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Showing papers on "Lead acetate published in 1994"


Journal ArticleDOI
TL;DR: In vivo experiments with the stable lead isotope, 204Pb, have confirmed that inorganic lead compounds can be absorbed through the skin, and it is possible that percutaneous absorption of lead could contribute significantly to lead body burden.

82 citations


Journal ArticleDOI
TL;DR: A linear relationship was observed between blood lead concentration and dose following intravenous administration of lead and this provided empirical support for using blood lead concentrations at supposed steady state to compute the bioavailability of lead administered by different routes and from different sources.

55 citations


Journal ArticleDOI
TL;DR: It is concluded from this study that higher Pb-B levels greatly influence the levels of other trace elements in human blood samples and also the activities of hepatic transaminases as well as alkaline phosphatase in experimental rats.
Abstract: Lead pollution and its impact on the status of four other trace elements—Fe, Zn, Br, and Rb—have been studied in the whole blood samples of different population groups employing energy dispersive X-ray fluorescence technique. These population groups included normal, automobile workers and lead battery manufacturers. The maximum increase in the concentration of trace elements in the blood samples of automobile workers and battery manufacturers was observed for Pb, when compared with normal Pb-B levels. The effect of lead pollution had significantly reduced Zn levels in automobile workers. Fe-B levels in automobile workers had been found to be reduced significantly as compared to control, whereas in battery workers the reduction was not significant. The concentration of Br was greatly enhanced in the blood samples of automobile workers, whereas Rb-B levels were significantly higher in both the automobile and battery workers. Oral administration of lead acetate (100 mg/kg body wt) to experimental rats significantly decreased the activities of hepatic transaminases after 3 and 4 mo of treatment, whereas the activity of hepatic alkaline phosphatase decreased significantly after 4 mo of treatment. It is concluded from this study that higher Pb-B levels greatly influence the levels of other trace elements in human blood samples and also the activities of hepatic transaminases as well as alkaline phosphatase in experimental rats.

45 citations


Journal Article
TL;DR: Rats poisoned with lead displayed lower total and HDL cholesterol levels in comparison to controls, but it was associated with increase of free cholesterol concentration and hypertriglyceridemia, while in rats treated with lead and cadmium jointly serum lipid peroxides level increased and superoxide dysmutase activity decreased.
Abstract: The aim of the present study was to investigate the impact of the combined exposure to lead and cadmium on serum lipids and lipid peroxides level in rats and to compare the obtained results with the effects of a single metal. Experiments were performed on male Buffalo rats which were intragastrically administered of lead acetate in doses of 70 mg Pb/kg body wt. twice a week and/or cadmium chloride in doses of 20 mg Cd/kg body wt. once a week for a period of seven weeks. One day after the feeding was over, the following parameters were measured: serum lipids, serum lipid peroxides, blood superoxide dismutase activity, and plasma cholesterol-lecithin-acyltransferase activity. Metal content (lead, copper, cadmium and zinc) in blood and liver was determined by means of atomic absorption spectrophotometry. No clinical signs of lead or cadmium toxicity were observed. In comparison to controls, rats poisoned with cadmium and simultaneously with lead and cadmium displayed lower total, free, and HDL-cholesterol concentrations in serum. Rats poisoned with lead displayed lower total and HDL cholesterol levels in comparison to controls, but it was associated with increase of free cholesterol concentration and hypertriglyceridemia. Rats poisoned with cadmium displayed decrease of serum lipid peroxides level and increase of blood dismutase activity. It may be a consequence of redistribution of zinc and copper (increase of copper and decrease of zinc concentrations in blood). In rats treated with lead and cadmium jointly serum lipid peroxides level increased and superoxide dysmutase activity decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

40 citations


Journal ArticleDOI
TL;DR: In this paper, the effects of low-level lead exposure on the postnatal development of cholinergic muscarinic receptors (mAChR) and a cholineacetyltransferase (ChAT) activity in the rat septum and hippocampus were investigated.

36 citations


Journal Article
TL;DR: The results show that lead can attack the synaptic neurotransmission in two ways: by depressing the Ca-KCl-evoked release of GABA, dopamine and histidine and by a selective stimulation of a spontaneous release (independent of depolarization conditions) of GABA and dopamine but not histidine.
Abstract: The effect of lead on the release of [14C]GABA, [3H]dopamine and [14C]histidine (as a precursor of histamine) was studied in synaptosomes obtained from chronically lead-treated rats and in synaptosomes with in vitro lead added. In vivo treatment of rats with lead acetate results in a decrease in the K(+)-depolarization-dependent release of GABA and dopamine and histidine. Lead given in vitro itself (independently of depolarizing condition) stimulated the release of previously accumulated neurotransmitters in synaptosomes (GABA and dopamine). This effect depends on lead acetate concentration. On the other hand lead, in different concentrations, did not cause changes in the histidine release. The results show that lead can attack the synaptic neurotransmission in two ways: by depressing the Ca-KCl-evoked release of GABA, dopamine and histidine and by a selective stimulation of a spontaneous release (independent of depolarization conditions) of GABA and dopamine but not histidine.

35 citations


Journal ArticleDOI
TL;DR: It is concluded that lead alters sperm function by altering the hormonal control of spermatogenesis rather than by direct toxic action on spermatozoa.

33 citations


Journal Article
TL;DR: The data suggest that chronic lead exposure induces an astrocytic reaction as a result of a direct action of lead on astroglial cells or as a response to underlying neural damage.
Abstract: The aim of this study was to characterize the cytoskeletal intermediate filaments, glial fibrillary acidic protein (GFAP), and vimentin in normal and lead treated rats, and to compare the astroglial response in the cerebellum and the hippocampus -two regions with great susceptibility to the toxic effects of lead. Experiments combined light and electron microscopy immunohistochemistry using antibodies to GFAP and to vimentin, and conventional transmission electron microscopy techniques. Chronic lead administration was provided through the drinking water (1 g% lead acetate solution) and started when pups were 7 days old through the mother's milk. Following weaning lead intoxicated offspring were continuously exposed during 9 months, and sacrificed, with their corresponding controls, by perfusion-fixation at 30, 60, 75, 90, 180 and 270 days of lead exposure. After 60 and 90 days of treatment, hypertrophic astrocytes were observed in the cerebellum and hippocampus. Additionally, in the same time-period more GFAP immunolabelled astrocytes were detected in the cerebellum but not in the hippocampus. These qualitative observations were confirmed by computerized image analysis quantification. This effect was transient, even though the lead treatment was prolonged for 9 months and the blood-lead levels remained high after 30 days of the lead-exposure. After 90 days of lead administration, hypertrophic astrocytes started to decline and a gradual increment in the number of dense bodies, lipofuscin-like, was evidenced in astrocytes, neurons, pericytes and microglial cells. The data suggest that chronic lead exposure induces an astrocytic reaction as a result of a direct action of lead on astroglial cells or as a response to underlying neural damage.

32 citations


01 Jan 1994
TL;DR: These studies suggest that low concentrations of lead are capable of inhibiting nitrite produced by the calcium-dependent constitutive form of nitric oxide synthase while the calcium/ calcium-independent, inducible form of Nitricoxide synthase is not affected.
Abstract: One of the mechanisms by which lead may cause a perturbation in the nervous system is the alteration of endothelial cell function. This study investigated the effect of lead acetate on constitutive and cytokine-induced production of nitrite, a marker of nitric oxide, in brain microvascular endothelial cells. Nitric oxide synthase may be a target for lead and changes in its function can result in a cascade of physiological effects seen in vivo. Concentrations of 10, 100, and 1000 nM lead acetate, in the presence or absence of 100 ng lipopolysaccharide/ml, 400 U interferon-gamma/ml and 100 U tumor necrosis factor-alpha/ml, were added to confluent cultures of brain microvascular endothelial cells. Concentrations of lead acetate as low as 10 nM decreased constitutive levels of nitrite by 50% without inhibiting the inducible levels. Addition of 1 microM lead acetate had no effect on [3H]L-leucine incorporation, lactate dehydrogenase release, or cellular morphology, indicating that the effect was selective. Increasing the concentration of extracellular calcium to 2 mM abolished the inhibitory effect of lead acetate on the constitutive production of nitrite. These studies suggest that low concentrations of lead are capable of inhibiting nitrite produced by the calcium-dependent constitutive form of nitric oxide synthase while the calcium-independent, inducible form of nitric oxide synthase is not affected. These data provide another testable hypothesis for the as yet undetermined mechanisms of lead neurotoxicity.

31 citations


Journal ArticleDOI
TL;DR: In this article, the effect of lead acetate on constitutive and cytokine-induced production of nitrite, a marker of nitric oxide, in brain microvascular endothelial cells was investigated.

29 citations


Journal Article
TL;DR: In this paper, the authors investigated the possible use of garlic feeding to clean up lead contents from chickens which had been exposed to natural or experimental lead pollution and consequently eliminate one of the sources of lead pollution to human consumers.
Abstract: Lead has been indicted to be involved in the aetiology of human and animal diseases. In view of earlier literature indicating that garlic antagonized lead toxicity, we have investigated the possible use of garlic feeding to clean up lead contents from chickens which had been exposed to natural or experimental lead pollution and consequently eliminate one of the sources of lead pollution to human consumers. Groups of chickens (10 birds each) were given lead alone (lead acetate equivalent to 5 mg lead/kg B.W.) or both lead and garlic simultaneously or lead followed by garlic post-treatment or garlic alone or distilled water. Lead concentrations were reduced in muscle and liver tissues of chickens given both lead and garlic simultaneously or as a post-treatment. Reduction in tissue-lead concentrations were greater in birds given garlic as a post-treatment than those given garlic simultaneously with lead. The results indicate that garlic contain chelating compounds capable of enhancing elimination of lead. Garlic feeding can be exploited to safeguard human consumers by minimizing lead concentrations in meat of food animals which had been grown in a lead polluted environment.

Journal ArticleDOI
TL;DR: The effects of exposure to lead on endocrine function and the reproductive parameters were studied in pubertal rats treated with lead acetate and the density of [125I]LH/human chorionic gonadotrophin binding sites in testicular homogenates was reduced by saturnism in both groups.
Abstract: The effects of exposure to lead on endocrine function and the reproductive parameters were studied in pubertal rats treated with 10 g l-1 lead acetate in drinking water for 20 days (subacute group) or 9 months (chronic group) in addition to iv injections of lead acetate (01 mg 100 g-1 body wt) every 10 (subacute group) or 15 days (chronic group) Although basal levels of testosterone were higher both in plasma and in testes of acutely intoxicated animals, the circulating levels of luteinizing hormone (LH) were not affected in either group, nor was the LH-releasing hormone content of the median eminence The density of [125I]LH/human chorionic gonadotrophin (hCG) binding sites in testicular homogenates was reduced by saturnism in both groups, concomitant with a significantly increased apparent affinity constant of the hormone-receptor complex These data can be viewed as the result of a mixture of specific lead toxicity (eg at the enzyme level) with other more general actions (eg at the level of the hypothalamus-pituitary-testicular axis)

Journal ArticleDOI
TL;DR: In this article, a spin-coated lead titanate thin film was spincoated onto various substrates and annealed at 425°C to obtain submicrometer grains of the order of 0.1 μm.

Journal ArticleDOI
TL;DR: The data indicate that the effects of environmental pollutants on reproduction in birds can be mediated through increased P450, thereby increasing the metabolism of steroid hormones and depressing concentration in circulation.
Abstract: In a previous study, the authors found that administration of phenobarbital to laying hens was associated with an increase in content of liver cytochrome P450 and a reduction of estradiol (E2) in serum. Thus, the authors hypothesized that other xenobiotics such as environmental toxicants that affect P450 might also affect E2 in laying hens. In experiment 1, the authors examined the effect of four environmental pollutants, three of which induced different isoenzymes of P450 and one inhibitor, on circulating E2 and related reproductive functions. Aroclor 1254 (PCB), 20 mg/d; dichlorodiphenyltrichloroethane (DDT), 40 mg/d; or benzo[a]pyrene (BZ), 5 mg/d, was administered for 5 d. An inhibitor, lead acetate, was injected for 2 d. Controls received corn oil or sodium acetate. No significant difference was observed due to administration of lead. Treatment with PCB or DDT decreased the concentration of E2 and increased P450. Only PCB significantly decreased plasma total calcium and egg lay. Therefore in experiment 2, the authors determined the dose-response effect of PCB. The PCB was given orally at doses of 0, 5, 10, and 25 mg in corn oil for 5 d. The depression of concentrations of E2 was associated with the induction of P450 in a dose-dependentmore » manner. Egg production and plasma total calcium were reduced by the two highest doses, but eggshell thickness was not different from control in all regimens. Plasma E2 and plasma total calcium were negatively correlated with induction of P450. BZ is not a strong inducer of P450 and had no effect on E2 or reproduction, whereas DDT and PCB had a profound effect on P450 with consequent depression of circulating E2. These data indicate that the effects of environmental pollutants on reproduction in birds can be mediated through increased P450, thereby increasing the metabolism of steroid hormones and depressing concentration in circulation.« less

Journal ArticleDOI
TL;DR: The effects of lead and lithium ingestion, separately and in combination, on the levels of K, Fe, Cu, Zn, Br, Rb, and As in rat blood were studied by the Energy Dispersive X-ray Fluorescence technique.
Abstract: The effects of lead and lithium ingestion, separately and in combination, on the levels of K, Fe, Cu, Zn, Br, Rb, and As in rat blood were studied by the Energy Dispersive X-ray Fluorescence technique. Two different doses of lead acetate, i.e., 50 and 100 mg/Kg body wt (low and high doses), were administered orally to rats, daily, for 1 and 4 months (short and long terms), whereas lithium in the form of lithium carbonate was given to rats in food (1.1 g/kg diet) for 1 and 4 mo separately, and also to rats receiving lower and higher doses of lead. K levels were found to be depressed significantly with lead treatment, whereas Fe contents were enhanced marginally after 1 mo of treatment when only the higher dose of lead was given. As, Br, and Rb contents were found to be elevated following lead treatment for short and long terms at both the dose levels. However, Cu contents were lowered, whereas Zn contents were raised only after long term treatment with lead. The Fe, Cu, As, and Br contents remained unaltered, whereas K, Rb, and Zn contents were reduced significantly when lithium was administered for short term. Moreover, Cu and Fe levels were also found to be reduced and Br contents were enhanced only after long term treatment. During the combined treatment with lead and lithium for short and long terms, the levels of K, As, and Rb were observed to decrease, whereas Fe contents were enhanced when estimated for both doses of lead. On the contrary, Cu levels were lowered only with the higher dose of lead acetate when given in combination with lithium for 1 and 4 mo. Br contents were only effectively decreased after 4 mo of treatment.

Journal Article
TL;DR: The results show that prolonged exposure of aggregating brain cell cultures to a low concentration of lead acetate causes distinct changes of cell type-specific parameters.
Abstract: Aggregating brain cell cultures were used as a model to study the effect of chronic exposure to low levels of lead acetate. Long-term maintenance of cultures could be improved by supplementation of the medium with albumin-bound lipids. Exposure for 9 days to 10 -6 -10 -4 M lead acetate caused a decrease of GABAergic (glutamic acid decarboxylase) and astrocytic (glutamine synthetase) markers which was also found after prolonged treatment 150 days) with 10 -7 M lead acetate. Total protein contentandcholine acetyl transferase were not changed

Journal Article
TL;DR: Results of this study shows that changes in the copper and zinc concentrations in tissues in the combined exposure to lead and cadmium are similar to those induced by a single lead (heart and brain) or single Cadmium (liver and kidney) intoxication.
Abstract: To learn whether a combined exposure to lead and copper provokes disturbances in essential trace elements homeostasis the distribution of zinc and copper in tissues (blood, liver, kidney, heart and brain) after combined and single exposure to lead and/or cadmium was compared. In the same regimen, single or combined exposure accumulation of cadmium and lead in tissues was also measured. Experiments were performed on male Buffalo rats, 5-6 weeks old. Lead acetate (70 mg Pb/kg body wt twice a week) and cadmium chlorate (20 mg Cd/kg body wt once a week) were administered intragastrically for 7 weeks singly or in combination. During the experiment no clinical signs of toxic effect of lead or cadmium were observed. The animals were killed after administration of the last doses of cadmium and/or lead and the level of trace and heavy metals in tissues were measured. The results of this study shows that changes in the copper and zinc concentrations in tissues in the combined exposure to lead and cadmium are similar to those induced by a single lead (heart and brain) or single cadmium (liver and kidney) intoxication. Lead and cadmium concentrations in the liver and kidneys of rats administered with Pb and Cd jointly were significantly lower than those in rats exposed to single doses of Pb or Cd.

Journal ArticleDOI
TL;DR: The results show that lead may produce very fast actions in the central nervous system and suggest that inhibition of water intake by lead may depend on impairment of central cholinergic and/or angiotensinergic functions.

Journal Article
TL;DR: The results suggest that Pb may specifically alter ODC activity via cytosolic interactions in developing tissue, and alterations in O DC activity may be indicative of subtle toxicant induced perturbations during early development.
Abstract: The developing brain is particularly susceptible to the neurotoxic effects of lead exposure. The ontological profile of ornithine decarboxylase (ODC) activity in the cerebellum was examined following lactational exposure of rats to 0.2% lead acetate (Pb). Relative to controls, Pb-exposure induced ODC activity levels in a transient manner with a 50% increase at postnatal day (PND) 6, a 20% increase at PND 9, returning to control basal levels by PND 15. These effects were seen at exposure levels of Pb that did not alter the normal growth and body weight of either the lactating dam or the developing pups. Basal cerebellar ODC activity in homogenates was increased with addition of low concentrations of Pb acetate (0.01 μM and 0.1 μM), while concentrations of 1 μM or greater were inhibitory. The effects of Pb acetate on tissue ODC activity in vitro were not mimicked by the addition of calcium chloride. Unlike tissue ODC activity, incubation of these metals with a pure ODC protein preparation exhibited fluctuations in ODC activity possibly due to the ionic interactions of Pb or calcium chloride. Calcium homeostatic mechanisms appeared to be unchanged with Pb exposure, at this dose, in that neither 45 Ca-uptake (both mitochondrial and microsomal) nor synaptosomal Ca 2+ -ATPase activity was altered. These data suggest that alterations in ODC activity may be indicative of subtle toxicant induced perturbations during early development. Although the precise mechanism by which Pb may induce ODC activity in developing tissue is unknown, our results suggest that Pb may specifically alter ODC activity via cytosolic interactions

Journal ArticleDOI
TL;DR: The results of this experiment showed that cocaine caused a significantly greater increase in extracellular nucleus accumbens dopamine in control animals relative to lead-treated animals.

Journal ArticleDOI
TL;DR: The results of this investigation demonstrated that the lead exposure in neonatal rats caused an increase in excitability, and a decrease in optimal temporal frequency, bandwidth at half amplitude, temporal resolution, and response phase of the retinal ganglion cells in adult rats.

Journal Article
TL;DR: It has been shown that the lead, when passing to the duct lumen of epididymis through cells and structures constructing the wall of that organ, is being excreted from the male genital system with the sperm.
Abstract: Over the period of the last 30 years there was a marked decrease in the number of spermatozoa produced by the gonads of men. It is felt that this observation is due to the influence of environmental pollution, wherein the lead plays quite an important role. In sperms of men, who are professionally exposed to lead compounds, oligo-, asteno-, and teratospermia is disclosed. Studies were performed on sexually mature male rats after 9-month-long exposure to lead acetate (II) as well as a group of animals after 3-month-long interval in the exposure. The changes provoked by the lead were evaluated by employing a number of study techniques, namely: morphological examination of testes with taking into account the stages of seminiferous epithelial cycle, and epididymis, giving due consideration to zones; electron microscopic examination of seminiferous cells and interstitial tissue, as well as the cells in the wall of epididymis and spermatozoa; X-ray microanalysis determining the presence and type of elements on ultrathin section; spectrophotometrical determination of Pb content in blood, testes and epididymides; determination of testosterone concentration (T) in blood serum. It has been revealed that the blood-testis barrier protects seminiferous epithelium against the toxic action of the lead. No deposits of Pb were observed either in germinal cells or Sertoli cells. The endocrine testicular cells outside the barrier had also unchanged ultrastructure, and contained no Pb. That finding was expressed by normal T level in blood serum. The only cells in the area of the testis, in whose cytoplasm there was Pb confirmed by X-ray microanalysis, were macrophages in the interstitial tissue of the testis. Apart from that, it has been disclosed that the blood-epididymis barrier does not provide a barrier against this element. Pb deposits were seen in smooth myocytes, epithelial cells and in the lumen of epididymal duct. That correlated with a marked decrease in the number of epididymal spermatozoa and numerous damages involving their ultrastructure. It has been shown that the lead, when passing to the duct lumen of epididymis through cells and structures constructing the wall of that organ, is being excreted from the male genital system with the sperm.

Journal Article
TL;DR: Homeopathic drugs plumbum 1M and Opium 30 were partially effective in the recovery of delta ALAD activity of the lead intoxicated rats and relieving anemia caused by chronic exposure of low doses of lead.
Abstract: Homeopathic drugs plumbum 1M and Opium 30 were partially effective in the recovery of delta ALAD activity of the lead (150 mg% lead acetate) intoxicated rats. Plumbum 1M did not exhibit protective effect when dietary lead at high concentrations (> 25 mg% lead acetate) were given concurrently as assessed by blood delta ALAD activity and hemoglobin concentration. However it was partially effective in the recovery of delta ALAD activity and relieving anemia caused by chronic exposure of low doses of lead (below 15 mg% lead acetate).

Journal ArticleDOI
TL;DR: The steady-state levels of monoamines were essentially unaltered after postnatal lead exposure in rats, while functional aspects of striatal dopamine transmission were affected after exposure to the higher dose of lead.

Journal Article
TL;DR: The findings suggest that an irritation of the mature astrocyte results in a change from the quiescent to the reactive state, which suggests an irreversible insult by low level lead exposure during this period of time.
Abstract: In this study we used in situ hybridization to examine the effects of chronic low level lead toxicity during different periods of brain development. Low level lead is known to affect astroglia. GFAP and Vimentin were chosen as glialtypic markers for neurotoxicity. The effects of lead were investigated on male Wistar rats. Animals were divided into four groups: a control group, a permanent group exposed during gestation, lactation and post-weaning (E0-P100), a perinatal group exposed during gestation and postnatally until weaning (E0-P16), and a post-weaning exposed group (P16-P100). All experimental animals were fed a diet containing 750 ppm lead acetate. With respect to Vimentin mRNA no major differences could be detected among the treatment groups. Significant differences in GFAP mRNA levels were detected in the post-weaning group relative to controls. In this group we observed a strong increase of GFAP mRNA in the polymorphic zone of the dentate gyrus and in the CA1 region of the hippocampus. Permanent and perinatal groups showed no overt changes compared to controls. Our findings suggest that an irritation of the mature astrocyte results in a change from the quiescent to the reactive state. The majority of astrocytes that have been exposed during their development and differentiation fail to react even if the exposure is continued to adulthood. This suggests an irreversible insult by low level lead exposure during this period of time.


Journal Article
TL;DR: Experimental ultrastructural examinations revealed groups in which lead impaired secretion of alveolar cells, damaged mitochondria and disturbed the lipid balance, and the greatest destructive changes were observed in group III.
Abstract: Clinical and experimental data point to the unfavorable effect of lead compounds on the oral cavity condition. The aim of this study was to analyse ultrastructural changes in the parotid gland of rats subjected to intoxication with lead acetate. The experiment was carried out on 24 Wistar rats divided into 4 groups, 6 animals in each. Group I animals were given aqueous solution of lead acetate of lead concentration 50 mg/dm3(50ppm), group II-500 mg/dm3(500ppm), group III-1,000 mg/dm3(1,000ppm). Control animals drank tap water. All the rats were sacrificed after six weeks of the experiment and material was collected for ultrastructural studies and evaluation of lead level in the tissue dry mass. A three fold increase in lead levels in the parotid gland was observed in group I and a tenfold increase in groups II and III. In all experimental ultrastructural examinations revealed groups in which lead impaired secretion of alveolar cells, damaged mitochondria and disturbed the lipid balance. The greatest destructive changes were observed in group III.

Journal Article
M. Atef1, S. A. H. Youssef, A. Ramadan, Afifi Na, Muity Aa 
TL;DR: Repeated oral administration of sulphadiazine caused a significant increase in serum AST, ALT, alkaline phosphatase and creatinine level in healthy and lead intoxicated rabbits, and the AST/ALT ratio in both healthy andLead intoxicated rabbits was found to decrease 1 h after the last dose as compared with before treatment.
Abstract: Two main equal groups of clinically healthy, non pregnant rabbits were classified into 4 subgroups (5 rabbits each). The 1st and 2nd subgroups were treated with sulphaquinoxaline or sulphadiazine in a single oral dose of 100 mg/kg b. wt., while the 3rd and 4th subgroups received a repeated oral dose of 100 mg/kg b. wt., daily for 5 successive days, respectively. The second main group received lead acetate in a dose of 4.2 mg/kg b. wt. per day for 2 months, then was classified as in case of the 1st main group and administered the respective sulphonamides in their recommended doses. The experimental lead intoxication was found to decrease the free delta-aminolevulinic acid dehydratase (delta-ALA-D) activity in blood of lead intoxicated rabbits after 4 and 8 weeks. Also, the ratio of free and with glutathione reactivated delta-ALA-D was increased 2.9 and 2.2 after 4 and 8 weeks, respectively as compared with before lead administration (1.19), indicating toxicity. The sulphonamide/creatinine ratio was increased after administration of both sulphonamides but higher in lead intoxicated rabbits as compared with healthy ones. The AST/ALT ratio was decreased 4 and 8 weeks after lead exposure. The AST, ALT and AST/ALT ratio, alkaline phosphatase, urea and creatinine were not altered in healthy rabbits. Repeated oral administration of sulphadiazine caused a significant increase in serum AST, ALT, alkaline phosphatase and creatinine level in healthy and lead intoxicated rabbits. On the other hand, AST/ALT ratio in both healthy and lead intoxicated rabbits was found to decrease 1 h after the last dose as compared with before treatment.

Journal ArticleDOI
TL;DR: Results indicated dose-dependent ethanol-induced hypoalgesia at all doses, but at the two higher doses the magnitude of the hypoAlgesic response was significantly greater in the group control animals than in thegroup lead animals across the 2-h postinjection period.
Abstract: Adult male rats were exposed to drinking fluid containing either 500 ppm lead acetate (group lead), or an equivalent concentration of sodium acetate (group control) for 61 days prior to pain reactivity testing using a tail-flick procedure. Rats were placed in restraining tubes for a 20 min acclimation period, and then baseline tail-flick latencies in response to a radiant heat source were measured. Subsequently, half the animals from each group were serially injected IP with either 1.0, 2.0, or 3.0 g/kg body weight of a 20% v/v ethanol solution, and the other half were injected with an equivalent volume of saline. Tail-flick latencies were reassessed at 20-min intervals over the next 2 h. Results indicated dose-dependent ethanol-induced hypoalgesia at all doses, but at the two higher doses the magnitude of the hypoalgesic response was significantly greater in the group control animals than in the group lead animals across the 2-h postinjection period. Results discussed in terms of an attenuation of the pharmacological properties of ethanol by lead.

Journal ArticleDOI
TL;DR: Results indicated that chronic lead exposure attenuated the reinforcing effect of brain stimulation, and suggest that a variety of motivational phenomena may be affected by contaminant exposure.
Abstract: Adult male rats were exposed to drinking water containing either 500 parts per million (ppm) lead acetate or an equal concentration of sodium acetate for 80 days. Bipolar electrodes were then implanted into the medial forebrain bundle (MFB), and rats were allowed to recover for 7 days. On Day 8 postsurgery, control and lead-treated rats were placed in an operant chamber and shaped to press a lever to receive 200-ms trains of current. Data from a range of current intensities and frequencies were recorded to obtain threshold values for each rat, defined as the stimulation needed to support half-maximal lever responding. Results indicated that chronic lead exposure attenuated the reinforcing effect of brain stimulation. Because of the large number of reward systems mediated by the MFB-nucleus accumbens pathway, these data suggest that a variety of motivational phenomena may be affected by contaminant exposure.