Showing papers on "Lead acetate published in 1985"

Effects of meals and meal times on uptake of lead from the gastrointestinal tract in humans.

Abstract: Twenty three adults ingested 203Pb as lead acetate on the 12th hour of a 19 h fast. Retention measured 7 days later in a whole-body counter was 61% and whole-body turnover rates suggested that initial uptake had been considerably greater. Balanced meals eaten with 203Pb reduced lead uptake to 4% and the influence of the food lasted for up to 3 h. The effects of phytate, ethylene-diaminetetra acetate (EDTA), caffeine, alcohol, glucose, a liquid meal and a light snack were tested separately with intermediate results. The effect of a meal was probably largely due to its content of calcium and phosphate salts but lead uptake was probably further reduced by phytate which is plentiful in whole cereals and it was probably increased by a factor in milk. Uptake with skimmed milk was the same as with whole milk and we suggested that the factor was not fat. Comestibles with low mineral and phytate contents reduced lead uptake by intermediate amounts, possibly by stimulation of digestive secretions. The avid uptake of lead during a fast, the large reduction of lead uptake with meals and the likelihood of variations in gastric-emptying rates and dietary habits may be major causes of variation in body burdens of lead in the population.

Lead toxicity and the hypothalamic-pituitary-testicular axis.

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. Clinical and animal studies indicate that abnormalities of spermatogenesis result from toxic lead exposure, but the pathogenetic mechanisms involved have not been identified. In order to ascertain what reproductive abnormalities occur in experimental animals when exposed to low levels of lead, 52-day-old animals were treated with water containing 0.0% (control), 0.1%, or 0.3% lead acetate for 30 days prior to killing. Whole blood serum lead levels were below detection (less than 7 micrograms/dl) in the control animals, 34 +/- 3 micrograms/dl in the 0.1% group, and 60 +/- 4 micrograms/dl in the 0.3% group (P less than 0.001). Significant negative correlations between whole blood lead levels and serum and intratesticular testosterone values were found (r = 0.64, P less than 0.001 and r = 0.6, P less than 0.001, respectively). As the level of lead exposure increased, intratesticular sperm counts significantly decreased (r = 0.81, P less than 0.001). No significant changes in serum luteinizing hormone (LH) values were found, but sperm follicle-stimulating hormone (FSH) values were significantly suppressed (P less than 0.05) after lead treatment. There was a significant decrease in ventral prostate weight (P less than 0.05), but no differences in testicular or seminal vesicle weights. Our data indicate that dietary exposure to lead resulting in whole blood serum lead values considered acceptable in the workplace (less than or equal to 40 micrograms/dl) causes inhibition of testicular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum lipid peroxide level and blood superoxide dismutase activity in workers with occupational exposure to lead

Abstract: We studied whether lead exposure increased the serum lipid peroxide (LPO) level and inhibited blood superoxide dismutase (SOD) activity in workers with occupational exposure to lead and rats injected with lead. We examined the following subjects: (1) manual workers (712 males) from 18 to 59-years-old in steel production with occupational exposure to lead, (2) office workers (155 males) without exposure to lead, (3) rats subcutaneously injected with lead in concentrations of 10 or 20 mg/kg as lead acetate. The nutritional intakes of manual workers and office workers were approximately equal. Serum LPO and high-density lipoprotein cholesterol (HDL-CL) levels in manual workers (LPO: 4.4 ± 1.9 nmol/ml, HDL-CL: 55.6 ± 14.2 mg/dl) were significantly higher than those in office workers (LPO: 4.0 ± 1.4 nmol/ml, HDL-CL: 53.0 ± 13.9 mg/dl). Serum LPO level in the manual workers increased with an increase of the lead concentration in the blood, while blood SOD activity decreased. Similar phenomena were observed in rats subcutaneously injected with lead acetate. Furthermore, the addition of lead at higher than 20-μM concentrations to non-treated rat liver microsomes increased NADPH-dependent lipid peroxidation, and these lead concentrations inhibited bovine erythrocyte SOD activity in vitro assay system. In conclusion, the present results seem to indicate that the increase of serum LPO level in workers with occupational exposure to lead is due not only to the stimulation of lipid peroxidation, but also to the inhibition of SOD activity by exposure to lead in the manufacturing processes.

Cytogenetic effects of lead acetate on rat bone marrow cells.

Abstract: The inducibility of chromosome aberrations and micronuclei by lead acetate was examined in vivo in bone marrow cells of rats after its single or repeated intraperitoneal administration. Lead acetate caused a small but significant increase in the frequencies of chromosomal aberrations (mostly chromatid gaps) and micronuclei. Chromatid breaks and acentric fragments were less frequent in occurrence. Complex aberrations such as chromatid exchanges and multiple breaks were never observed. Our findings suggest that lead acetate exerts a weak clastogenicity on rat bone marrow cells.

Retention of lead in the rat

Abstract: This study compares the relative effectiveness of different diets, therapeutic agents, and chelation in reducing the elevated tissue concentrations of lead in rats. Young male rats were given lead by exposure to drinking water containing 350 ppm of lead as lead acetate. After four weeks of exposure, the source of lead was removed, surviving rats randomized among eight groups, and subjected to one of the following: (1) terminated (positive control-1); (2) returned to the previous exposure to lead (positive control-2); (3) given the control diet (positive control-3); (4) increased minerals (diet); (5) increased ascorbic acid (diet) and thiamine (injection); (6) increased cellulose (diet); (7) ethylenediaminetetraacetic acid (EDTA) (injection); and (8) dimercaptosuccinic acid (DMSA) (injection). After six weeks, the experiment was terminated, the following tissues were harvested, and the lead concentrations determined: blood, brain, calvaria (flat bone), femur (long bone), kidney, and liver. Histopathological examinations of kidneys were provided, and the hematocrit and hemoglobin were measured. The highest lead concentrations were found in the femurs of rats following ten weeks exposure. All groups receiving lead had significantly higher lead concentrations than the controls. None of the diets produced a significant reduction in the concentration of lead in the tissues when compared with the positive control-3 (the leaded rats not receiving treatment). A reduction in the lead concentration in the brain and liver was obtained by chelation.

Neoplasia induced in male rats fed lead acetate, ethyl urea, and sodium nitrite.

Abstract: Sprague-Dawley rats were exposed to 0, 26, or 2600 ppm lead as lead acetate in drinking water for 76 weeks. At 28 weeks of lead exposure, a portion of each group was exposed simultaneously to 6.36 g/kg ethyl urea (EU) and 2.0 g/kg sodium nitrite (NaNO2) for a duration of 20 weeks, and then continued an additional 28 weeks on standard diet free of EU and NaNO2. The animals were observed for incidence, latency, and distribution of tumors. Rats exposed to 2600 ppm lead alone had 81% renal tumors, while rats given 2600 ppm lead in combination with EU/NaNO2 had a 50% incidence. Renal tumors did not occur in the EU/NaNO2 only or EU/NaNO2-26 ppm lead groups. The major tumor type found in EU/NaNO2-exposed rats was lymphosarcoma. Lead did not appear to be syncarcinogenic to the activity of ethylnitrosourea, the carcinogen formed by oral exposure to EU and NaNO2. The lead-induced renal neoplasms were histologically similar to those which occur spontaneously in man and, therefore, may serve as an animal model to study human disease.

Effects of marginal zinc deficiency on subclinical lead toxicity in the rat neonate

Abstract: Influence of maternal dietary zinc intake on tissue distribution of lead and zinc in neonatal rats administered lead acetate by gavage during lactation was examined. Milk from dams fed a marginally deficient diet (6 micrograms Zn/g diet) contained a lower zinc concentration at the beginning of lactation than did that from control dams (30 micrograms Zn/g diet); no differences were seen by d 11 of lactation. Dams fed the deficient diet had lower plasma zinc values in comparison with pair-fed or ad libitum-fed dams and lower femur zinc concentration in comparison with pair-fed dams. Pups suckling marginally deficient dams had lower concentrations of zinc in plasma, femurs and kidneys although hippocampal and cerebellar zinc were unaltered. Body weights of pups from marginally zinc-deficient dams were lower than those from ad libitum-fed dams, but similar to those from pair-fed dams. Lead ingestion had no effect on body weight. Marginally zinc-deficient pups had greater lead accumulation in blood, femurs, hippocampi and cerebella, but not kidney, than did zinc-adequate pups. Marginal zinc deficiency during lactation increases the body lead burden of suckling rats, an effect not attributable to increased transfer of lead into milk in response to suboptimal maternal zinc status.

Interactions between selenium and tin, selenium and lead, and their effects on alad activity in blood.

Abstract: Interactions of tin and selenium, as well as of lead and selenium, were investigated in male ICR mice. The toxic effects of selenium on mortality and body weight loss were reduced by simultaneous injection with tin or lead; among mice that were injected ip with selenium at 100 μmol/kg, the 24 h survival rate was 20%, whereas among mice that were administered selenium and tin or selenium and lead at the dose of 100 μmol/kg each, the rates were 100% and 90%, respectively. As for δ-aminolevulinic acid dehydratase (ALAD, EC 4.2.1.24), lead and tin were strong inhibitors, which is well known; selenium showed no effect. When more than an equimolar dose of sodium selenite was injected ip simultaneously with stannous chloride, the ALAD activity was completely retained. On the other hand, in the simultaneous injection with sodium selenite and lead acetate of differing ratios (Se/Pb), 1, 2.5, 5, and 7.5, selenium did not exhibit an obvious protective effect against the inhibition of ALAD activity caused by lead. It is suggested that selenium protects essential thiol groups in ALAD that are otherwise blocked by invading tin; in contrast, selenium, under similar conditions, does not prevent interactions of lead with enzyme thiol groups.

Effects of organic and inorganic lead on synaptosomal uptake, release, and receptor binding of glutamate in young rats.

Abstract: Chemical changes in central glutamate neurotransmission were assessed by measuring synaptic membrane receptor binding, the uptake and release by synaptosomes of glutamate in rats treated acutely with tetraethyl lead and chronically with lead acetate. The activity of Na+, K+-ATPase in synaptosomes was measured to correlate with the changes in uptake/release studies. The affinity of receptor binding and uptake systems was significantly reduced although the number of receptor sites and the capacity of uptake systems were increased. The activity of Na+, K+-ATPase was also found to be increased in synaptosomes. The changes were more marked in inorganic lead toxicity, and all three regions studied—cerebral cortex, cerebellum, and brainstem—showed significant alterations.

Experimental lead neuropathy: inorganic lead inhibits proliferation but not differentiation of Schwann cells.

Abstract: Schwann cells were prepared from the sciatic nerves of newborn rats and cultured in a monolayer. Addition of lead acetate at concentrations between 0.4 and 10.0 micrograms/ml, levels comparable to those occurring in neural tissues and physiological fluids of lead-intoxicated rats, diminished both the baseline rate of proliferation of the Schwann cells and their response to the mitogens, axolemmal fragments, glial growth factor, and the adenosine 3':5'-cyclic monophosphate (cAMP) analogues 8-bromo-cAMP and dibutyryl-cAMP. This demonstrates a direct toxic effect of inorganic lead on Schwann cells. Lead acetate in this concentration range did not, however, inhibit the cAMP analogue-induced appearance of the "myelin marker" lipid galactocerebroside on the surfaces of the cultured Schwann cells.

Acute Lead Intoxication due to Intravenous Injection

Abstract: A case of acute lead poisoning due to intravenous injection of lead acetate is reported. The patient developed clinical and biochemical symptoms characteristic for acute hepatic porphyrias. Elevated urinary 5-aminolaevulinic acid and low porphobilinogen correlated to a lead-induced inhibition of 5-aminolaevulinic acid dehydrase with diagnostically indicative reactivation rates by zinc and dithiothreitol. Urinary coproporphyrin excretion was also increased. Additional findings included anaemia and toxic hepatitis. Under the influence of elimination therapy with D-penicillamine pathologic parameters normalized. Except for transient neuralgic pains the patient did not experience any neurologic dysfunctions, thus contrasting the findings in chronic lead intoxication.

Differential vulnerability of mixed and cutaneous nerves in lead neuropathy.

Abstract: The prevalence of demyelinated fibers in mixed nerve (sciatic) and cutaneous nerve (sural) and the change in lead levels in various tissues over time were assessed in a model of lead neuropathy in the rat. Long-Evans rats were given drinking water containing 4% lead acetate and killed between one and 213 days of exposure. Lead levels in blood, brain, kidney, and femur increased over the 213-day period. Lead levels in sciatic nerve appeared to increase rapidly during the first few weeks of exposure and then decline to a lower plateau. The neuropathy was characterized by segmental demyelination and remyelination; neither axonal degeneration nor a microangiopathy was found. Sciatic nerve had a significantly greater prevalence of demyelinated fibers than sural nerve; the prevalence of demyelinated fibers was similar in proximal and distal sciatic nerve. The variable, brain-lead concentration times days on lead, which is an indicator of cumulative brain exposure, was the best predictor of the prevalence of demyelination. The differential involvement of sciatic and sural nerves in lead neuropathy may either indicate that Schwann cells myelinating different nerve-fiber populations have different susceptibilities to lead toxicity, or that lead preferentially enters sciatic nerve.

Behavioral effects following rehabilitation from postnatal exposure to lead acetate.

Abstract: At 21 days of age three groups of male hooded rats of the Sprague-Dawley strain were exposed to either untreated water or lead acetate at concentrations of 25 or 50 ppm provided ad lib in the drinking water for 40 days When tested for spontaneous alternation, the subjects receiving both 50 ppm and 25 ppm lead acetate exhibited significantly reduced rates of alternation below those of untreated control subjects Immediately subsequent to testing, lead was removed from the diet of the experimental groups and water substituted which was provided ad lib for the duration of the experiment This regimen of rehabilitation was continued for 70 days at which time all subjects were tested on the problems of the Hebb-Williams closed-field maze-learning task No significant differences were found in the time taken to traverse the maze enclosure, the number of squares traversed, or in the total number of error zones entered over the 12 test problems, although significantly increased latencies to leave the start box were noted for subjects previously exposed to lead acetate These data indicate that some deficits produced by postweaning lead acetate exposure may be reversible and not persist beyond a period of rehabilitation

Influence of Chronic Lead Ingestion on Igg Subclass Expression of the Immune Response to Bovine Serum Albumin

Abstract: Rats were given free access to drinking water containing 2% lead acetate for 30 days prior to intraperitoneal inoculation with 100 meg of bovine serum albumin (BSA) in Freund's complete adjuvant. Three weeks later, the animals were boosted with the antigen in Freund's incomplete adjuvant. After an additional three weeks, the animals were bled and the sera assayed for total IgG by radial immunodiffusion and for specific IgM, IgG and IgG subclasses by the enzyme-linked immunosorbent assay (EL1SA). BSA-inoculated rats exhibited similar levels of total IgG regardless of exposure to lead, but showed significant increases in IgG compared to nonimmunized controls. However, levels of IgG specific for BSA were significantly lower in the lead exposed group. Analysis of the IgG subclasses specific for BSA revealed that BSA-inoculated rats which were not exposed to lead had greater titers of lgG2b and IgG2c as compared to the lead exposed group. Chronic lead ingestion appears to diminish the overall IgG respo...

Effects of lead poisoning on properties of brain mitochondria in young rats

Abstract: When the litters were 14 days old, wistar rat pups received lead ions. The suckling mother was fed by a powdered laboratory chow containing lead carbonate (1%, 2%, 4%). The intoxication was going on for 3 days to 9 weeks. While lead-fed pups showed a decrease in body-weight gain and in neurologic development, lead ions were without effects on oxygen consumption, ADP-phosphorylation and activity of several enzymes of cerebral mitochondria. On the other hand, the important lead accumulation into cerebral mitochondria was in a straight ratio with lead doses in the feedings. To explain the in vivo data, the effects of lead acetate were investigated in vitro on brain mitochondria of young male wistar rats. Our findings indicate that lead ions alter mitochondrial respiration and ADP-phosphorylation and that inorganic phosphate has a protective effect.

Zinc lead-interaction in the rabbit.

Abstract: Subacute lead poisoning was performed in a group of rabbits by dissolving lead acetate (5 g/l) in the drinking distilled water. Another group of rabbits was left to drink the same lead acetate solution containing 0.435 g/l acetate to study the effects of zinc on lead poisoning. A third group drinking 0.435 g/l zinc acetate solution alone was studied for comparison. Intake of zinc caused a relative decrease of blood, urine and faecal lead, significant activation of the lead-inhibited erythrocyte delta-aminolaevulinic acid dehydratase (ALAD) activity and a relative decrease of urinary delta-aminolaevulinic acid (ALA) level. The analysis of several tissues for lead indicated that zinc caused biotransformation of lead from blood to some other tissues, leading to excess storage in bone, kidney and liver and less extent in the lung, brain and muscle.

Effects of lead on the renal response to extracellular volume expansion

Abstract: Subacute lead exposure has been observed to inhibit the natriuretic response to isotonic saline expansion in adult female rats. Three-week exposure to 0.5% lead acetate in drinking water resulted in a moderately high blood lead concentration of 57 ..mu..g/100 ml and up to 60% inhibition of the natriuretic response to extracellular volume expansion. This ability of lead to inhibit natriuresis following volume expansion (an induced stress) may be a more sensitive index of lead poisoning than alterations of renal function in nonstressed animals. Lead exposure had no effect on glomerular filtration rate (GFR) or plasma aldosterone concentrations, and in the presence of large doses of DOCA (a mineralocorticoid) this inhibitory effect of lead was still persistent. Amiloride completely blocked the antinatriuretic effect of lead in volume-expanded lead-poisoned animals, causing a twofold increase in water and electrolyte excretion while having minimal effects on volume-expanded controls. It is concluded that lead interferes with the action of a third factor, controlling natriuresis.

Effect of Lead Intake on Extinction of Short-Term Memory Trace (CTA) in Rats

Abstract: The effect of lead acetate on the extinction of conditioned taste aversion (CTA—short-term memory trace) was studied in albino rats. Three groups of animals of both sexes weighing between 150 and 200 g and 2 to 3 months old were selected and maintained with a staple diet under uniform husbandry conditions. The CTA was induced by 30-min saccharin (0.1%) drinking followed 30 min later by poisoning (lithium chloride 25 mg/100 g body weight). Retention trials were done 1 to 5 days later by offering the animal saccharin again; in Group 1 (n = 20) only one trial was done, whereas in Groups 2 (n = 22) and 3 (n = 22) regular trials were done in between 1 to 7 days. Only Groups 1 and 3 were exposed to lead (2500 μg/kg) a day before each extinction trial, and saccharin was injected per os by mouth if their consumption of fluid was inadequate. The extinction of CTA for saccharin in unexposed rats lasted about 2 weeks. Lead had no effect on the water consumption of CTA-trained animals. Lead retarded extincti...

Inability to experimentally produce a polyneuropathy in dogs given chronic oral low level lead.

Abstract: Electromyographic examinations were performed at various times over a 40 week period in four mature dogs receiving chronic oral low doses of lead acetate and a control dog receiving sodium acetate. Blood lead levels in the four dogs were elevated (mean values 1.15, 2.18, 1.13 and 1.72 mumol/liter). No clinical signs of lead intoxication were present. Two dogs had evidence of a nonregenerative anemia. Neither needle electromyographic nor nerve conduction velocity studies showed evidence of a polyneuropathy. Teased nerve fiber preparations of proximal and distal segments of the ulnar and tibial nerves and muscle biopsies of distal appendicular muscles were normal in all dogs. Light microscopic examination of the brain, kidneys and liver revealed no abnormalities in the two dogs necropsied. In conclusion, a polyneuropathy was not produced experimentally in dogs ingesting low doses of inorganic lead for up to 40 weeks.

Neutrophilic granulocytosis following lead acetate in female mice

Abstract: Lead induces an abrupt neutrophilic granulocytosis with the peak response detected 4 days after treatment. Using the incorporation of tritiated thymidine as an index of neutrophil production, autoradiographic analysis revealed that only about 16% of the total neutrophil increase is associated with a stimulatory effect on production. The remainder of the increase appears to be linked to the panhistotoxic action of lead, promoting migration of neutrophils from reserve sites in the wake of tissue damage.

Process for the manufacture of hydrated oxides and tri- and tetra- basic lead sulphates.

Abstract: Process for the manufacture of hydrated lead oxides in the bivalent state characterized by the steps of (1) reacting metallic lead with acetic acid (e.g. ammonium acetate, 5%-30% solution) at a temperature up to 200 C (e.g. 50 C-200 C) under an atmosphere of an oxygen containing gas (e.g. oxygen) of between 1 and 10 atmospheres absolute pressure to form lead acetate, then (2) reacting the lead acetate with a source of ammonium ion (e.g. ammonia) under an absolute pressure between 1 and 5 atmospheres at a temperature up to 100 C (e.g. 60 C - 90 C) to precipitate lead oxides. Optionally, to produce tri- and tetra- basic lead sulphates, by (3) adding to the lead oxides so precipitated sulphuric acid in the stoichiometric amount to produce tri- or tetra- basic lead sulphate, then (4) separating and drying the tri- or tetra- basic lead sulphate so formed.