate in the drinking water, commencing either after weaning (in normotensive or spontaneously hypertensive male rats) or from conception (normotensive rats only) altered the susceptibility of the heart to arrhythmias induced either by coronary artery occlusion or by noradrenaline Treatment with lead alone had no marked effect on the arrhythmias elicited by either method Spontaneously hypertensive rats treated with either dose of lead exhibited more ectopic beats following coronary artery occlusion than normotensive rats but not more than those observed in control spontaneously hypertensive rats An enhanced arrhythmogenic effect of noradrenaline was observed only in hypertensive rats administered 250 ppm lead Both doses of lead accelerated the development of high blood pressure and in normotensive rats the higher dose also resulted in an elevated pressure Following administration of lead, blood lead concentrations were elevated to 096 and 211 μmol 1−1 after 250 and 1000 ppm, respectively Accumulation of lead in heart and bone was also observed We conclude that chronic exposure to these concentrations of lead, when combined with high blood pressure, slightly enhances the susceptibility of the heart to arrhythmias induced by myocardial ischaemia
TL;DR: It is found that a group of iron workers occupationally exposed to inorganic lead excreted high levels of urinary beta-AIB, a normal degradation product of thymine, a constituent of DNA and, to a lesser extent, of transfer RNA, in humans.
Abstract: beta-Aminoisobutyric acid (beta-AIB), a normal degradation product of thymine, a constituent of DNA and, to a lesser extent, of transfer RNA, is excreted in low levels in human urine. We found that a group of iron workers occupationally exposed to inorganic lead excreted high levels of urinary beta-AIB. Elevated urinary excretion of beta-AIB was also observed in marmosets, Callithrix jacchus, that received lead acetate in drinking water. Our results suggest that increased urinary excretion of beta-AIB could stem from damage to DNA on exposure to lead.
TL;DR: The hypothermic response to acute lead acetate treatment may be beneficial to survival and be potentiated with increasing Ta, which augmented the lead-induced hypothermia.
TL;DR: Gradual increase in blood and testis lead alongwith the proportional inhibition of 3-aminolevulinic acid dehydratase levels indicated the intensity of lead toxicity in rats.
Abstract: Lead acetate treatment intraperitoneally at the dosages of 1 mg, 2 mg, 4 mg and 6 mg/kg over a period of 30 days altered spermatogenesis in rats. Inhibition of ƒ¢5-3ƒÀ-hydroxysteroid dehydrogenase was parallel with the high concentration of testicular cholesterol and low concentration of ascorbic acid, alkaline phosphatase and protein in most of the treated groups. Gradual increase in blood and testis lead alongwith the proportional inhibition of 3-aminolevulinic acid dehydratase levels indicated the intensity of lead toxicity in rats. Data revealed that alteration of spermatogenesis in lead treated rats might be due to the inhibition of steroidogenesis.
TL;DR: It is demonstrated that Pb significantly impairs the defense mechanism of the lens, which comprises both the glutathione and superoxide dismutase systems.
Abstract: Effects of lead (Pb) were studied on rat lenses after oral exposure to lead acetate (0.1 %) in drinking water given ad libitum for up to 3 months. Activities of the key enzymes involved in the glutathione metabolic pathway were found to be severely impaired along with an increase of blood/lens Pb level. Activity of superoxide dismutase, which is responsible for scavenging the free radicals, was also significantly decreased. Depletion of reduced glutathione content with a concomitant elevation of peroxide levels showed an oxidative stress in the ocular lens as a result of Pb exposure. The results of the present study demonstrate that Pb significantly impairs the defense mechanism of the lens, which comprises both the glutathione and superoxide dismutase systems.
TL;DR: The results indicate that lead intoxication did not impair the contractile apparatus of the forestomach smooth muscle, and the lack of net effect on activation of intramural cholinergic neurons, despite the enhanced sensitivity to a Cholinergic agonist, may indicate reduction in acetylcholine release in lead-treated tissue.
TL;DR: This paper focuses on the most unique properties of LPSI, namely it's alteration of activity after heating or the addition of lead acetate, compared with those properties of inhibitors for endotoxin which have been previously demonstrated by a number of investigators.
TL;DR: The results suggest that latent learning may be a particularly sensitive measure of Pb exposure in the neonatal rat model despite the increased body burden of PB.
Abstract: Complex maze learning was investigated in male neonatal and adult rats using a latent learning task. The neonates received (intragastric administration) either lead acetate (50 mg Pb/kg) or equimolar sodium acetate on days 6, 9, 12, and 18 postpartum. The adult subjects were exposed to 100 ppm Pb acetate or equimolar sodium acetate in drinking water for 112 days beginning at weaning (day 21 postpartum). Training for the latent learning task began on day 31 postpartum for the neonates and on day 143 for the young adults. The training sequence included free exploration (under conditions of satiation) of a symmetrical latent learning maze or an open field of the same shape and area by the Pb-treated and control subjects (randomly distributed). Subsequently, all subjects were food deprived and appetitively tested in the latent learning maze. Neonatal lead exposure perturbed latent learning: the Pb-treated subjects showed no evidence of latent learning. However, pretest exploratory activity was similar for Pb-...
TL;DR: In this paper, a Canadian co-operative blood-Pb interlaboratory survey was conducted based on lyophilized bovine blood samples with different endogenous lead contents, and the mean values computed for the three samples analyzed by 12 participants were 40, 229, and 91 μg Pb/l, respectively.
Abstract: A Canadian co-operative blood-Pb interlaboratory survey was conducted based on lyophilized bovine blood samples with different endogenous lead contents The samples were prepared from whole blood of a non-exposed cow and another fed with a single dose of lead acetate trihydrate The mean values computed for the three samples analyzed by 12 participants were 40, 229, and 91 μg Pb/l, respectively These results showed a negative bias of 20%, 04% and 14% with respect to the target values of 50, 230 and 106 μg Pb/l, respectively
Patent•
25 Feb 1987
TL;DR: The characteristic steps of producing di-valent lead hydroxide are: (1) the metallic lead reacts with acetic acid at temp. no more than 200 deg.C and under pressure of 1 to 10 absolute atmosphere at the presence of oxygen atmos, forming lead acetate; (2) the leadacetate formed reacts with ammonium ionic source at or below 100 deg.
Abstract: The characteristic steps of producing di-valent lead hydroxide are: (1) The metallic lead reacts with acetic acid at temp. no more than 200 deg.C and under pressure of 1 to 10 absolute atmosphere at the presence of oxygen atmos., forming lead acetate. (2) The lead acetate formed reacts with ammonium ionic source at or below 100 deg.C under 1 to 5 atmo., precipitating lead hydroxide.
TL;DR: It is concluded that, although small amounts of dietary lead reduce fluoride bioavailability, small amountsof dietary fluoride do not appear to significantly influence the utilization of Dietary lead.
Abstract: A factorial experiment was conducted with weanling rats fed a purified diet to determine the influence of dietary lead (0 or 100 ppm) as either lead acetate or lead carbonate on fluoride bioavailability (2 or 10 ppm as sodium fluoride). During the 6-wk study, both forms of lead depressed weight gain, regardless of the fluoride level, despite the fact that food intake was similar for all treatment groups. Both forms of lead produced a small, but significant, reduction in femur and second molar fluoride. This effect, however, could only be demonstrated in rats fed diets containing 10 ppm fluoride, indicating a significant interaction between lead and fluoride for these indices of fluoride bioavailability. This interactive effect between fluoride and lead was also demonstrated for apparent fluoride absorption. Both forms of dietary lead significantly increased the lead concentration of plasma, femur, liver, and kidney, and both forms of lead significantly increased the urinary excretion of delta-aminolevulinic acid. The level of dietary fluoride failed to influence these measurements. We therefore conclude that, although small amounts of dietary lead reduce fluoride bioavailability, small amounts of dietary fluoride do not appear to significantly influence the utilization of dietary lead.
Journal Article•
TL;DR: The elevated blood lead level, increased urinary delta-amino-levulinic acid (ALA-U) excretion, depletion in RBC and haemoglobin content and more number of reticulocytes in peripheral blood indicated the increased intensity of lead toxicity and inhibitory effect on haem biosynthesis.
Abstract: Erythropoietic alterations in normal and splenectomized mature male rats treated with aqueous lead acetate intraperitoneally at dosages of 4 mg/kg and 6 mg/kg body weight were observed over a period of 30 days. Significant retardation in growth might be due to gradual increases in lead toxicity. The elevated blood lead level, increased urinary delta-amino-levulinic acid (ALA-U) excretion, depletion in RBC and haemoglobin content and more number of reticulocytes in peripheral blood indicated the increased intensity of lead toxicity and inhibitory effect on haem biosynthesis. The accelerating action of lead on erythropoietic cellular series i.e. pronormoblast, early and intermediate normoblast and late normoblast was evident by the significant increase in number of cellular count both in intact and splenectomized rats after treatment with lead.
TL;DR: In this article, the synthesis of Pb(NO3)2, PbO2 and PbCrO4 were used to synthesize lead carbonate and lead acetate.
Abstract: Uses and synthesis of Pb(NO3)2, PbO2, PbCrO4, PbS, PbO, lead carbonate, lead acetate, and lead metal itself.