Showing papers on "Lead acetate published in 1976"
Journal Article•
TL;DR: Experimental animal studies of leads effects are reviewed, evidence that women are more susceptible than men to the toxic effects of lead is evaluated, and evidence that the difference between the sexes may be due to hormonal effects of drug metabolism.
Abstract: Reported data regarding leads effect on human pregnancy are summarized experimental animal studies of leads effects are reviewed and published evidence that women may be more susceptible than men to the toxic effects of lead is evaluated. Numerous reports during the nineteenth century had shown that lead had a damaging effect on fertility the course of pregnancy and the development of the fetus. Exposure to lead by either sex has been shown to result in reproductive failure. Abnormal lead content of water supplies has been associated with increased coproporphyrin in urine and frequent abnormal pregnancies. Lead has been found in umbilical cord blood in concentrations paralleling those of the mother and lead has been found to be transported into maternal milk during lactation. Long-term ingestion by the mother of "moonshine whiskey" containing a high concentration of lead has resulted in damage to the infant. The reproductive ability of men exposed to lead is reduced by altered spermatogenesis. Animal experiments have shown that lead inhibits hepatic detoxification mechanisms in both male and female animals. In the presence of cadmium the teratogenic effect of lead is potentiated in hamsters. Chromosomal aberrations have been shown to be frequent in leukocyte cultures from mice fed a diet of 1% lead acetate. Chromosomal aberrations have been shown in the peripheral blood lymphocytes of male workers in a lead oxide factory. There is evidence that women are more susceptible than men to the toxic effects of lead. The difference between the sexes may be due to hormonal effects of drug metabolism.
118 citations
TL;DR: Results are interpreted to indicate that the effects produced by exposure to lead may involve an increase in responsiveness to aversive situations.
Abstract: Rats contineously exposed to lead acetate solutions were tested on a visual discrimination reversal problem, on the open field and in 2 shuttle avoidance situations. High lead intake produced slower acquisition of the visual discrimination problem but had no effect on reversal performance. High lead intake reduced activity on the open field and improved performance on both shuttle avoidance problems. Results are interpreted to indicate that the effects produced by exposure to lead may involve an increase in responsiveness to aversive situations.
72 citations
Journal Article•
TL;DR: The data indicate that chronic exposure to low doses of heavy metals produces differential changes in regional levels of various brain biogenic amines, which may represent the early signs of adverse effects on CNS function since they occur before any overt symptoms of neurotoxic effects ofheavy metals become apparent.
Abstract: Effects of chronic (45 days) treatment with different doses of cadmium chloride (0.25 and 1.0 mg/kg/day), methylmercury chloride (0.4 and 4.0 mg/kg/day) and lead acetate (0.2 and 1.0 mg/kg/day) and of 28-day withdrawal of treatment on the levels of acetylcholine (ACh) and activity of acetylcholinesterase (AChE) in cerebral cortex, and concentration of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in brain-stem were examined in rats. Exposure to both cadmium and methylmercury produced significant decreases in cortical ACh and brain-stem 5-HT levels. In addition, brain-stem NE concentration was increased in methylmercury-treated rats. In contrast, chronic treatment with lead resulted in enhanced cerebrocortical ACh levels but a decreased brain-stem NE concentration. Treatment with cadmium also produced a transient enhancement of striatal dopamine levels. Cadmium-induced decrease in brain-stem 5-HT and lead-induced accumulation of cortical ACh persisted even after 28 day withdrawal of treatment. The data indicate that chronic exposure to low doses of heavy metals produces differential changes in regional levels of various brain biogenic amines. These changes may represent the early signs of adverse effects on CNS function since they occur before any overt symptoms of neurotoxic effects of heavy metals become apparent.
58 citations
TL;DR: Twenty wether lambs were individually fed for 84 days to study the effect of dietary lead on performance and mineral composition of selected tissues and the percentage of apparent absorption and net retention of lead was not significantlydifferent among treatments.
Abstract: Twenty wether lambs were individually fed for 84 days to study the effect of dietary lead on performance and mineral composition of selected tissues. The treatments included 0, 10, 100, 500 and 1000 ppm supplemental lead as lead acetate added to a practical diet. Increased dietary lead did not affect feed consumption, weight gain or feed conversion ratio. Hemoglobin, hematocrit and blood lead were not affected by dietary treatments. Lead concentrations were higher (P < .01) in liver, bone, brain and spleen when 500 and 1000 ppm dietary lead was fed. High dietary lead also resulted in higher (P < .05) lead concentrations in kidney, heart and muscle. As dietary lead increased, zinc levels in heart and brain increased (P < .01) and iron levels in the brain decreased (P < .01). In a second study, six sheep each were assigned to diets containing either 50 or 1000 ppm supplemental lead, respectively, to determine the effect of dietary lead on nutrient digestibility, nitrogen and lead balance. Supplemental lead did not affect nutrient digestibility or nitrogen balance. More lead was absorbed and retained with the greater intake but the percentage of apparent absorption and net retention of lead was not significantlymore » different among treatments.« less
36 citations
TL;DR: Urinary levels of ALA and lead were comparable with the usual urinary levels of chronically lead exposed humans at the end of the intoxication period, and in kidney homogenates of poisoned rats succinate dehydrogenase, cytochrome oxidase and lactate dehydrogenases were unmodified, malate dehydrationrogenase and glutamate dehydrogen enzyme were decreased, while Dt diaphorase and glucose-6-phosphate dehydrogensase were greatly increased compared with controls.
21 citations
TL;DR: The results of this study seem to verify that absorption of lead through the skin does occur and the findings confirm lead naphthenate to be more toxic than lead acetate.
20 citations
TL;DR: The lead-treated cells were interpreted to contain lead ions on the basis of energy-dispersive X-ray analysis and some cells, however, showed evidence that intracytoplasmic materials had been leached from the cells.
Abstract: Aeromonas sp. will methylate trimethyl lead acetate (Me/sub 3/PbOAc) to volatile tetramethyl lead (Me/sub 4/Pb). Examination of cultures grown in the presence of Me/sub 3/PbOAc revealed no major irregularities between cells of the treated and untreated cultures. Some cells, however, showed evidence that intracytoplasmic materials had been leached from the cells. The lead-treated cells were interpreted to contain lead ions on the basis of energy-dispersive x-ray analysis.
16 citations
TL;DR: It is shown that weanling rats made calcium deficient increased their voluntary ingestion of lead to levels much greater than those of control rats, and experimented with rhesus monkeys which were subjected to a moderately deficient diet providing 64% of their recommended daily calcium levels.
Abstract: VOLUNTARY ingestion of lead (lead pica) by children is a puzzling phenomenon. The resulting lead poisoning can lead to painful physical symptoms, mental retardation and brain damage1–5. Yet ingestion often persists after toxic symptoms appear if the child has access to lead6. We have shown that weanling rats made calcium deficient increased their voluntary ingestion of lead to levels much greater than those of control rats7. It was suggested that, because of the metabolic similarity of lead to calcium, ingestion of lead might relieve symptoms of calcium deficiency, attenuate the normal aversive effects of lead ingestion, and thus maintain continued ingestion. Rats, however, are not completely appropriate for an analogy to human lead ingestion because calcium metabolism differs considerably in the two organisms8,9. Rats seem to find lead acetate an aversive taste7,10, whereas humans refer to it as “lead sugar” and report a sweet taste (paper presented at meeting of Midwestern Psychological Association, 1975 by R. W. Henderson and J. Dawley). Furthermore, the diet used with rats has been almost completely deficient in calcium (2 mg Ca per 100 g) producing severe symptoms of calcium deficiency, which have not been reported in humans with lead pica. If calcium deficiency leads to lead pica in humans, it must be a moderate or subclinical deficiency. We have therefore experimented with rhesus monkeys which were subjected to a moderately deficient diet providing 64% (108 mg Ca per 100 g) of their recommended daily calcium levels11.
14 citations
TL;DR: The animals incurred moderate to extreme elevations of lead in blood, most lost weight, or had depressed weight gains, and developed Burtonian lines, some died suddenly and unexpectedly, and many terminated in a moribund state with profound anemia.
Abstract: Lead-containing paints were administered orally to 27 rhesus monkeys for periods of 18-667 days. Lead acetate was fed to nine monkeys of three different species for 9-156 days. Excretion of one week's dose of lead in six primates ranged from 35 to 94%. The animals incurred moderate to extreme elevations of lead in blood, most lost weight, or had depressed weight gains, and developed Burtonian lines, some died suddenly and unexpectedly, and many terminated in a moribund state with profound anemia. Only one neonate had obvious signs of lead encephalopathy. The monkeys' ages, dose and source of lead, and possibly other factors, affected their response to lead.
14 citations
TL;DR: The density of the cerebral cortex capillaries of the infant rats and their convolution rate were studied morphometrically and noted to increase significantly according to the duration of lead treatment, as demonstrated by two-way analysis of variance.
Abstract: Pregnant rats were fed a diet containing 1.8% lead acetate for 8 days before delivery until the young were 3 month old. The density of the cerebral cortex capillaries of the infant rats and their convolution rate were studied morphometrically and noted to increase significantly according to the duration of lead treatment, as demonstrated by two-way analysis of variance. On the other hand, the thickness of the cortex reduced progressively. The increase of both capillary density and convolution rate is supposed to be related with this involution of cortex. This provides a quantitative insight of the previously described ‘capillary activation’ phenomenon, caused by lead encephalopathy and reveals it as a significant sequel of saturnine action.
7 citations
TL;DR: It is concluded that some experimental models of acute inflammation in the rat are also accompanied by altered liver function, and serum amylase decreases in rats treated with various endotoxins and the hepatoxins, CCl 4 and lead acetate.
Journal Article•
TL;DR: The chronic nephropathy and microcytic hypochromic anemia resulting from long-term administration of lead to the gerbil are comparable to those observed in man, and may be useful as amore model to study chronic lead poisoning in man.
Abstract: The rat, commonly used for studies of toxicity and cellular effects of lead, has disadvantages as a model for effects on humans. The rat has spontaneous enzootic pneumonia and progressive nephropathy as well as lead-induced kidney tumors. Studies with the Mongolian gerbil indicated large accumulations of lead in the kidneys, e.g., three times as much as in rats after 2 weeks of diets containing 1% lead. During 12 weeks of 0.25% dietary lead, intranuclear inclusions in epithelial cells of the proximal convoluted tubules were found. Increasing numbers of tubules containing little or no epithelium were noted. There were also cytoplasmic changes representing lead inclusions similar to those in the rat. Diets with 0.25% lead acetate, fed to gerbils for 30 months, produced chronic progressive nephropathy with tubular degeneration, interstitial fibrosis, and intranuclear inclusions. Blood cell volume and corpuscular hemoglobin values approximately 30% lower than control values indicated microcytic hypochromic anemia. Red cells exhibited anisocytosis, polychromatophilia, and basophilia: their shape varied, and many of the cells were normoblasts or reticulocytes. The chronic nephropathy and microcytic hypochromic anemia resulting from long-term administration of lead to the gerbil are comparable to those observed in man. Thus, the gerbil may be useful as amore » model to study chronic lead poisoning in man.« less
Journal Article•
Journal Article•
TL;DR: Intranuclar acid-fast inclusions in the cells of the proximal convulted tubules of the kidney were demonstrated in 9 of 12 lead treated goats and in the liver parenchymal cells of 2 of these animals.
Abstract: The effects of orally administered lead acetate were investigated in 9 adult and 3 kid goats by clinical and necropsy studies. One kid and 6 adults died after having received from 100 to 1392.5 Gm each, given over periods of from 10 to 52 days. Anorexia, diarrhea and body weight loss occurred in all lead treated goats in the study. Basophilic strippling of red blood cells was found in 6 of 8 animals on which weekly hemograms were performed. The pathologic changes were essentially the same as those that have been recorded for other ruminant species with lead poisoning. Intranuclar acid-fast inclusions in the cells of the proximal convulted tubules of the kidney were demonstrated in 9 of 12 lead treated goats and in the liver parenchymal cells of 2 of these animals.
Journal Article•
01 Nov 1976
TL;DR: The data indicated that chronic exposure to low doses of heavy metals produces differential changes in regional levels of various brain biogenic amines, which may represent the early signs of adverse effects on CNS function since they occur before any overt symptoms of neurotoxic effects ofheavy metals become apparent.
Abstract: Effects of chronic (45 days) treatment with different doses of cadmium chloride (0.25 and 1.0 mg/kg/day), methylmercury chloride (0.4 and 4.0 mg/k/day) and lead acetate (0.2 and 1.0 mg/kg/day) and of 28-day withdrawal of treatment on the levels of acetylcholine (ACh) and activity of acetylcholinesterase (AChE) in cerebral cortex, and concentration of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in brain-stem were examined in rats. Exposure to both cadmium and methylmercury produced significant decreases in cortical ACh and brain-stem 5-HT levels. In addition, brain-stem NE concentration was increased in methylmercury-treated rats. In contrast, chronic treatment with lead resulted in enhanced cerebrocortical ACh levels but a decreased brain-stem NE concentration. Treatment with cadmium also produced a transient enhancement of striatal dopamine levels. Cadmium-induced decrease in brain-stem 5-HT and lead-induced accumulation of cortical ACh persisted even after 28 days withdrawal of treatment. The data indicated that chronic exposure to low doses of heavy metals produces differential changes in regional levels of various brain biogenic amines. These changes may represent the early signs of adverse effects on CNS function since they occur before any overt symptoms of neurotoxic effects of heavy metals become apparent.
TL;DR: Change of glycine cleavage activity in liver mitochondria of lead-intoxicated rats was studied and in vitro the activity in the normal rat Liver mitochondria was markedly inhibited by addition of lead acetate.
Abstract: Change of glycine cleavage activity in liver mitochondria of lead‐intoxicated rats was studied in this paper. The following results were obtained: (1) The activity in hepatic mitochondria of rats was decreased by a single administration of lead (4 mg/100 g body weight); (2) in vitro the activity in the normal rat liver mitochondria was markedly inhibited by addition of lead acetate (4 mM).
Journal Article•
TL;DR: Activation of lysosomal enzymes (alpha-manosidase and beta-acetylglucosaminidase) in the blood serum as soon as the third day after daily administration of lead acetate is demonstrated.
Abstract: Examination of the effect of experimental lead poisoning on permeability of lysosomal membranes in albino rats demonstrated activation of lysosomal enzymes (alpha-manosidase and beta-acetylglucosaminidase) in the blood serum as soon as the third day after daily administration of lead acetate (20 mg/kg). Apparently damage of the lysosomal membrane played an important role in the pathogenesis of lead poisoning.
TL;DR: Certain factors were found to prevent quantitative recovery of soluble alkaline phosphatase from homogenates of chick duodenal mucosa during treatment with n-butanol.
Abstract: Certain factors were found to prevent quantitative recovery of soluble alkaline phosphatase from homogenates of chick duodenal mucosa during treatment with n-butanol. Divalent cations such as calcium, manganese and lead interfered when present at 0.1-0.2 mM. Magnesium and zinc were found to reduce enyme recovery when present at 1.0 mM during extraction. These metals had little effect on enzyme activity per se, whether added to the homogenates or enzyme extracts before dilution for assay. However, lead acetate may have a protective or activating effect on phosphatase, at 0.1-10 mM. Other factors affecting the recovery of enzyme activity after butanol solubilization are the state of dilution and pH of the homogenate and individual animal variation.
TL;DR: Innury to the lysosomal membrane evidently plays an important role in the pathogenesis of lead poisoning.
Abstract: The effect of experimental lead poisoning on the permeability of the lysosomal membrane was investigated in albino rats. Activation of two lysosomal enzymes, α-mannosidase and β-acetylglucosaminidase, was found in the blood serum as early as on the third day of daily administration of lead acetate (20 mg/kg) to the rats. Innury to the lysosomal membrane evidently plays an important role in the pathogenesis of lead poisoning.
TL;DR: It was suggested that steroid 5ƒÀ-reductase activity was an important factor in affecting the heme synthesis in lead poisoning.
Abstract: The increase of urinary ƒÂ-aminolevulinic acid in lead poisoning is well observed. In this paper, the effects of lead acetate on the activities of ƒ¢4-reductase and 5ƒÀ-reductase to cortisol, cortisone, testosterone and ƒ¢4-androstene-3, 17-dione and of dehydrogenase to 3ƒ¿-hydroxysteroid and 3ƒÀ-hydroxysteroid were examined. To measure the activities, 12,000•~g and 105,000•~g supernatant of rat liver were used. The ƒ¢4-reductase activity to cortisol and testosterone showed a significant decrease twenty-four hours after the administration of lead acetate, but that to testosterone showed a remarkable increase seventy-two hours after the administration of lead acetate. The 5ƒÀ-reductase activity to testosterone decreased significantly twenty-four hours after the administration of lead acetate, but increased seventy-two hours after administration of lead acetate. No significant difference was found in ƒ¢4-androstene-3, 17-dione. From these results, it was suggested that steroid 5ƒÀ-reductase activity was an important factor in affecting the heme synthesis in lead poisoning.
TL;DR: While a continuous ingestion of lead acetate added in drinking water suppressed the rat growth, depressing in some degree the level of hepatic δ-aminolevulinate (ALA) dehydratase, a very small amount of sclerin (SCL) added simultaneously in the water restored the growth and dehydrat enzyme level.
Abstract: While a continuous ingestion of lead acetate added in drinking water suppressed the rat growth, depressing in some degree the level of hepatic δ-aminolevulinate (ALA) dehydratase, a very small amount of sclerin (SCL) added simultaneously in the water restored the growth and dehydratase level. Moreover, subcutaneous injection of SCL to the rat not only maintained the ALA dehydratase level, but prevented a marked depression of the level of mitochondrial ALA synthetase in liver caused by intraperitoneal injection of lead acetate. Injection of SCL alone increased tolerably (about 1.8 times) the mitochondrial ALA synthetase, but little the extramitochondrial synthetase. The treatment by SCL was attended by a initial decrease, then a gradual increase in the activity of microsomal drug metabolizing enzyme.