Showing papers on "Lead acetate published in 1997"
TL;DR: The data suggest a balance between increased NO synthesis and degradation (by reactive oxygen species) in lead-treated rats, which results in normal levels of NO.
Abstract: An elevation of mean blood pressure was found in rats treated with low lead (0.01% lead acetate) for 3 months, as contrasted to paired Sprague-Dawley control rats. In these rats, measurement of plasma and urine endothelins-1 and -3 revealed that plasma concentration and urinary excretion of endothelin-3 increased significantly after 3 months (plasma: lead group, 31.8+/-2.2, versus controls, 23.0+1.7 pg/mL, P<.001; urinary excretion: lead group, 46.6+11.7, versus controls, 35.6+6.7 pg/24 h, P<.05), whereas endothelin-1 was unaffected. Plasma and urinary nitric oxide (NO) and cyclic GMP concentrations were not significantly changed. However, assay of plasma and kidney cortex malondialdehyde by high-pressure liquid chromatography, as a measure of reactive oxygen species, was elevated in lead-treated rats compared with that in control rats (plasma: lead group, 4.74+1.27, versus controls, 2.14+.49 micromol/L, P<.001; kidney cortex: lead group, 28.75+3.46, versus controls, 16.38+2.37 nmol/g wet weight, P<.001). There was increased NO synthase activity in lead-treated rat brain cortex and cerebellum. In lead-treated rat kidney cortex, the endothelial constitutive NO synthase protein mass was unaffected, whereas the inducible NO synthase protein mass was increased. These data suggest a balance between increased NO synthesis and degradation (by reactive oxygen species) in lead-treated rats, which results in normal levels of NO. Thus, the hypertension may be related to an increase in the pressure substances, endothelin-3 and reactive oxygen species, rather than to an absolute decrease in nitric NO.
190 citations
TL;DR: An interaction arsenic/lead on the central monoaminergic systems of the adult mouse is demonstrated, with a higher accumulation of lead and a lower arsenic accumulation in the brain.
116 citations
TL;DR: It is concluded that lead exposure probably affected the sperm function by activating one of the pathways of ROS generation.
112 citations
TL;DR: It is suggested that the intact membrane structure is a must for 5'D-I activity and the administration of vit E may prevent the lead induced thyroid dysfunction by maintaining membrane architecture.
75 citations
TL;DR: Data suggest that a change in the activation of hippocampal PKC may be involved in the lead-induced deficit in learning, and continuous and longer duration of lead exposure appears to affect the learning performance and hippocampus PKC activation.
Abstract: Long-term exposure to a low level of lead is associated with learning deficits. Several types of learning have been correlated to hippocampal protein kinase C (PKC) activation. This study was designed to determine if there is a correlation between the effects of lead on hippocampal PKC activation and those on learning performance. Rats were exposed to 0.2% (w/v) lead acetate at different developmental stages including a maternally exposed group, a postweaning exposed group, and a continuously exposed group. The continuously lead exposed rats tended to avoid less frequently and not respond more frequently in two-way active avoidance training than did controls. This training process was associated with translocation of hippocampal PKC activity from cytosol to membrane. Two-way analysis of variance of data indicates that there is a significant training and lead treatment interaction in the ratio of membrane to cytosolic PKC activity (F3,32 = 3.013; p = 0.044). The interaction is attributable to the absence of the training-induced PKC translocation in the continuously lead exposed rats. In addition, no significant changes were observed in learning performance and training-induced hippocampal PKC activation after maternal and postweaning lead exposure. Continuous and longer duration of lead exposure appears to affect the learning performance and hippocampal PKC activation. These data suggest that a change in the activation of hippocampal PKC may be involved in the lead-induced deficit in learning.
46 citations
TL;DR: It is revealed that while small and medium follicles were significantly affected even at the lowest dose, the large follicle were affected mostly at the highest dose, and these findings correlated well with increased blood lead levels.
Abstract: Lead, a potent reproductive toxicant in humans and experimental animals, was used to detect the morphological basis of ovarian toxicity in mice by counting the various stages of follicular development using different doses of lead acetate (0, 2, 4 or 8 mg/kg/d) for 60 d (5 d/wk) by oral gavage. Our results revealed that while small and medium follicles were significantly affected even at the lowest dose (2 mg), the large follicles were affected mostly at the highest dose. Atresia even in the medium follicles reflected the extent of damage caused by lead. These findings correlated well with increased blood lead levels. Therefore, lead seems to affect the follicular development and maturation, if mice are exposed to sufficiently high concentrations of metal through the oral route.
46 citations
TL;DR: Chronic developmental lead exposure prevented the full expression of LTP in the CA1 region of the rat hippocampus and induced long-term potentiation in control and 100 ppm lead-treated animals.
32 citations
TL;DR: A concentration dependent decrease in root nitrate reductase (EC1661) activity (NRA) by 1 to 20 mM lead acetate was noticed in three cultivars of Vigna radiata (L) Wilczek (K851, MH8320 and ML337) as mentioned in this paper.
Abstract: A concentration dependent decrease in root nitrate reductase (EC1661) activity (NRA) by 01 to 20 mM lead acetate was noticed in three cultivars of Vigna radiata (L) Wilczek (K851, MH8320 and ML337) Leaf NRA, on the other hand, increased significantly with increasing lead concentration which was more pronounced in cvs MH8320 and ML337 than in cv K851 Total nitrogen content of root and shoot was generally increased due to supply of the lead acetate, whereas the total nitrogen content of the colyledons was hardly affected in cvs MH8320 and ML337 and decreased in cv K851 during the early growth phase The inhibition of root NRA could be alleviated by addition of inorganic salts (K2HPO4 and KNO3, but not CaCl2) or 6-benzylaminopurine (BAP) in the incubation medium Lead mediated inhibition of root NRA was similar in light and dark grown seedlings, but lead induced increase in leaf NRA was more pronounced in the light than in the dark
32 citations
TL;DR: Evidence is presented that liver synthesis of human transferrin is suppressed by both the toxic metal lead and bacterial lipopolysaccharide, an inducer of the hepatic acute phase response, and that lead may also affect iron metabolism in humans by interfering with transferrin levels.
28 citations
TL;DR: Addition of lead acetate to PC 12 pheochromocytoma cells elicits induction of c‐fos, an immediate early response gene, which has the potential to deregulate the expression of other genes.
23 citations
TL;DR: All the tissues taken for experimentation, generated significantly higher amount of TBA-RS in lead-treated mice when compared with the respective control value, however, none of the tissues could correspond to the control value after the lapse of four weeks post-treatment.
Abstract: A single intraperitoneal injection of lead acetate (200 mg/kg body weight) increased the lipid peroxidation potential (LPP) measured as thiobarbituric acid-reactive substance (TBA-RS) in different tissues of Swiss mice. All the tissues taken for experimentation, generated significantly higher amount of TBA-RS in lead-treated mice when compared with the respective control value. However, none of the tissues could correspond to the control value after the lapse of four weeks post-treatment. Possibilities of differential responsiveness of tissues to generate lipid peroxides in lead-treated mice have been discussed.
TL;DR: The rate enhancing effects of cocaine were less pronounced in lead-exposed animals than controls, at least at the 20 mg/kg dose, and accent the need to examine further the interactive relations between the external chemical environment and drug sensitivity.
Abstract: Chronic lead exposure has been shown to attenuate cocaine-induced increases in extracellular dopamine levels in the region of the nucleus accumbens, and antagonize the locomotor stimulating effects of the drug. The purpose of this study was to determine if similar lead-induced disturbances in the effects of cocaine include the impact of the drug on schedule-controlled responding. Adult male rats exposed ad libitum to water containing 500 ppm lead acetate (Group Lead), or a comparable concentration of sodium acetate (Group Control), were placed on a restricted diet (12–15 g food/day) prior to commencing fixed-interval (FI-5 min) schedule training on Day 33 of exposure. After 27 days of operant training, animals received a sequence of no injection, saline injection, and cocaine injection tests, repeating the sequence for 3, 10, 20 and 40 mg/kg cocaine HCl (ip). Local rates were determined for successive 30 s segments of the interval and the pattern of responding was compared under conditions of saline and cocaine injection. For both groups, cocaine increased responding, especially early in the interval. However, the rate enhancing effects of cocaine were less pronounced in lead-exposed animals than controls, at least at the 20 mg/kg dose. These data extend earlier findings and accent the need to examine further the interactive relations between the external chemical environment and drug sensitivity.
TL;DR: Results suggest that glucocorticoid signal transduction pathways in HTC cells involve calcium-mediated cellular events and PKC isoforms and Western blot results indicated that lead exposure may increase PKC beta and decrease PKC alpha translocation from cytosolic to particulate fractions, respectively.
Journal Article•
TL;DR: It is demonstrated that lead exposure affects the dopaminergic retinal amacrine cells by reducing the TH-content in these neurones and that this neurotoxic effect persists beyond the end of exposure.
Abstract: One of the toxic effects of lead in the CNS is an altered functional state of the catecholamine system, especially a reduction in the activity of tyrosine hydroxylase (TH), the rate-limiting enzyme of catecholamine synthesis. Here we report on a lead-induced decrease in TH-content in neurones of the rhesus monkey retina. Rhesus monkeys were pre- and postnatally exposed to 0, 350, or 600 ppm of lead acetate (Pb) in the diet over 9 years. Lead exposure was followed by a 35-month period of lead-free diet. During this period, blood lead levels of the treated animals declined to nearly those of the untreated controls. Subsequently the animals were sacrificed and the retinas processed for TH immunocytochemistry. The fluorescent dye FITC was used to visualise the antibody reaction. Photometric measurements of the fluorescence intensity of stained neurones were made with a laser scanning microscope. In the rhesus monkey retina two types of TH-immunoreactive neurones are present. In the bright fluorescent type, lead exposure resulted in decreased fluorescence intensity and altered the intensity profile of the TH-immunoreactive cells in a dose-dependent manner. In these cells, fluorescence intensity was 0.53 and 0.22 for 350 ppm Pb and 600 ppm Pb respectively when the fluorescence intensity of the untreated controls (0 ppm Pb) is taken as 1. Both lead doses also reduced the number of ascending fibres in the inner nuclear layer and the dense staining of fibres in sublayer 1 of the inner plexiform layer. The weakly fluorescent cell type disappeared to a large extent under 350 ppm Pb treatment and was not detectable in the 600 ppm Pb group. The results demonstrate that lead exposure affects the dopaminergic retinal amacrine cells by reducing the TH-content in these neurones and that this neurotoxic effect persists beyond the end of exposure.
TL;DR: Results show that lead exposure results in a reduction of cardiac beta-adrenoceptor density, which was closely related to elevation of blood and heart lead levels.
TL;DR: Hepatic and renal lipid peroxidative process increased significantly following lead treatment, whereas the levels of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) were decreased.
Abstract: A study has been made to reveal the mode of action of lead inhibiting type-I iodothyronine 5′-monodeiodinase (5′-D) activity in the Indian rock pigeon,Columba livia. Administration of lead acetate (6 mg/kg body weight/day) for 20 days decreased 5′-D activity and glutathione content in the liver and kidney homogenates. It also reduced the serum concentration of 3, 3′, 5-triiodothyronine (T3) with a marginal increase in serum thyroxine (T4). Hepatic and renal lipid peroxidative process increased significantly following lead treatment, whereas the levels of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) were decreased. The possible involvement of lipid peroxidative process in the inhibition of 5′-D activity inColumba livia is suggested.
TL;DR: Morphological modifications after early lead exposure, induced nNOS reduction in NOS expressing neurons thereby interfering in NO synthesis.
TL;DR: Results show no detectable effect of a low‐body burden of lead on major myocardial proteins of the rabbit.
Abstract: Despite reported adverse effects, the cardiovascular toxicity of lead remains controversial. The purpose of the present study was to determine if low-level subchronic exposure of rabbits to lead would produce detectable, concentration-dependent changes in myocardial proteins. Lead was administered to male Dutch Belted rabbits as a lead acetate solution, adjusted weekly to achieve and maintain the target blood lead levels of 0, 20, 40, and 80 microg/dL for 15 weeks. Lead exposures did not affect heart or body weights. Myocardial concentrations of lead at sacrifice were 58+/-25, 69+/-23, 102+/-62, and 105+/-37 ng/g. Of 808 individual proteins resolved by two-dimensional electrophoresis (2-DE) in ventricular homogenates, 162 had coefficients of variation < 20%. A number of proteins were tentatively identified based on coordinate positions homologous to other established 2-DE patterns. Despite variable expression of some protein spots, none of the protein abundances analyzed were found to be significantly altered (P < 0.001) by the lead exposures studied. Therefore results show no detectable effect of a low-body burden of lead on major myocardial proteins of the rabbit.
TL;DR: It is suggested that lead acetate exerts a weak clastogenicity on salivary gland polytene chromosomes of D. melanogaster.
Abstract: In this study, the effects of lead acetate on the third instar larvae salivary gland polytene chromosomes of D. melanogaster have been investigated.In this research, the effects of a heavy metal compounds, lead acetate, were examined on the polytene chromosomes in D. melanogaster. The various clastogenic effects such as weak points (breaks, semibreaks, constrictions, etc.), hairpin and asynapsis were observed but not chromosomal aberrations in control groups (in the larvae untreated with lead acetate). Our findings suggest that lead acetate exerts a weak clastogenicity on salivary gland polytene chromosomes of D. melanogaster.
TL;DR: The color change is gradual, continuous, and reversible with temperature, even through the liquid-glass transition as discussed by the authors, due to the rotation of two acetate ligands that become bidentate.
Abstract: Compositions of lithium acetate and lead acetate form homogeneous liquids when heated above 100°C. When such liquids are doped with Co2+, the liquid/glass is colored blue at relatively high temperatures (100°C–150°C) and varying shades of red under ambient conditions. The color change is gradual, continuous, and reversible with temperature, even through the liquid-glass transition. This thermochromic property has been attributed to Co2+ changing coordination from tetrahedral to octahedral with decreasing temperature, due to the rotation of two acetate ligands that become bidentate. Additives to the glass composition can control the acetate glass structure, which preferentially stabilizes a specific coordination site of Co2+ and the resulting color of the liquid/glass. The color changes are not directly attributable to changes in the basicity or polymerization of the acetate liquid/glass network. Acetate liquids/glasses lack a covalently bonded network, and thus are not appropriate models for silicate structures.
TL;DR: The observed effects of toxicologically relevant lead concentrations on high-threshold calcium currents in chronically exposed mammalian cells provide further support for the notion that at least one cellular target of the heavy metal's neurotoxic action may be the voltage-gated calcium channel.
TL;DR: A marked decrease both in the body and testes weight in the lead injected animals associated with a significant decrease in the ascorbic acid content in the testicular tissue have been observed.
Abstract: The toxicity of lead acetate in the male germ cells of Swiss mice has been studied. A single intraperitoneal dose of lead acetate (50 mg/kg body weight) not only caused testicular atrophy but also affected the normal sperm count to decline significantly with the production of a significantly increased amount of morphologically abnormal sperm in the treated animals. Further, a marked decrease both in the body and testes weight in the lead injected animals associated with a significant decrease in the ascorbic acid content in the testicular tissue have been observed.
TL;DR: The effects of lead acetate after repeated intraperitoneal injection were examined in parotid and submandibular saliva and blood in rats and lead concentrations were determined to be significantly different from their respected controls.
Abstract: The effects of lead acetate (100 mg/ kg) after repeated intraperitoneal (ip) injection were examined in parotid and submandibular saliva and blood in rats. Animals were treated with 1, 2, or 3 injections of lead acetate and were sacrificed 1 and 7 d after the last injection. Lead concentrations were determined by flame atomic absorption spectroscopy, in whole blood and in submandibular and parotid salivas. Lead concentrations in submandibular and parotid salivas were determined to be 50% and 22% of whole blood lead concentrations, respectively. Lead concentrations in whole blood and in submandibular and parotid salivas were determined to be significantly different from their respected controls. Submandibular saliva lead concentrations were correlated with whole blood lead concentrations ( r = .78) and parotid saliva lead concentrations were correlated ( r = .93) only on d 1 with respect to whole blood level after the first administration (acute poisoning).
TL;DR: Although Fe composition of placenta remained within normal range with increasing load of endogeneous Pb, Zn decline was not consistent after oral feeding of Pb acetate and analysis of trace elements following Pb exposure showed low levels of Mn and Cu.
Abstract: The present study was carried out to find the effects of Pb acetate (10-50 mg/kg body wt) after oral administration on:
Pb toxicity expressed on a dry-wt basis was reflected in terms of deficiency of δ-ALAD and PAP and enhanced content of GSH. Analysis of trace elements following Pb exposure showed low levels of Mn and Cu. Although Fe composition of placenta remained within normal range with increasing load of endogeneous Pb, Zn decline was not consistent after oral feeding of Pb acetate. Deficiency of PAP after Pb exposure did not correlate with the endogeneous levels of Pb or Zn therein, but correlated with endogeneous levels of Mn. Placental deficiencies of Cu and Mn have been related to the disturbed placental functions by Pb accumulation.
TL;DR: The results suggest that acute exposure of C6 cells to lead may inhibit processes involved in glucocorticoid-mediated signal transduction events within central nervous system hormonal target cells.
Journal Article•
01 Jan 1997
TL;DR: Ultrastructural analysis of the rat pancreas following the long-term exposure to lead revealed the presence of numerous intermediate cells in animals receiving lead acetate in doses of 500 ppm and 1000 ppm for 4 and 6 weeks.
Abstract: Ultrastructural analysis of the rat pancreas following the long-term exposure to lead revealed the presence of numerous intermediate cells in animals receiving lead acetate in doses of 500 ppm and 1000 ppm for 4 and 6 weeks. The cells included acinar-beta, beta-acinar and intermediate cells containing two kinds of endocrine granules- alpha and beta, and zymogen granules.
Journal Article•
TL;DR: Both nitrite and lead significantly decrease free sulfhydryl groups and tryptophan levels in blood, and it is observed that lead administrated together with sodium nitrite does not increase methemoglobin concentration.
Abstract: The study was performed on 4 groups of male Wistar rats, receiving p.o. through 3 months every day: 1) distilled. water (control group); 2) sodium nitrite in dose 30 mg/kg b.w. x day (20% LD50); 3) lead acetate in dose 10 mg/kg b.w. x day (6.7% LD50); 4) lead acetate and sodium nitrite in amounts as above. The methemoglobin and hemoglobin were determined in whole blood, tryptophan--in plasma and free sulfhydryl groups--in erythrocytes. There was shown methemoglobin creative effects by nitrite (4.17%) and lead (3.02%) after 90-days intoxication. Both nitrite and lead significantly decrease free sulfhydryl groups and tryptophan levels in blood. There was also observed that lead administrated together with sodium nitrite does not increase methemoglobin concentration.