Showing papers on "Lead acetate published in 1988"

Genetic toxicology of lead compounds

Abstract: We have investigated the activity of insoluble and soluble lead compounds in inducing mutagenesis, cell transformation and sister chromatid exchange in mammalian cells. Insoluble lead sulfide, readily phagocytized, was more than four times as toxic to V79 cells on a microM basis, than two moderately soluble lead compounds although the exposure time for the soluble salts was five times longer. These findings demonstrate the importance of different cellular mechanism(s) of metal uptake and bioavailability. Both insoluble lead sulfide and more soluble lead nitrate were mutagenic at the HPRT locus in V79 cells. Although less mutagenic at the higher concentrations, lead nitrate at a concentration of 500 microM enhanced the mutation frequency greater than 6-fold above background following a 5-day exposure. Although the mechanism(s) by which lead induces mutations is unknown, failure of both compounds to induce SCE and DNA single-strand breaks, detectable by alkaline elution, suggests that lead-induced mutations may not be a result of direct damage to DNA but may occur via indirect mechanisms including disturbances in enzyme functions important in DNA synthesis and/or repair, or in DNA-helical structure. Lead acetate also transformed SHE cells in a dose-response fashion following a 48-h exposure. Our results indicate that lead compounds may be genotoxic by an indirect mechanism, and lend support to the view that lead is a carcinogen.

Effect of diet on the response in rats to lead acetate given orally or in the drinking water

Abstract: Liver lead levels were higher for rats that were orally dosed with 100 mg lead acetate/kg body wt and fed a semipurified diet than those fed a pelleted diet. The activities of delta-aminolevulinic acid dehydratase in blood were decreased in the group given 10 μg lead acetate/mL in their drinking water and fed the semipurified diet, but not in the blood from the group treated with lead and fed the pelleted diet. The levels of glutathione in the liver decreased in response to lead acetate in the drinking water of rats fed the semipurified diet, but not in the livers from the group fed the pelleted diet and treated with lead. The levels of lead in the kidneys were higher in the group given lead acetate in their drinking water and fed the semipurified diet than in the lead treated group fed the pelleted diet. Rats dosed orally with lead or given lead in the drinking water and fed the semipurified diet were more sensitive to lead treatment than those fed the pelleted diet.

Perinatal lead exposure alters the development of δ‐but not μ‐opioid receptors in rat brain

Abstract: 1. Low level lead exposure has been shown to impair the development of opioid peptide levels in the brain, and to impair antinociceptive responses to opioid drugs. We have now studied the effects of lead exposure on the development of opioid receptors using ligand binding studies. 2. The ontogenesis of mu- and delta-opioid binding sites was studied using rat whole brain membranes and [3H]-[D-Ala2MePhe4-Gly-ol]enkephalin and [3H]-[D-Pen2,D-Pen5]enkephalin as binding ligands. Rats were exposed to lead during development by addition of lead acetate (at 100-1000 p.p.m.) to the maternal drinking water from conception to postnatal day 14. 3. Perinatal lead exposure had no significant effects on the binding affinity (KD) or binding capacity (Bmax) for the mu-opioid receptor measured at postnatal days 10, 21 and 30. Lead exposure (at 1000 p.p.m.) increased the KD for the delta-opioid receptor at postnatal days 15, 21, 35 and 50 but had no effect on the binding capacity. No indications of overt toxicity were observed and blood lead levels were in the ranges considered to represent subclinical lead toxicity in man. 4. The lack of effect of lead on mu-receptor binding contrasts with previously described impairment of antinociceptive effects of mu-agonists suggesting that the toxicity is not manifested at the mu-binding site. However, the delta-opioid receptor appears to be more sensitive to lead exposure and the persistent changes in delta-site affinity after cessation of lead exposure suggest irreversible damage in the production of the receptor protein.

Preparation of Pb-containing glass by the sol-gel process Reduction of Pb-migration during drying

Abstract: Conditions for preparing a homogeneous glass of the PbOB 2 O 3 SiO 2 system by a sol-gel process from silicon methoxide, boric acid and lead acetate have been investigated. The migration of lead ions toward the gel surface during drying was reduced by replacing water in a wet gel with isopropanol. The X-ray transmission of a xerogel obtained by drying a wet gel after the replacement of water with isopropanol was constant at respective points on the diameter of a disc cut out of a cylindrical sample. The X-ray transmission of a xerogel dried without isopropanol treatment, on the other hand, was low at the center and high at the perimeter, suggesting a higher concentration of lead at the center than at the perimeter. The concentration of lead in the glass obtained by sintering the former gel was found to be uniform throughout the glass body.

Genotoxicity of Two Heavy Metal Compounds-Lead Acetate and Mercuric Chloride in the Mosquito, Anopheles stephensi Liston (Culicidae: Diptera)

Abstract: The effects of two heavy metal compounds viz., lead acetate and mercuric chloride were studied on the polytene chromosomes in Anopheles stephensi. Various chromotoxic effects such as inversions, translocations, and breaks were observed. In the larvae treated with lead acetate, an increased incidence (as compared to controls) of asynapsis in the X-chromosome was also observed. From the present studies, it is evident that lead acetate is a weak mutagen, whereas the use of mercury needs more cautions.

Effect of lead and niacin on growth and serotonin metabolism in chicks.

Abstract: Interactions of lead and niacin were studied in growing broiler chicks fed one of four experimental diets from day-old to 3 wk of age. The diets were a low niacin basal diet (LN), the basal diet supplemented with 40 mg of niacin/kg (control), the basal diet supplemented with 2000 mg lead/kg, as lead acetate (LN + Pb) and the basal diet supplemented with both niacin and lead (control + Pb). Growth and feed efficiency were reduced significantly by lead. The lead-associated growth depression was less severe in chicks fed the low niacin diet as indicated by a significant lead X niacin interaction. The relative weights of two brain regions (telencephalon and diencephalon) and the adrenal glands were greater in lead-treated chicks than in their nonlead-treated counterparts. Plasma and telencephalon tryptophan were lower in lead-treated chicks than in nonlead-treated chicks. Diencephalon tryptophan was lower in chicks fed the LN diet than in chicks fed the control diet. Brain serotonin was lower and 5-hydroxyindoleacetic acid was higher in both brain regions of lead-treated chicks than in nonlead-treated chicks. The data indicate that tryptophan and serotonin metabolism were altered by lead treatment, whereas niacin was without effect. The interaction of lead and niacin on growth does not appear to be related to alterations of serotonin metabolism in the central nervous system.

Functional disturbance of rat sexual accessory glands in an early phase of lead intoxication.

Abstract: In order to investigate the effects of chronic lead intoxication on sexual accessory glands adult male Wistar rats were poisoned by ad libitum ingestion of lead acetate at concentrations of 0.5 g/l and 1.0 g/l for 90 d. Blood lead exhibited a significant increase in both treated groups. A decrease in hematocrit and hemoglobin, besides a rise in glycemic levels, confirmed lead intoxication. No sign of lesion was detected upon histologic examination of prostate, seminal vesicle, and coagulating gland. A morphometric technique revealed that, in this early phase of intoxication, no alteration occurred in the prostate's and seminal vesicle's epithelial height. However, a significant decrease in fructose content was observed in both lead treated groups. The results, revealing a precocious envolvement of male sexual accessory glands in lead intoxication, were related to disturbance in plasma testosterone level and also probably in androgen receptors.

Morphometric and stereological analysis of rat testis and epididymis in an early phase of saturnism.

Abstract: Adult male Wistar rats were poisoned by ad libitum ingestion of lead acetate at concentrations of 0.5 g/l and 1.0 g/l in drinking water, for 90 days. Blood lead exhibited a significant increase in both treated groups. A decrease in haematocrit and haemoglobin, together with a rise in glucose levels, confirmed lead intoxication. No signs of lesion were detected upon histological examination of testes, caput and cauda epididymidis. In this early phase of intoxication, no alteration occurred in the seminiferous tubule diameter, in the germinal epithelium height, nor in the rate of spermatogenesis and the production of spermatozoa. The caput epididymidis also showed no structural change. In the cauda epididymidis, however, an increase in ductal diameter, and a decrease in epithelial height, were observed. The concentration of spermatozoa stored in the caudal region of the epididymis exhibited a significant increase in lead-treated animals. The results, which reveal an early involvement of cauda epididymidis in lead intoxication, are discussed in terms of a disturbance in the neuroendocrine mechanism controlling the multiple epididymal functions.

Effects in rats of iron on lead deprivation

Abstract: In two fully crossed, two-factor experiments, F1 generation male rats were fed a basal diet supplemented with lead (lead acetate) at 0 or 2 μg/g and iron (ferric sulfate) at 50 or 250 μg/g (Experiment 1). Supplements in Experiment 2 were lead at 0 or 1 μg/g and iron at 50, 250, or 1000 μg/g. After 28 or 50 d in Experiment 1, and 35 d in Experiment 2, a relationship between lead and iron was found. Body weight was lower in low-lead than lead-supplemented 28-d-old rats regardless of dietary iron, whereas hematocrit and hemoglobin were lower in low-lead than lead-supplemented rats fed 50 μg iron/g diet. A similar finding was obtained with hematocrit and hemoglobin in 35-d-old rats. Dietary lead did not affect rats fed 250 or 1000 μg iron/g diet. Also, feeding low dietary lead did not affect 50-d-old rats regardless of dietary iron. Liver and bone concentrations of lead were markedly affected by dietary lead and iron. The concentration of lead in liver and bone was lower in low-lead than lead-supplemented rats. Compared to rats fed 50 μg iron/g diet, rats fed 250 μg iron/g diet exhibited a decreased lead concentration in liver and bone. This decrease was accentuated by lead supplementation. The findings suggest that lead acted pharmacologically to affect iron metabolism in rats.

Localization of lead in the kidney and liver of rats treated in vivo with lead acetate: ultrastructural studies on unstained sections.

Abstract: The subcellular distribution and ultrastructural effects of lead have been studied in the kidneys and liver of rats given lead acetate (600 ppm Pb2+) in their drinking water for 6 months. Control rats were given sodium acetate. Tissue samples were fixed in glutaraldehyde and examined by electron microscopy with and without staining. Unstained sections of both kidney and liver from lead-treated animals showed small particles (2-5 nm diameter) of very high electron density which appear to represent a deposited form of Pb2+. Ultrastructural changes in the kidneys were largely confined to glomeruli (swelling of endothelial cells, fusion of foot processes, thickening of basement membrane) and proximal tubules (ranging from minimal sub-lethal changes to necrotic disorganization). The electron-dense particles of Pb2+ occurred in large clusters in basement membranes. As individual particles, or small groups, they were numerous in nuclei of proximal epithelium but usually only a few, largely confined to vesicles or inclusion bodies, were present in the cytoplasm. Only when cells were markedly damaged morphologically were particles more generally distributed in the cytoplasm. Liver damage by Pb2+ was largely confined to centrilobular regions. Endothelial and Kupffer cells were the most affected; they often sequestered large numbers of the particles. In parenchymal cells, particles were few and mainly in vesicles, but they were more widely distributed in the cytoplasm when morphological injury was apparent. The free distribution of Pb2+ in liver and kidney seems to be limited by its deposition in basement membranes and sequestration in reticulo-endothelial cells; intracellular distribution in healthy cells is also limited, by deposition in nuclei (in kidney only) or cytoplasmic vesicles.

Effect on blood, liver, and kidney variables of age and of dosing rats with lead acetate orally or via the drinking water.

Abstract: Levels of lead in the livers and kidneys of rats increased in proportion to the dose of lead acetate that the rats were given orally or in the drinking water. The activities of delta-aminolevulinic acid dehydratase (DALAD) in blood and liver decreased when the rats were dosed with lead, whereas glutathione levels in the blood increased. The decrease in the activity of blood DALAD was the most sensitive indicator of lead toxicity. Levels of lead in the livers and kidneys decreased after 3, 7, and 14 d of lead withdrawal. The activities of blood DALAD increased after 3 d of lead withdrawal. Groups of rats that initially weighted an average of 140 g were killed at weekly intervals for 6 wk. Blood hematocrits and liver glutathione levels increased, and blood DALAD and activated DALAD from blood decreased with increasing age of the rats. Activated DALAD activities from liver increased after the first week of the study.

Ultrastructural aspects of the small intestinal lead toxicology. Part I: Surface ultrastructure of the small intestine mucosa in rats with lead acetate poisoning.

Abstract: The effects of low concentration of lead acetate on the apical surface of the jejunal enterocytes were studied. Young male rats were divided into 2 groups which received 0.01% lead acetate solution in drinking water during 30 and 60 d respectively. Blood lead concentrations of poisoned rats were elevated to 30.33 micrograms Pb/100 ml at d 30 of intoxication, then slightly depressed at the end of experiment. Weight gain was impaired only in the 60-d group in comparison with controls. Samples from jejunum were processed for scanning electron microscopy using a critical point drying method and gold evaporation. The fine structure of the surface enterocytes was always determined in the epithelial bands above the levels of crypts nearly half a distance from crypt to villous top. The shape of the jejunal villi in poisoned rats was similar to that in non-poisoned rats. A marked feature of the rats' jejunum exposed to heavy metal for 30 d was a rough appearance of the surface villi, probably associated with distortion of the glycocalyx layer. Extensive areas with degenerative lesions were observed on the surface of the most villi on the 60th d of intoxication. Microvilli of enterocytes distributed within these areas were deformed and sometimes could be completely absent. All enterocytes exhibited various degrees of glycocalyx disturbance. It was concluded that the pronounced toxic effects of lead were related to modification of biochemical properties of the surface coat of enterocytes. This abnormal function of the glycocalyx could result in damage and microvillous malformations.

Recovery of the early cellular changes induced by lead in rat peripheral nerves after withdrawal of the toxin.

Abstract: A morphological and quantitative investigation was carried out in the peripheral nerves of adult rats, which were first exposed to 4% lead acetate in the drinking water and then restored to standard laboratory conditions. After six weeks of continuous lead exposure, the only cells involved were Schwann cells (SC) and endothelial cells (EC). As compared to age-matched controls, the most conspicuous changes observed by light and electron microscopy in these cells included the presence of nuclear inclusion bodies (NIB), cytoplasmic hypertrophy, mitochondrial abnormalities, an increased number of myelin-derived SC intracytoplasmic structures, and vesiculation of myelin sheaths. By counting the number of nuclear profiles containing NIB in semithin sections stained with basic fuchsin and methylene blue, we found that SC from predominantly cutaneous (sural) nerves were less vulnerable to lead than SC from mixed (peroneal) and muscular (tibial) nerves. With respect to EC, however, no significant differences were found among these three nerves. After termination of lead exposure, we observed a gradual decrease of most of the above cellular changes, which finally disappeared at day 30 post-intoxication. However, the number of myelin-related SC cytoplasmic bodies still remained above normal levels at the time of the termination of the experiment (60 days post-intoxication). The nature of the changes induced by lead in peripheral nerve cells as well as the rapid and nearly complete recovery suggest that they reflect a compensatory response to overcome the adverse effects of the lead on cell metabolism.

Studies on application of a lead acetate solution as filter to the photochemical reaction of ergosterol to improve the yield of vitamin D.

Abstract: Since a lead acetate solution can remove most of the ultraviolet (UV) light in the range below 275 nm which usually gives undesirable by-products in the photochemical conversion of ergosterol to vitamin D, it is useful as a filter solution for the reaction to obtain higher yield of vitamin D. When a 5% lead acetate solution was used as the filter, the yield of vitamin D was 20-25% higher than that without using filter solution.

Ultrastructural aspects of the small intestinal lead toxicology. Part II. The small intestine goblet cells of rats during lead poisoning.

Abstract: Summary The purpose of the present study was to evaluate the detoxification significance of the small intestinal goblet cells in rats on prolonged treatment with 0.01 % lead acetate in the drinking water.These goblet cells were analysed using a submicroscopic demonstration of heavy metals with the sulphide silver method and the X-ray microanalysis probe.Male Wistar rats, weighing 80 g, were sacrificed after 2, 30 and 60 d of exposure to oral administration of lead.The small intestines were perfused with Sorensen buffer with H2S, then blocks of tissue were removed from the border between the duodenum and jejunum and processed for transmission electron microscopy according to Grzybek (3) and Dancher (2).At first the silver containing salt precipitates were distributed in the extracellular space between epithelial cells after 2 d of the experiment.Treatment of rats with lead acetate for 30 d produced the characteristic appearance of the goblet cells at the electron microscopic level.The presence of lead in conjunction with the goblet cell membrane has been observed.If administration of lead to rats is continued longer than 30 d, in the mucus droplets located in the cytoplasm of goblet cells some deposits of silver salts may be demonstrated.For the electron probe X-ray microanalysis the bulk specimens were prepared using a critical point drying apparatus.The specimens were scanned along a line on the villous surface parallel to its long axis.The X-ray studies indicated that accumulation of lead in the epithelial cells increased during the time of experiment.

Magnetic field effects on the electrodeposition of lead from lead acetate-ammonium acetate solutions.

Abstract: Cathodic polarization curves were measured using electrolytes of 0.01-0.05mol·dm-3 Pb (CH3COO)2-0.5-3mol·dm-3CH3 COONH4 containing 0-0.5g/dm-3 gelatin. At a magnetic flux density of 0.12T, polarization decreased, the limiting current density increased, and the formation of dendrites was inhibited. Current efficiency increased by 10%. It was considered that the thickness of the diffusion layer decreased due to Lorentz force.

Effects of lead and niacin on tryptophan and serotonin metabolism.

Abstract: Studies were conducted to investigate the effects of lead and niacin on tryptophan and serotonin metabolism in growing broiler chicks A low-niacin basal diet based on soybean meal and glucose was supplemented with either 40 ppm niacin/kg feed or 2,000 ppm lead, as lead acetate trihydrate, or a combination of the two in a 2 x 2 factorial arrangement The experimental diets were fed from 1 day to 3 weeks of age The activities of several enzymes involved in tryptophan and serotonin metabolism were assayed in chicks fed each of the experimental diets Lead reduced the activity of liver tryptophan pyrrolase but had no effect on the activity of hepatic picolinic carboxylase Low dietary niacin had no effect on the activity of either of these enzymes Brainstem tryptophan 5-hydroxylase activity was unaltered by either lead or niacin Brain and liver monoamine oxidase activity was reduced by lead but was not affected by niacin No interactions of lead and niacin were observed with any of the enzymes examined Lead had no consistent effect on brain serotonin (5-HT) steady-state level, but it increased the level of the major metabolite of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA) Monoamine oxidase blockade failed to reduce the elevated 5-HIAA level in lead-treated chicks The drug probenecid produced an increase in 5-HIAA that was comparable to the increase caused by lead The effects of probenecid and lead were additive It is concluded that lead significantly altered the activity of several enzymes involved with tryptophan metabolism, whereas the dietary niacin levels employed were without effect Additionally, lead caused the accumulation of 5-HIAA in the brain, which appeared to result from inhibition of the probenecid-sensitive acid transport system

Chondrocyte metabolism in growing and definitive cartilage exposed to lead acetate

Abstract: Intensity of biosynthesis of glycogen, glycosaminoglycans and collagen by chondrocytes has been studied. It is established that the degree of influence of the lead compounds on these processes depends on dose, duration of chondrocytes' entry into the organism and intensity of their functioning. Lead acetate has the greatest effect on metabolism of chondrocytes in bones of the fetal skeleton during its entry in the gestation period. The inhibition of glycosaminoglycans biosynthesis in chondrocytes delays their transition into the hypertrophic state, thus inhibiting the skeleton growth. The more intense is the skeleton growth, the greater is the lead effect.

Electrodeposition of Lead on Copper in Acidic Ammonium Acetate Solutions.

Abstract: Lead deposited on copper from aqueous acidic ammonium acetate solutions containing either Pb(NO 3 ) 2 or Pb(CH 3 COO) 2 was impure and showed a tendency to form dendrites. When PbSO 4 was used in the same acidic acetate medium, the lead deposits were both pure and compact as confirmed by ex-situ X-Ray Diffraction and Auger Electron Spectroscopy techniques. The effect of PbSO 4 on the kinetics of under- and overpotential deposition was notable in cyclic voltammetric and potential step studies. Lead sulphate decreased the current density and shifted nucleation potentials to more negative values than those observed through the addition of either lead acetate or lead nitrate. In the UPD region, the deposition of lead appears to be formed by an instantaneous two-dimensional nucleation and growth mechanism. In the overpotential regime, multilayer deposition was three-dimensional in nature. The bulk deposition region showed instantaneous nucleation with diffusion control, whereas in the dendritic region, the nucleation and growth process was found to follow a 3-D progressive pattern.