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Showing papers on "Lead acetate published in 1998"


Journal ArticleDOI
TL;DR: In vivo evidence is provided supporting the hypothesis that lead induces oxidative stress in RBCs, which is reversible by treatment with a thiol antioxidant (NAC), as well as a chelating agent (succimer).

245 citations


Journal ArticleDOI
TL;DR: The results indicate that exposure of mothers to moderate levels of lead produces chronic immune modulation in their F344 rat offspring exposed in utero, consistent with the possibility that lead may bias T helper subset development and/or function, resulting in alterations in the balance among type 1 and type 2 immune responses.

134 citations


Journal ArticleDOI
TL;DR: It appears from these results that lead may exert its toxic effect via peroxidative damage to renal and hepatic cell membranes after 24 hours, and selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of the superoxide dismutase and glutathione reductase and the glutATHione content.
Abstract: Male albino rats were intramuscularly administered a single dose of lead acetate (100 micromol/kg b.wt). Another group of rats were injected with sodium selenite (10 micromol/kg b.wt) before lead intoxication. After 3 and 24 hours, lead treatment resulted in significant increases in acid and alkaline phosphatases, GOT and GPT, total proteins, and cholesterol in serum. The total triglycerides in serum was decreased after 24 hours of intoxication. Lead treatment also produced significant elevation of lipid peroxidation in liver and kidney. The antioxidant capacity of hepatic and renal cells in terms of the activities of superoxide dismutase, glutathione reductase, and glutathione content was diminished. It appears from these results that lead may exert its toxic effect via peroxidative damage to renal and hepatic cell membranes after 24 hours. Selenium administration prior to lead injection produced pronounced prophylactic action against lead effects, and it is observed that selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of the superoxide dismutase and glutathione reductase and the glutathione content. As a result, the lipid peroxidation was decreased in both liver and kidney.

113 citations


Journal ArticleDOI
TL;DR: Zinc supplementation ameliorates lead-induced testicular damage both at the cellular and subcellular level and improvement in the inhibition of delta-ALAD and in the ubiquitous cellular enzyme SOD suggests less testicular tissue damage due to detoxification of free radicals.

104 citations


Journal ArticleDOI
TL;DR: The reproductive axis is particularly sensitive to lead during specific developmental periods, resulting in delayed sexual maturation produced by suppression by sex steroid biosynthesis and surprisingly little effect is observed on adult reproductive endocrinology and physiology.
Abstract: A dose-response study was conducted in a rat model to examine the effects of lifetime lead exposure on the development of the reproductive system and the endocrine mechanisms underlying these effects. Time-impregnated female Sprague-Dawley rats (n = 10-15/group) were exposed to lead acetate in the drinking water at levels of 0.05%, 0. 15%, or 0.45% (w/v) initiated on gestational day 5. At birth, litters were culled to four male and four female pups. Exposure of dams to lead was continued until weaning, following which, the pups continued to be exposed to lead acetate in drinking water until sacrifice. One male and one female pup from each litter were sacrificed at age 21, 35, 55, and 85 d. A significant dose-responsive decrease in birth weight and crown-to-rump length was observed in all lead-exposed litters. However, no marked effects were observed on anogenital distance/crown-to-rump length ratios. Lead exposure resulted in a delay in sexual maturity as measured by prostate weight in male pups and time of vaginal opening in female pups, which increased with lead dose. These disruptions in reproductive physiology were accompanied by a significant decrease in neonatal sex steroid levels and suppression of the plasma concentrations of testosterone (male) and estradiol (female) during puberty. In male pups, this was accompanied by a significant decrease in plasma luteinizing hormone (LH), elevated pituitary LH content, and a decrease in plasma testosterone/LH ratios at the highest dose. In female pups, although no effects were observed on plasma LH concentration, a similar significant elevation in pituitary LH content was observed during early puberty. Postpuberty, plasma LH and sex steroid concentrations were unaffected at any dose in spite of continued lead exposure. No significant effects were observed on epididymal sperm count in male pups at 85 d of age. In female pups, estrus cycling was only significantly disrupted at the highest lead dose. These data suggest that the reproductive axis is particularly sensitive to lead during specific developmental periods, resulting in delayed sexual maturation produced by suppression by sex steroid biosynthesis. The mechanisms underlying this appear to involve lead actions on both LH release and gonadal function. At low, environmentally relevant blood lead concentrations, adaptation to the continuous presence of the metal ion occurs and surprisingly little effect is observed on adult reproductive endocrinology and physiology.

102 citations


Journal ArticleDOI
TL;DR: Data suggest that the mechanisms underlying the greater suppression of somatic growth observed at puberty in lead-exposed male offspring may be due to the additional hypoandrogenization produced by the action of lead on the hypothalamic-pituitary-testicular axis.
Abstract: A dose-response study was conducted to examine the growth suppression associated with developmental lead exposure in a rat model and to determine the endocrine mechanisms underlying these effects. Ad libitum intake of lead acetate (0.05% to 0.45% w/v) was initiated in time-impregnated female Sprague-Dawley rats (n = 10-15/group) at gestational day 5. At birth, pups were culled to four male and four females per litter. Lead exposure of dams continued until weaning, following which lead exposure of pups was continued until sacrifice at age 2 , 35, 55, and 85 days. Birth weight and prepubertal and pubertal growth rates were significantly suppressed. Growth rates were suppressed to a much greater degree in male as compared to female pups. Decreased growth rates were accompanied by a significant decrease in plasma insulin-like growth factor 1 (IGF1) concentrations and (1) a significant increase in pituitary growth hormone (GH) content during puberty in pups of both sexes, (2) a delay in the developmental profiles of the GH-dependent male-specific liver enzymes cytochrome P-450 CYP2C11 and N-hydroxy-2-acetylaminofluorene sulfotransferase, and (3) continued suppression of these enzymes in lead-exposed adult male pups. In addition, significant decreases in plasma sex steroids, testosterone (male) and 17beta-estradiol (female), were observed during puberty. Postpuberty, at age 85 d, both IGF1 and sex steroid levels were indistinguishable from control pups despite continued lead exposure. Growth rates were also similar in control and lead-exposed pups between age 57 and 85 d. Data suggest that the mechanism underlying lead-induced sex-independent suppression of growth observed in these studies involves disruption of GH secretion during puberty. It is possible that the mechanisms underlying the greater suppression of somatic growth observed at puberty in lead-exposed male offspring may be due to the additional hypoandrogenization produced by the action of lead on the hypothalamic-pituitary-testicular axis.

99 citations


Journal ArticleDOI
TL;DR: It is demonstrated that acute lead exposure causes dramatic changes in the subcellular distribution and expression of rat kidney GSTs, and that these changes are not a result of oxidative stress.

95 citations


Journal ArticleDOI
TL;DR: Male rats exposed to lead had decreased serum testosterone levels and that this metal produced early onset of capacitation by one of the pathways of ROS generation, which might result in premature acrosome reaction and reduced zona-intact oocyte-penetrating capability.
Abstract: The relationships between sperm reactive oxygen species (ROS) generation, the capacitation process and acrosome reaction, and the spermoocyte penetration rate (SOPR) were investigated to understand the effect of lead toxicity on sperm functions and the mechanisms of these effects. Male Sprague-Dawley rats received weekly intraperitoneal injections of 20 mg or 50 mg lead acetate/kg or 20 mg or 50 mg sodium acetate/kg (control) for 6 wk. Serum testosterone was measured by radioimmunoassay. In cauda epididymal spermatozoa, the chemiluminescence was measured to evaluate the sperm ROS generation. Chlortetracycline fluorescence assay was used to study the status of capacitation and acrosome reaction on fresh cauda epididymal spermatozoa and after 2, 4, or 24 h of incubation with 5 mg/ml bovine serum albumin. In lead-exposed rats, the serum testosterone levels were reduced, and the percentage of capacitation and the chemiluminescence were significantly increased in fresh cauda epididymal spermatozoa. The serum testosterone levels were negatively associated with the percentage of acrosome-reacted spermatozoa. Sperm chemiluminescence was positively correlated with the percentage of both capacitated and acrosome-reacted spermatozoa. The SOPR was negatively associated with the percentage of both capacitated and acrosome-reacted spermatozoa. In summary, this study showed that male rats exposed to lead had decreased serum testosterone levels and that this metal produced early onset of capacitation by one of the pathways of ROS generation. These effects might consequently result in premature acrosome reaction and reduced zona-intact oocyte-penetrating capability.

87 citations


Journal ArticleDOI
TL;DR: The results suggest that the long-term ingestion of manganese sulfate, aluminum chloride, lead acetate and copper chloride would have adverse effects on sexual behavior, territorial aggression, fertility and the reproductive system of the adult male rat.
Abstract: 1. The effect of long-term ingestion of the industrial metals salts, manganese sulfate, aluminum chloride, lead acetate and copper chloride was investigated on aggression, sexual behavior and fertility in male rat. Adult male rats ingested solutions of these salts along with drinking water at a concentration of 1000 p.p.m. for 12 weeks. 2. Male rat sexual behavior was suppressed after the ingestion of manganese sulfate, aluminum chloride, lead acetate and copper chloride. The ingestion of solutions of these salts markedly prolonged the intromission and ejaculation latencies. Aluminum chloride and copper chloride reduced the copulatory efficiency. 3. Male rat aggression was also abolished after the ingestion of manganese sulfate, aluminum chloride, lead acetate and copper chloride. The ingestion of solutions of these salts markedly suppressed lateralizations, boxing bouts, fight with stud male and ventral presenting postures. 4. Fertility was reduced in male rats ingested with lead acetate. The total number of resorptions was increased in female rats impregnated by males ingested with manganese sulfate and lead acetate. 5. Body, absolute or relative testes, seminal vesicles weights were dropped in adult male rats ingested with manganese sulfate, aluminum chloride, lead acetate and copper chloride. However, the absolute or relative preputial gland weights were not affected. Collectively, these results suggest that the long-term ingestion of manganese sulfate, aluminum chloride, lead acetate and copper chloride would have adverse effects on sexual behavior, territorial aggression, fertility and the reproductive system of the adult male rat.

66 citations


Journal ArticleDOI
TL;DR: Delayed female reproductive development and suppression of adult male serum testosterone concentration required continuous exposure to the heavy metal, and exposure during early development (pregnancy and lactation) resulted in no permanent effects in this model.
Abstract: The reproductive, endocrine, and growth effects of developmental lead exposure were assessed using a rat model in which 0.6% lead acetate (w/v) was administered in the drinking water ad libitum during different developmental periods to determine if lead actions were a result of direct effects of continuous exposure to the metal ion or secondary to disrupted neonatal "endocrine imprinting." Sprague Dawley rats were exposed to lead: (1) from gestational d 5 through birth; (2) during pregnancy and lactation; (3) during lactation only; (4) from birth through adulthood; or (5) from gestational d 5 through adulthood. Lead effects were measured on the development of aspects of the reproductive system, adult sex steroid levels, and growth rates in both male and female animals. The relative weights of male secondary sex organs in adult offspring were not significantly affected in any of the lead-treated groups. In contrast, female pups exposed to lead from birth through adulthood or from gestational day 5 through adulthood were observed to have significantly delayed vaginal opening and disrupted estrus cycling. These effects on female reproductive physiology were not observed in animals where lead exposure was confined only to pregnancy or lactation. Significant suppression of adult mean serum testosterone levels was only observed in male pups exposed to lead continuously from gestational age 5 d throughout life. Lead decreased birth weight in all animals exposed in utero and mean body weights were significantly decreased in all lead-treated groups up to weaning. Analysis of growth curves revealed that all lead-treated groups had significantly reduced growth rates during lactation. However, in addition, in male pups exposed to lead during pregnancy and lactation, from birth or from gestational age 5 d, growth rates were also significantly reduced during puberty. Postpubertal growth rates were unaffected in any lead-treated group. Thus, delayed female reproductive development and suppression of adult male serum testosterone concentration required continuous exposure to the heavy metal. Little evidence was observed for an alteration of "endocrine imprinting" by lead on either reproductive or growth parameters. Exposure during early development (pregnancy and lactation) resulted in no permanent effects in this model other than small (10%) decreases in the body weight of pups postpuberty.

51 citations


Journal ArticleDOI
TL;DR: The results suggest that cadmium and lead may both act as tumour promoters in diploid human fibroblasts, and that reactive oxygen species is more important in Cadmium- than lead-induced cytotoxicity and anchorage-independence.
Abstract: Cadmium and lead have been shown to induce cellular transformations and gene mutations in cultured rodent cells, as well as tumours in live animals. However, the mechanisms by which these metals cause cellular transformations and mutations in human cells have not been explored. In this study, we investigated the abilities of cadmium and lead to induce anchorage-independent transformations and hprt gene mutations in diploid human fibroblasts. Human fibroblasts were exposed to either cadmium acetate (0-60 microM) or lead acetate (0-2 mM) for 24 h. After removal of the metals, the cells were kept in exponential growth for 7 and 9 days before mutation and anchorage-independence assays were taken, respectively. Both cadmium and lead significantly induced anchorage-independent colonies in dose-dependent manners; the frequencies of anchorage-independent colonies induced by these metals were similar to those induced by N-methyl-N'-nitro-N-nitrosoguanidine at approximately equal cytotoxic dose ranges (30-10% survival). 3-Aminotriazole at non-cytotoxic dosages decreased catalase activity by >80%, and markedly enhanced cadmium-induced cytotoxicity and anchorage-independent colonies. Cadmium uptake by human fibroblasts was not affected by 3-aminotriazole co-administered with 10 microM of cadmium; whereas cadmium uptake and accumulation were enhanced 1.5-fold by 3-aminotriazole co-administered with 1-2.5 microM of cadmium. Lead-induced anchorage-independence or cytotoxicity was not affected by 3-aminotriazole co-treatment; however, 3-aminotriazole did significantly enhance lead uptake and accumulation in human fibroblasts. Neither cadmium- nor lead-induced 6-thioguanine-resistant mutation frequency in human fibroblasts. Co-administering these metals with 3-aminotriazole did not enhance mutations in human fibroblasts. These results suggest that cadmium and lead may both act as tumour promoters in diploid human fibroblasts, and that reactive oxygen species is more important in cadmium- than lead-induced cytotoxicity and anchorage-independence.

Journal ArticleDOI
TL;DR: The effects of elevated blood lead on semen quality were evaluated in the rabbit model and compared to published effects in humans as mentioned in this paper, showing that increased blood lead levels were associated with adverse changes in the sperm count, ejaculate volume, percent motile sperm, swimming velocities, and morphology.

Journal ArticleDOI
TL;DR: In this article, the influence of heavy metals on the hepatic level of reduced glutathione (GSH), S-transferase, and reductase activities in the liver of male mice after single-dose and repeated-dose treatments was investigated.
Abstract: Glutathione S-transferases catalyze the metabolism of reactive substances of exogenous or endogenous origin and are involved in inactivation processes of xenobiotics and their metabolites. The present study aims at investigating the influence of heavy metals on the hepatic level of reduced glutathione (GSH), glutathione S-transferase, and glutathione reductase activities in the liver of male mice after single-dose (1 and 24 h) and repeated-dose treatments (three consecutive days). The hepatic level ofGSH was depleted after single-dose treatments with cadmium chloride, mercuric chloride, cobalt chloride, cesium chloride, lead acetate, and silver nitrate, and percentage of GSH depletion was greater still after the repeated-dose treatments. Nickel chloride, on the other hand, did not cause any change in the level of GSH after any period of treatment. Glutathione reductase activity was increased 24 hours after treatment with cadmium chloride, mercuric chloride, lead acetate, and silver nitrate, whereas cobalt chloride decreased such activity after repeated doses. With the exception of cadmium chloride, glutathione S-transferase activity was significantly decreased 24 hours after a single-dose treatment with all of the tested heavy metals. Such alterations in the activities of phase II drug-metabolizing enzymes as a result of heavy metal treatment may change the hepatic capacity for the detoxification of many toxic compounds from endogenous or exogenous sources.

Journal ArticleDOI
TL;DR: The results indicate that renal GST increases occur at lead levels which are environmentally significant, that these changes precede cellular damage, and suggest that GST may serve as a tissue biomarker of lead exposure.

Journal ArticleDOI
TL;DR: The results suggest that lead might selectively interfere with specific neurochemical pathways in the hippocampus and demonstrate that NO may be a messenger molecule in areas CA1 and CA3.

Journal ArticleDOI
TL;DR: The results suggest that lead exposure without concomitant undernutrition alters rat development, affecting specific subsets of motor skills.
Abstract: We investigated the effects of lead exposure during the pre- and postnatal period on the neurobehavioral development of female Wistar rats (70-75 days of age, 120-150 g) using a protocol of lead intoxication that does not affect weight gain. Wistar rats were submitted to lead acetate intoxication by giving their dams 1.0 mM lead acetate. Control dams received deionized water. Growth and neuromotor development were assessed by monitoring daily the following parameters in 20 litters: body weight, ear unfolding, incisor eruption, eye opening, righting, palmar grasp, negative geotaxis, cliff avoidance and startle reflex. Spontaneous alternation was assessed on postnatal day 17 using a T maze. The animals' ability to equilibrate on a breaker rim was measured on postnatal day 19. Lead intoxication was confirmed by measuring renal, hepatic and cerebral lead concentration in dams and litters. Lead treatment hastened the day of appearance of the following parameters: eye opening (control: 13.5 +/- 0.6, N = 88; lead: 12.9 +/- 0.6, N = 72; P < 0.05), startle reflex (control: 13.0 +/- 0.8, N = 88; lead: 12.0 +/- 0.7, N = 72; P < 0.05) and negative geotaxis. On the other hand, spontaneous alternation performance was hindered in lead-exposed animals (control: 37.6 +/- 19.7; lead: 57.5 +/- 28.3% of alternating animals; P < 0.05). These results suggest that lead exposure without concomitant undernutrition alters rat development, affecting specific subsets of motor skills.

Journal Article
TL;DR: Findings are interpreted as myopathical reaction due to chronic low level lead exposure, as there were no signs of neurogenical lesion in Rhesus monkeys exposed pre- and postnatally to lead acetate in the diet.
Abstract: Morphological changes in the central nervous system and other organs have been reported in numerous studies investigating low level lead exposure. To date, however, there are no investigations on the effect of low level lead exposure on striated muscles, although varying neuromuscular changes in different species have been known for years. Rhesus monkeys were exposed pre- and postnatally to lead acetate in the diet (350 ppm or 600 ppm) over 9 years, followed by a lead free period of 32 months, while a control-group received regular diet. No signs of muscular dysfunction were evident. To elucidate neuromuscular pathomorphology frozen sections of the vastus medialis muscle were processed for routine and enzymohistological staining (Hematoxilin and Eosin, Sudan Black, Gomori, NADH, ATPase). Resin histology was processed for electron microscopy. Morphometric analysis was made with commercial software. Light microscopy revealed dose-related signs of myopathy in the lead-exposed groups. The scatter of fibre diameters was increased, and split fibers and internal nuclei were more frequent. Fibres became separated from each other by copious endomysial connective tissue. Ultrastructural examination showed hydropic mitochondria and a massively dilated sarcotubular system in the 600 ppm group. Dose-related extracellular collagen deposition increased. A heavy fibrosis was seen in the 600 ppm group. These findings are interpreted as myopathical reaction due to chronic low level lead exposure, as there were no signs of neurogenical lesion. It remains unknown how the fibrosis developed. A primary fibrosis could be based upon a developmental delay of satellite cells (expressing metalloproteases for collagen-catabolism). Lead is known to inhibit regular development in many ways if exposure has started prenatally. As the skeletal muscle is a common target of toxicity, the myotoxic effects of chronic low level lead exposure comes into question.

Journal ArticleDOI
TL;DR: Results show that neuron-glia interactions attenuate the cellular lead uptake and the glial susceptibility to lead, but they do not support the idea of a protective role of astrocytes.

Journal ArticleDOI
TL;DR: In this paper, the effects of concurrent exposure to lead (Pb) and cadmium (Cd) on kidney function were studied in 20 goats for 42 days, and the results showed that concurrent exposure of goats to Pb and Cd did not enhance nephrotoxic effects produced by either of the metals given separately and Cdr reduced toxic effects of Pb indicating a possible antagonistic relation between the two metals.

Journal ArticleDOI
TL;DR: The results indicate that any lead-related functional alterations at this dose may be subtle and require a sufficient demand on the system for detection.

Journal ArticleDOI
TL;DR: Lead-induced alterations of ligand binding to NMDA receptors in the hippocampal formation and cortical areas may play a role in lead-induced neurotoxicity.
Abstract: The NMDA receptor non-competitive antagonist, [3H] MK-801, was used as a ligand for an autoradiographic study to determine the effects of lead on NMDA receptor in rat brain. Adult male rats were given lead acetate, 100 mg/kg, or sodium acetate, 36 mg/kg (control), by i. p. for 7 days. Lead levels were detected in blood (41.1μg/dl) and brain (16.7-29.4μg/g). Concentrations of lead in various brain regions did not differ. [3H] MK-801 binding was heterogeneous throughout the brain with the following order of binding densities : hippocampal formation>cortex>caudate-putamen>thalamus>brainstem. Lead exposure caused a decrease in [3H] MK-801 binding to NMDA receptors in the hippocampal formation including CA2 stratum radiatum, CA3 stratum radiatum and presubiculum, and in the agranular insular, cingulate, entorhinal, orbital, parietal and perihinal areas of cerebral cortex. In another experiment, female rates were exposed pre-and post-natally from the 4th±1 post cconception day with 1, 000 ppm lead in their drinking water. This treatment continued after weaning. No effects of lead on [3H] MK-801 binding were found at postnatal day (PM) 28. However, lead caused a significant increase in [3H] MK-801 binding in the hippocampus including CA1 and CA2, and in the occipital and temporal cortical areas at PN 56 and at PN 112. Increases in [3H] MK-801 binding were also found in entorhinal cortex and dentate gyrus at PN 112. The hippocampal formation is a critical neural structure for learning and memory processes, whereas cortical and subcortical regions are involved in the modulation of complex behavioral processes. NMDA receptors have been shown to play a key role in synaptic plasticity underlying learning and memory. Therefore, lead-induced alterations of ligand binding to NMDA receptors in the hippocampal formation and cortical areas may play a role in lead-induced neurotoxicity.

Journal ArticleDOI
TL;DR: In this article, the removal of polycyclic aromatic hydrocarbons (PAHs) in the presence and absence of heavy metals by bacteria isolated from a contaminated area of Poland was examined.
Abstract: The elimination of polycyclic aromatic hydrocarbons (PAHs), in the presence and absence of heavy metals by bacteria isolated from a contaminated area of Poland was examined. Among fifty four isolates ten strains had an ability to utilize at least one of the following xenobiotic substrates: anthracene (250 mg/l), phenanthrene (250 mg/l) and pentachlorophenol (10 mg/l) at a rate of 50n100%. The strains were also found to be able to grow at high concentration of lead added as a lead acetate. The isolated strain, most active in utilization of applied xenobiotics was identified as Rhodococcus equi. Although the degradation of anthracene was inhibited in the presence of lead acetate, protein synthesis and the xenobiotic uptake was observed (at lead concentration of 1000 mg/l). Acetate as a more readily metabolized organic substrate was found as a co-metabolic substrate. The further experiments with cells entrapped on glass membrane filter indicated that Rhodococcus equi IM 6KB3 could be useful for the rapid removal of lead and anthracene from contaminated liquids.

Journal Article
TL;DR: The highest deposits of lead were observed in placenta and chorionic membranes, though here only about 60% are collagen-bound, and at 0.8% of lead in drinking water considerable accumulation was observed in all tissues investigated.
Abstract: Lead administered to laboratory rats in drinking water (0.1-0.8%) as lead acetate solution tends to accumulate in collagen-rich tissues such as tendons and the skin. The amount of lead deposited (and also zinc present in the tissue without its supplementation) correlates with the blood supply to the tissue investigated. The highest deposits of lead were observed in placenta and chorionic membranes, though here only about 60% are collagen-bound. No differences in the drinking habits of the animals were observed and also at lower concentrations of lead in the drinking water no dose dependence was revealed. However, at 0.8% of lead in drinking water considerable accumulation of lead was observed in all tissues investigated.

Journal Article
TL;DR: It was found that all parameters remained unaltered within normal ranges, with the exception of reticulocyte counts which was significantly increased compared to the in controls, and it is suggested that the selective change found in reticULocyte count might be considered as an early response of a biomarker to sublethal exposition of Bufo arenarum to lead.

Journal ArticleDOI
TL;DR: Results of this study on the primate, following extrapolation to humans, could influence further refining of the impact of environmental lead contamination concentrations vis-à-vis the health of children, adults, and aged human beings.
Abstract: Although reproductive consequences of high circulating blood lead levels (> or = 60 micrograms/dL) have been reported, potential adverse effects of chronic lead exposure in males that result in low to moderate blood lead levels (10-25 and 26-60 micrograms/dL, respectively) are unknown. Effects of chronic lead exposure to testis ultrastructure were determined in the cynomolgus monkey after oral administration of lead acetate (1500 micrograms/kg BW/day) in a vehicle in the following groups: from birth to 10 years (lifetime), postnatal day 300 to 10 years (postinfancy), and postnatal day 0-400 (infancy); monkeys in the control group received only the vehicle (95% glycerol and 5% distilled water). At age 10 years, circulating lead concentrations in lifetime and postinfancy-dosed monkeys were approximately 35 micrograms/dL, and in control and infancy animals the concentrations were < 1.0 microgram/dL. Sertoli and spermatogenic cells of dosed monkeys from the infancy and lifetime groups revealed injuries. Chronic exposure to lead that results in moderate blood lead concentrations induced persistent ultrastructural alterations in the cynomolgus monkey testis. Results of this study on the primate, following extrapolation to humans, could influence further refining of the impact of environmental lead contamination concentrations vis-a-vis the health of children, adults, and aged human beings.

Journal ArticleDOI
TL;DR: In this article, the pyrolysis of organic components in the sol-gel preparation of lead zirconate titanate (PZT) from lead acetate and Zr4+ and Ti4+ in methoxyethanol was studied with simultaneous differential thermal analysis, thermogravimetry and infrared spectroscopy.
Abstract: The pyrolysis of organic components in the sol-gel preparation of lead zirconate titanate (PZT) from lead acetate and zirconium and titanium propanolate in methoxyethanol is studied with simultaneous differential thermal analysis, thermogravimetry and infrared spectroscopy. The first pyrolysis step of the dried PZT gel, yielding acetone and CO2 similar to the pyrolysis of lead acetate, indicates that most of the acetate groups are bonded to Pb2+. In the second step, the remaining organic components are oxidized to CO2 and H2O. The formation of undesired carbon residues during pyrolysis from unhydrolysed alkoxide groups and acetate groups bonded to Zr4+ and Ti4+ can be prevented by steam treatment of the dried gels. Activation energies for the different pyrolysis steps of lead, zirconium and titanyl acetate, lead decanoate and PZT gels are given. © 1998 Kluwer Academic Publishers

Journal Article
TL;DR: The ultra-structural lesions of lead poisoning and the deposition of lead in liver, kidney, peritoneum, cerebellum and retina of dogs were studied and revealed degeneration of the epithelial cells of the urinary tubules, the endothelial Cells of the renal capillaries and the hepatocytes.
Abstract: The ultra-structural lesions of lead poisoning and the deposition of lead in liver, kidney, peritoneum, cerebellum and retina of dogs were studied. Specimens were obtained from 5 3-4 mo-old crossbreed dogs each injected i.p. with a total dose of 120 mg lead acetate, divided in 10 equal doses of 12 mg, administered every other day. Two dogs were controls. Histopathological examination revealed degeneration of the epithelial cells of the urinary tubules, the endothelial cells of the renal capillaries and the hepatocytes. Characteristic lead inclusion bodies were observed intracytoplasmically and intranuclearly in mesothelial and giant cells of the peritoneum. Lead needle-like inclusions were intracytoplasmically in the interstitial connective tissue cells of the kidney, and substantial quantities of lead were in collagen fibers of the interstitial kidney tissue.

Journal Article
TL;DR: In this article, the toxicity of lead in the form of lead chloride or lead acetate to microbial biomass in the red soil was evaluated and the results suggest that the solubility and the acconlpanying anions of the lead compounds are the most important factors determining their toxicity to the soil microbial biomass.
Abstract: A laboratory incubahon experiment was conducted to evaluate the toxicity of lead in the form oflead chloride or lead acetate to microbial biomass in the red soil. tead was applied at six different levels i. e.,0 (background), 100, 200, 300, 450 and 600 w/10- 6 either in the form of lead chloride or lead acetate.tead app1ied as lead acetate markedly reduced the soil microbial biomass carbon (Cmic) and the microbialbiomass nitrogen (Nmic ) compared with the lead applied as lead chloride at all the tested levels. The biomassC: N ratios" m (Cmic ): m (Nmic )" and the total organic carbon to biomass carbon ratios" m (orsanic C): m(biomass C)" in the soil were markedly increased by increasing the level of the lead in the form of lead acetate.While, the magnitude of change was much smaller in the case of lead chloride at the same lead levels. Theresults suggest thal the solubility and the acconlpanying anions of the lead compounds are the most importantfactors determining their relahve toxicity to the soil microbial biomass.

Journal ArticleDOI
TL;DR: Chronic exposure to low levels of lead resulted in sustained hypertension without affecting urinary excretions of 6-keto-PGF1-alpha or TXB2, suggesting that occurrence of lead-induced hypertension under the given conditions in rat may not involve alterations of renal production of vasodilating or vasoconstrictive eicosanoids.

Journal Article
TL;DR: The results indicate that lead exposure to the mother affects excitatory amino acid systems during the development of the offspring.
Abstract: To determine changes in response to N-methyl-D-aspartate (NMDA) and kainic acid (KA) in cerebellar granule cells of offspring of lead-exposed mothers, pregnant rats received 0.25% lead acetate in their drinking water 2 days after mating. The control animals were given sodium acetate (0.125%) in their drinking water. The cerebellar granule cells were cultured from 8-day old pups. Changes in the levels of cytosolic Ca++ and cGMP and the release of glutamic acid were measured using fura-2 spectrofluorometer, radio-immunoassay, and HPLC, respectively. Increases in cytosolic Ca++ in response to 50 microM of NMDA and KA were less responsive (77%) in the lead exposed group as compared to that of the control group. However, the maximum responses to KA were not different. The NMDA- and KA-stimulated release of glutamate from cerebellar granule cells prepared from lead-exposed pups were also significantly reduced. While the NMDA-induced elevation of cGMP was not affected in the lead-exposed pups, the normal KA-induced increases in cGMP level in cerebellar granule cells of lead-exposed pups was not observed. The specific binding of [3H]MK-801 was significantly lower in cerebellar granule cells of the lead-exposed pups. These results indicate that lead exposure to the mother affects excitatory amino acid systems during the development of the offspring.