Showing papers on "Lead acetate published in 2009"
TL;DR: The extract succeeded to improve the histological pictures of liver and kidney and the biochemical parameters towards the normal values of the control and this improvement was pronounced in the animals treated with the extract after LA intoxication.
123 citations
TL;DR: Total lipids, cholesterol, triglycerides and LDL-c were significantly increased by lead acetate treatment, while HDL-c levels were decreased in the serum and liver extracts, and the morph metric analysis of the dorsal aorta revealed that, the histological alterations induced after lead acetates treatments were markedly reduced.
120 citations
TL;DR: Risk assessment and/or remediation of small arms ranges should assume high bioavailability of lead, and two widely accepted methods were used for lead bioavailability and bioaccessibility.
Abstract: Although small arms ranges are known to be contaminated with lead, the full extent of metal contamination has not been described, nor has the oral bioavailability of lead in these soils. In this work, soil samples from ranges with diverse geochemical backgrounds were sieved to <250 microm and analyzed for total metal content. Soils had consistently high levels of lead and copper, ranging from 4549 to 24 484 microg/g and 223 to 2936 microg/g, respectively, while arsenic, antimony, nickel, and zinc concentrations were 100-fold lower. For lead bioavailability measurements, two widely accepted methods were used: an in vivo juvenile swine relative bioavailability method measuring lead absorption from ingested soils relative to equivalent lead acetate concentrations and an in vitro bioaccessibility procedure which measured acid-extractable lead as a percent of total lead in the soil. For eight samples, the mean relative bioavailability and bioaccessibility of lead for the eight soils was about 100% (108 +/- 18% and 95 +/- 6%, respectively) showing good agreement between both methods. Risk assessment and/or remediation of small arms ranges should therefore assume high bioavailability of lead.
109 citations
TL;DR: Exposure of rat proximal tubular cells to low-concentration lead led to cell death, mediated by an apoptotic and a necrotic mechanism, and a group of cells survived lead action,mediated by their ability to activate antioxidant defense systems.
Abstract: Lead is a known nephrotoxic element. In this study, primary cultures of rat proximal tubular (rPT) cells were treated with different concentrations of lead acetate (0.25, 0.5 and 1 μM) to investigate its cytotoxic mechanism. A progressive loss in cell viability together with a significant increase in the number of apoptotic and necrotic cells and lactate dehydrogenase release were seen in the experiment. Simultaneously, elevation of reactive oxygen species levels and intracellular [Ca2+]i, depletion of mitochondrial membrane potential and intracellular glutathione were revealed during the lead exposure. In addition, apoptotic morphological changes induced by lead exposure in rPT cells were demonstrated by Hoechst 33258 staining. The apoptosis was markedly prevented by N-acetyl-l-cysteine, while the necrosis was not affected. Moreover, catalase and superoxide dismutase activities in the living cells rose significantly. In conclusion, exposure of rPT cells to low-concentration lead led to cell death, mediated by an apoptotic and a necrotic mechanism. The apoptotic death induced by oxidative stress was the chief mechanism. Meanwhile, a group of cells survived lead action, mediated by their ability to activate antioxidant defense systems.
97 citations
Journal Article•
TL;DR: In this article, the effect of heavy metals such as lead, mercury, cadmium, chromium, selenium and arsenic on male reproduction has been studied in details in various experimental species.
Abstract: Reproductive hazards from metal exposure in males are one of the fastest growing areas of concern in toxicology today. Exposure to different heavy metals causes irreversible toxic insult to male reproductive system. Heavy metals produce cellular impairments at structural and functional level in male reproductive system. The effect of heavy metals, such as lead, mercury, cadmium, chromium and arsenic on male reproduction has been studied in details in various experimental species. But data on humans are steadily building up. Metals could interfere with the gametogenic cells or Leydig cell or spermatozoa directly in semen. These effects may results in reduced fertility or associated with pregnancy wastage, congenital malformation associated with genetic diseases. Moreover, the features of heat stress protein (hsp), Androgen-Binding Protein (ABP), Cadherin and many other stressor protein along with reactive oxygen species (ROS) and neuro-endocrine mechanism are highly affected by these heavy metals exposure. Still the data are inadequate and need confirmation. The rapid industrialization and overgrowing urbanization, the toxic effects of heavy metals on male reproduction system have become a major health concern in the globe(1-2). The evidence of the past twenty years have shown disturbing trend in male reproductive health hazards due to careless use of these chemicals which caused detrimental effects on different organs. Therefore, broad-spectrum irreversible toxic actions at cellular and molecular level were observed mainly on reproductive system of human and experimental animals (3-4). Adverse effect of heavy metals on male reproduction: The potential toxicity of Metals, i.e., lead, cadmium, chromium, selenium and arsenic, caused alteration in sperm morphology, count, motility as well as biochemical disruptions of enzymes and hormones. Lead: Lead is widely used in acid battery plant refinery, smelter, fuel combustion industry, printing press and automobile exhaust where tetraethyl lead acts as anti- knocking agent. Toxicity is manifested in male reproductive system by deposition of lead in testes, epididymis, vas deferens, seminalvesicle and seminal ejaculate. Lead has an adverse effect on sperm count and retarded the activity of alive sperm. Moreover, motility as well as prolonged latency of sperm melting both in exposed person and experimental animals were observed after lead exposure (5-6).Study with male CF-1 mice indicated the significant decrease in epididymal sperm count at low dose of lead exposure (0.25% via drinking water). Moreover the decreased motility and increased incidence of teratospermia at higher dose of lead exposure (0.50%) along with inhibition of post-meiotic cells mainly pachytene spermatocyte were noted. In the same experiment the detachment of gemminal cell layer from basal membrane, atrophy of Leydig cells plus interstitial edema and low density of seminal plasma were also observed. Experimental studies were conducted to note the potential comparative effects of lead acetate considering different routes of
80 citations
TL;DR: It is indicated that cadmium, lead and zinc can induce micronucleated cells, SCEs and sperm abnormalities in Algerian mice and that the clastogenic potential is dependent on the time of exposure and the interaction between the three elements, confirming the environmental damage that may result from the simultaneous action of several metals.
Abstract: As a consequence of human activities, large amounts of cadmium, lead and zinc are released in the environment, often simultaneously. The aim of this study was to investigate under experimental conditions the DNA damage induced in Algerian mice (Mus spretus) exposed to cadmium (Cd), lead (Pb) and zinc (Zn) separately, or in selected combinations. Three cytogenetic end points were considered: the frequencies of micronucleated cells (MN) and sister chromatid exchange (SCE) in the bone marrow and the frequency of sperm abnormalities. Mice were treated by intraperitoneal (i.p.) injections with 5 or 10 doses of aqueous solutions of cadmium acetate, lead acetate and zinc acetate in concentrations corresponding to 1/10 of the LD50, respectively, 21.5, 0.46 and 1.5 mg/kg bw. The control groups were injected in the same way with distilled water. With only one exception (Cd + Zn group treated with 5 doses), the results show a significant increase of MN in all groups for both treatments (5 and 10 doses). Similarly, the results concerning the SCE revealed a statistically significant increase in all treated animals, with the exception of the Zn group treated with 5 doses. The number of sperm abnormalities was significantly higher in animals treated with 5 doses, except in the group Pb + Zn. In animals treated with 10 doses the number of sperm abnormalities was always statistically higher compared with controls. This study indicates that cadmium, lead and zinc can induce MN, SCEs and sperm abnormalities in Algerian mice and that the clastogenic potential is dependent on the time of exposure and the interaction between the three elements, confirming the environmental damage that may result from the simultaneous action of several metals. Most relevant is the toxic potential for Zn, related with the dose, which may compromise its protective effect against other metal contaminations, such as cadmium.
61 citations
TL;DR: Exposure to lead before and after birth can damage short-term and long-term memory ability of young rats and hippocampal ultrastructure, however, the current study does not provide evidence that the expression of rat hippocampal mGLUR3 and mGluR7 can be altered by systemic administration of lead during gestation and lactation.
Abstract: A complete explanation of the mechanisms by which Pb2+ exerts toxic effects on developmental central nervous system remains unknown. Glutamate is critical to the developing brain through various subtypes of ionotropic or metabotropic glutamate receptors (mGluRs). Ionotropic N-methyl-D-aspartate receptors have been considered as a principal target in lead-induced neurotoxicity. The relationship between mGluR3/mGluR7 and synaptic plasticity had been verified by many recent studies. The present study aimed to examine the role of mGluR3/mGluR7 in lead-induced neurotoxicity. Twenty-four adult and female rats were randomly selected and placed on control or 0.2% lead acetate during gestation and lactation. Blood lead and hippocampal lead levels of pups were analyzed at weaning to evaluate the actual lead content at the end of the exposure. Impairments of short -term memory and long-term memory of pups were assessed by tests using Morris water maze and by detection of hippocampal ultrastructural alterations on electron microscopy. The impact of lead exposure on mGluR3 and mGluR7 mRNA expression in hippocampal tissue of pups were investigated by quantitative real-time polymerase chain reaction and its potential role in lead neurotoxicity were discussed. Lead levels of blood and hippocampi in the lead-exposed rats were significantly higher than those in the controls (P < 0.001). In tests using Morris Water Maze, the overall decrease in goal latency and swimming distance was taken to indicate that controls had shorter latencies and distance than lead-exposed rats (P = 0.001 and P < 0.001 by repeated-measures analysis of variance). On transmission electron microscopy neuronal ultrastructural alterations were observed and the results of real-time polymerase chain reaction showed that exposure to 0.2% lead acetate did not substantially change gene expression of mGluR3 and mGluR7 mRNA compared with controls. Exposure to lead before and after birth can damage short-term and long-term memory ability of young rats and hippocampal ultrastructure. However, the current study does not provide evidence that the expression of rat hippocampal mGluR3 and mGluR7 can be altered by systemic administration of lead during gestation and lactation, which are informative for the field of lead-induced developmental neurotoxicity noting that it seems not to be worthwhile to include mGluR3 and mGluR7 in future studies.
54 citations
TL;DR: From this experiment it is revealed that Garlic and vitamin B-complex has protective and curative effect in lead toxicity.
Abstract: The experiment was performed on 25 adult mice, (Swiss albino), weighing about 25 gm, maintained on standard pellet diet and drinking water ad libitum . All the mice were randomly divided into five equal groups (5x5). Each group comprised of five mice was marked as group A, B, C, D and E. In the present study an attempt has been taken to study the effect of Garlic and vitamin B-complex in lead induced toxicities in mice with the observation of some parameters as toxic signs and body weight, some haematological parameters like total erythrocyte count (TEC), total leukocyte count (TLC), haemoglobin content (Hb%) and Packed cell volume (PCV), some biochemical parameters such as serum glutamate pyruvate transaminase SGPT/ALT, Serum glutamate Oxaloacetate transaminase (SGOT/AST) and postmortem changes in mice. An attempt was also made to estimate the residual deposition of lead in body tissues i.e. blood, liver, kidney, brain and bone in mice. Mice treated with lead acetate showed severe toxic signs and significantly reduced total erythrocyte count, total leukocyte count, haemoglobin content and packed cell volume and significant elevation of SGPT and SGOT. But in case of mice treated by lead acetate along with Garlic and vitamin B-complex showed almost normal levels of haematological and biochemical parameters. From this experiment it is revealed that Garlic and vitamin B-complex has protective and curative effect in lead toxicity. The mean body weight of mice of group B (only lead acetate) was significantly (p Garlic > Vitamin Bcomplex. Key words: Garlic, vitamin B-complex, lead acetate, mice  doi: 10.3329/bjvm.v6i2.2337 Bangl. J. Vet. Med. (2008). 6 (2): 203-210
44 citations
TL;DR: Findings indicate that exposure to toxic metals affects primary spermatocyte DNA and are suggestive of possible direct testicular toxicity.
Abstract: Toxic agents can interfere with the male reproductive system at many targets. One of the major unresolved questions concerning male infertility is identification of its molecular origins. Clinical and animal studies indicate that abnormalities of spermatogenesis result from exposure to three toxic metals (lead acetate, cadmium chloride, and arsenic trioxide), but the effects on primary spermatocyte DNA of the male rat after chronic exposure to these metals have not been identified. The aims of this study were to analyze, in three independent experiments, the DNA damage induced by lead (Pb), cadmium (Cd), and arsenic (As) in rat germinal cells during three time periods, and to determine the relationship between DNA damage and blood Pb, blood Cd, and urine As levels. For lead acetate and cadmium chloride experiments, blood was collected by cardiac puncture, while for arsenic trioxide a 24-h urine sample was collected. Afterward, the animals were sacrificed by decapitation. Pachytene spermatocytes from rat testes were purified by trypsin digestion followed by centrifugal elutriation. After establishment of cell purity and viability, DNA damage (tail length) was measured employing a single cell gel/comet assay. Significant DNA damage was found in primary spermatocytes from rats with chronic exposure (13 weeks) to toxic metals. In conclusion, these findings indicate that exposure to toxic metals affects primary spermatocyte DNA and are suggestive of possible direct testicular toxicity.
43 citations
Journal Article•
TL;DR: No significant change was observed in neutrophil, eosinophil, basophil and monocyte count in any treatment groups, whereas the lymphocyte count decreased significantly in group III and IV, and dose dependant significant reductions in TEC, Hb, PCV and TLC were observed.
Abstract: An experiment was conducted to study the haemato-biochemical alterations induced by lead acetate toxicity in 48 Wistar rats of either sex, divided uniformly into four different groups. The rats of group I received only deionised water as control while, group II, III and IV were given lead acetate @ 1 PPM, 100 PPM and 1000 PPM, in drinking deionised water respectively for 28 days. In group III and IV dose dependant significant (P<0.05) reductions in TEC, Hb, PCV and TLC were observed. No significant change was observed in neutrophil, eosinophil, basophil and monocyte count in any treatment groups, whereas the lymphocyte count decreased significantly (P<0.05) in group III and IV. A dose dependant significant (P<0.05) increase in AST, ALP, AKP, GGT, BUN and creatinine was experiential while TP and albumin levels were decreased in group III and IV.
41 citations
TL;DR: Ascorbic acid combined with thiamine exhibited protective effect on reproductive system by inhibiting Pb-induced excessive cell apoptosis, which is confirmed by initial research.
Abstract: Lead is a ubiquitous environmental and industrial pollutant that may have toxic effects on the male. Vitamins may protect against toxic effects of lead in the liver and reproductive system, which is confirmed by our initial research. The aim of this study was to further investigate the protective effects of vitamins (ascorbic acid combined with thiamine) on lead acetate (Pb)-induced reproductive toxicities in mice and study the possible mechanisms underlying these effects. Forty-five male mice were randomly divided into 3 groups, 15 mice in each and received daily intragastric administration with control, Pb (20 mg/kg), and Pb+vitamins (ascorbic acid of 420 mg/kg+thiamine of 30 mg/kg) for 6 weeks, respectively. The Pb-treated animals showed significant decreases in the epididymal sperm count and motility compared to the control group, while the Pb+vitamins group had significant increases for these variables. Moreover, an increasing apoptosis of germinal cells induced by Pb was reduced by vitamin treatment. Pb induced the activation of Caspase-3, Fas/Fas-L and Bcl-2 with elevated levels, and the adaptor protein primarily regulated signaling through Fas and required for Fas-induced apoptosis. In conclusion, ascorbic acid combined with thiamine exhibited protective effect on reproductive system by inhibiting Pb-induced excessive cell apoptosis.
TL;DR: There was an obvious synergistic effect of lead combined with cadmium on the expression of metallothionein in the kidney of rats.
Abstract: Lead acetate (300 mg/L) and/or cadmium chloride (50 mg/L) were administered as drinking water of Sprague-Dawley rats for 8 weeks to investigate the possible combined effect of these metals on the expression of metallothionein (MT) in kidneys. Immunohistochemical staining and real-time quantitative polymerase chain reaction analyses were performed on kidney samples to identify the distribution of MT and to quantify the relative expression levels of MT-1 and MT-2 gene, respectively. There is no significant difference in distribution of the intensity, amount of MT immunostaining, and expression level of MT-1 and MT-2 gene in the kidneys between the lead group and control group (P > 0.05), whereas those in the cadmium group and (Pb + Cd) group were significantly higher than that in the control group (P < 0.01). Compared to the (Pb + Cd) group with the lead or cadmium group, the expression level of MT-1 and MT-2 gene increased significantly (P < 0.01). In summary, there was an obvious synergistic effect of lead combined with cadmium on the expression of metallothionein in the kidney of rats.
TL;DR: The results suggest that lead induces region-specific response of expression in apoptotic proteins of rat brain showing more effect in hippocampus and cerebellum and less effect in frontal cortex and brain stem and it is tissue specific.
TL;DR: In this article, the toxicity of arsenic trioxide and lead acetate was assessed in adult hepatic stem cells induced in the 2-acetyl-aminofluorene/partial hepatectomy rat model.
Abstract: In the present study, the toxicity of arsenic trioxide and lead acetate was assessed in adult hepatic stem cells induced in the 2-acetyl-aminofluorene/partial hepatectomy rat model. Isolated oval cells were incubated separately for 6 h with 40 μM each of arsenic trioxide and lead acetate. 3-(4,5-Dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide assay denoted significant time-dependent cell death in arsenic and lead treated oval cells. The degree of stress imposed by these metals was evidenced by induction of heat shock protein (HSP) 70 and HSP 90. Arsenic and lead were found to trigger apoptosis as revealed by DNA ladder formation, Western blots of apoptotic factors, and reverse transcriptase polymerase chain reaction analyses of bax and bcl-2. Results clearly indicate that both arsenic and lead induced apoptosis is caspase-mediated and accompanied by extracellular signal-regulated kinase (ERK) dephosphorylation. Full-length BH3-interacting-domain death agonist expression in presence of caspase 3 inhibitor unravels a direct involvement of caspase in As and Pb induced apoptosis. Expression patterns of apoptosis inducing factor, B cell lymphoma-2 (Bcl-2) antagonist of cell death, Bcl-2-associated X protein, and Bcl2 also signify mitochondrial regulation of apoptosis effected by lead and arsenic. It is concluded that stimulation of caspase cascade and simultaneous ERK dephosphorylation are the most significant operative pathways directly associated with apoptotic signals triggered by arsenic and lead in the oval cells.
TL;DR: The data indicate enhanced glutathione peroxidase activity at most of the intervals for cerebellum, frontal cortex and brain stem, suggesting conversion of GSH to GSSG, while the hippocampus showed decreased levels, which indicates protection against lead acetate toxicity.
Abstract: This study is intended to determine the effect of lead acetate on glutathione and its associated enzymes of rat brain. Wistar male rats were treated with lead acetate (500 ppm) through drinking water for a period of 8 weeks and parallel controls were maintained. They were sacrificed at the first, fourth and eighth week to isolate whole brains, which were separated into cerebellum, hippocampus, frontal cortex and brain stem. The data indicate enhanced (P < 0.05) glutathione peroxidase (G-Px) activity at most of the intervals for cerebellum, frontal cortex and brain stem, suggesting conversion of GSH to GSSG, while the hippocampus showed decreased levels. In contrast, glutathione reductase (GR) decreased significantly (P < 0.05) in cerebellum, frontal cortex and brain stem at all intervals except the fourth week in frontal cortex and brain stem. Hippocampus exhibited a gradual and significant (P < 0.05) increase in GR activity. Glutathione-S-transferase (GSTase) activity increased with exposure time in all four brain tissues, showing protection against lead acetate toxicity. The GSH and GSSG levels correlated well with the activities of GPx, GR and GSTase in all four regions of the brain. Overall the results indicate that lead acetate affects glutathione-related enzymes differentially and these changes can be attributed to differences in tissue susceptibility.
TL;DR: Treatment with methanolic extract of A. aspera after lead induction completely ameliorated the lead-induced renal damage and changes in kidney weights encountered upon lead administration improved after extract with A.Aspera.
Abstract: The present study was designed to evaluate the nephroprotective role of methanolic extract of Achyranthes aspera (A.aspera) an important herb in the Indian system of medicine against lead acetate-induced nephrotoxicity in rats. Toxicity was induced in male albino rats (Wistar strain) by administering lead acetate (0.2%) in drinking water for 6 weeks, followed by extract of A. aspera (200 mg/kg body weight). Changes in kidney weights encountered upon lead administration improved after extract with A. aspera. Lead damage to the urine was evident from increase in the activity of γ-glutamyltranspeptidase (γ-GT), Cathespin D, alkaline phosphatase (ALP), acid phosphatase (ACP), β-glucuronidase lactate dehydrogenase (LDH) and N-acetyl-β-D-glucosaminidase (NAG) in urine along with some urinary constituents (urea, uric acid, creatinine, protein and phosphorous). The effects of lead were also studied in kidney (γ-GT, β-glucuronidase, NAG, Cathespin D and LDH) and showed a decline upon extract administration. Increased activities of urinary enzymes were accompanied by increase in the urinary constituents. Treatment with methanolic extract of A. aspera after lead induction completely ameliorated the lead-induced renal damage.
TL;DR: It is concluded that lead exposure to rats during pregnancy led to varying degrees of fetal growth retardation as well as delayed ossification of some craniofacial bones which were dose dependent and the concomitant supplementation with vitamin E greatly improved the deleterious effect of lead.
Abstract: Lead exposure during intrauterine life was found to result in reduced birth weight, impaired skeletal development and post-natal neurotoxic effects. In this study, the effect of pre-natal exposure to different doses of lead on the development of craniofacial skeleton in rat fetuses was investigated. Vitamin E was tested as a concomitant treatment, aiming to improve the fetotoxic effects of lead. Positively pregnant female rats were randomly divided into four groups; groups I and II (L250 and L500), exposed to lead acetate in doses of 250 and 500 mg/l respectively, group III (L500 + E), exposed to lead acetate (500 mg/l) wit concomitant vitamin E and group IV (Control) which was given sodium acetate only. All the treatments started from the first day of gestation till the 20th day, where all rats were sacrificed and the fetuses were recovered. Fetuses were processed to alizarin red staining for ossified components. Twenty-seven bones of the craniofacial skeleton were studied in each fetus where the ossification was scored as being complete, delayed or absent. In all studied fetuses from all groups, changes were found only in eight bones while the remaining craniofacial bones were normally ossified. In affected bones there was a significant decrease in the number of completely ossified bones; associated with a significant increase of both partially ossified and absent bones in L(250) and L(500) treated groups when compared to the control group. These differences were more significant in the L(500) treated group. Giving vitamin E improved the percentage of completely ossified craniofacial bones and decreased the percentage of both partially ossified and absent bones. The most affected bone was presphenoid, then to a lesser extent supraoccipital, squamosal, parietal, interparietal and frontal bone respectively. In conclusion, lead exposure to rats during pregnancy led to varying degrees of fetal growth retardation as well as delayed ossification of some craniofacial bones which were dose dependent and the concomitant supplementation with vitamin E greatly improved the deleterious effect of lead.
TL;DR: Low dose of melatonin given from weaning for two months impaired LTP in the DG area of hippocampus and induced learning and memory deficit in the control rats.
Journal Article•
TL;DR: The results showed that the levels of both oxidized (ubiquinone) and reduced (UBiquinol) forms of coenzyme Q in serum, brain, liver and kidney of lead-treated rats are quite different depending on the organ tissue type.
Abstract: Lead is a persistent and common environmental contaminant, which chiefly plays a significant role in modern industry. Coenzyme Q acts as electron and proton carrier in mitochondria and functions as an antioxidant in its reduced form (ubiquinol). To investigate the hazardous effects of lead on the coenzyme Q level, rats were injected i.p. with lead acetate (5 mg/kg b.wt. daily for 6 weeks). Our results showed that the levels of both oxidized (ubiquinone) and reduced (ubiquinol) forms of coenzyme Q9 and Q10 in serum, brain, liver and kidney of lead-treated rats are quite different depending on the organ tissue type.
TL;DR: The findings suggest that lead exposure at various gestational periods produce varied effects, with NF-kappaB activation following lead exposure, which may be contribute to abnormal pregnancy outcomes.
TL;DR: Lead ions moderately inhibit both phosphoribosyltransferases in erythrocytes, this influence being detectable even at very low concentrations, which indicates the necessity of further research on the role of lead-induced APRT and HPRT inhibition as one of the mechanisms of lead toxicity.
TL;DR: In this paper, the authors investigated the toxic effects of lead on the pituitary-testicular axis, and endocrine and exocrine testicular functions in male Wister rats.
TL;DR: The findings indicate that SA and LA separately induced the formation of micronucleated polychromatic erythrocytes in the bone marrow of the rats significantly and when fed simultaneously, the induction was about 22 folds as compared with the negative control group.
Abstract: Continuous exposure of humans to arsenic through long-term ingestion of contaminated drinking water and its attendant health problems has been widely reported. It is also known that arsenic interact with other substances, metals inclusive thereby potentiating its effects or vice versa. In this study, we examined the effects of sodium arsenite (SA) and lead acetate (LA) in wistar rats. Sodium arsenite (2.5mg/kg bd.wt) and lead acetate (14mg/kg bd.wt) were fed to rats by gavage for fourteen consecutive days alone or simultaneously. Control rats were fed with distilled water. Clastogenic effects were observed in the bone marrow cells using the micronucleus assay. In addition, serum activities of gamma glutamyl transferase (γ-GT), alkaline phosphatase (ALP), alanine amino transferase (ALT ) and aspartate amino transferase (AST) were monitored . The findings indicate that SA and LA separately induced the formation of micronucleated polychromatic erythrocytes (mPCEs) in the bone marrow of the rats significantly (P < 0.05) by about 9 and 8 folds respectively. When fed simultaneously, the induction was about 22 folds as compared with the negative control group. SA significantly induced the serum activity of all the enzymes while LA significantly induce the activity of only γ-GT and ALP (P < 0.05). Simultaneous feeding of SA and LA also markedly induced the activity of all the enzymes in the serum. Mild infiltrative haemorrhage was observed in the lungs of rats exposed to the two compounds. This study underscores the enhanced toxic effect of combined or simultaneous exposure to toxic substances.
TL;DR: The data suggest that mGluR5 might be involved in lead-induced neurotoxicity by disturbing mGLUR5-induced long-term depression and decreasing N-methyl-D-aspartic acid receptor (NMDAR)-dependent or protein synthesis-dependent long- term potentiation.
Journal Article•
TL;DR: The treatment with C.sempervirens methanol extract and its flavonoids may provide a partial protection against the toxic effect induced by lead acetate, indicating that C. semperviren methanl extract may be capable of greatly modifying rodents’ susceptibility to blood and liver toxicity in addition to oxidative stress induced byLead acetate.
Abstract: The toxicological effect of lead acetate to the liver and the possible protective effect of Cupressus sempervirens (C. sempervirens) plant and its flavonoids (quercetin and rutin) was evaluated. 30 Male albino rats and divided into five groups (six per group). Group I, served as control, group II exposed to 0.5 mg/g concentrations of lead acetate in diet for 60 days. Group III was received daily doses of 8 mg/100g of rat b.wt of C. sempervirens (liophilized from methanol extract of seeds) two weeks prior to lead acetate administration. Group IV received daily doses of 0.3 mg/100g of rat b.wt of the flavonoid quercetin two weeks prior to lead acetate administration; Group V was received daily doses of 0.1 mg/100g of rat b.wt of the flavonoid rutin two weeks prior to lead acetate administration. Lead acetate caused a significant increase in serum and tissue AST, ALT, ALP, bilirubin, serum and tissue MDA, plasma and tissue NO, in addition to, highly significant increase in serum cholesterol, LDL, triglycerides and HDL. On the contrary, lead induced a significant decrease in serum and tissue total protein, albumin, globulin, albumin/globulin ratio, blood and tissue SOD and GPx compared to control group. The administration of C. sempervirens methanol extract, quercetin and rutin two weeks prior to lead acetate prevents these parameters to the normal levels. In conclusion, the treatment with C.sempervirens methanol extract and its flavonoids may provide a partial protection against the toxic effect induced by lead acetate. This indicates that C. sempervirens methanol extract may be capable of greatly modifying rodents’ susceptibility to blood and liver toxicity in addition to oxidative stress induced by lead acetate.
Journal Article•
TL;DR: Serum chemistry revealed changes in concentrations of glucose and sodium owing to lead treatment and simultaneous exposure to a combination of chlorpyrifos and lead is considered to be more dangerous than to an exposure of either alone.
Abstract: Chlorpyrifos, a well known organophosphorus insecticide and heavy metal lead, was challenged to Wistar rats to study their interactive effects on biochemical parameters (clinical pathology) after acute exposure via oral gavaging. Hematology and clinical chemistry parameters were estimated after 14 days of exposure. In addition, serum butryl and RBC cholinesterase was estimated on days 3 rd and 15 th of experimentation. The study was conducted using two different dose levels of chlorpyrifos and lead acetate and grouped into seven groups. The parameters of hematology and serum chemistry were analysed through automatic analyzers. No treatment related or interactive effects were noticed in hematology values except for the reduced RBC, Hb content and HCT values in lead treated animals at 1000mg/kg. A significant decrease in both serum and RBC cholinesterase enzymes were noticed in animals treated with chlorpyrifos at 50 mg/kg and in combination group (chlorpyrifos 50 + lead 1000 mg/kg), and increased inhibition along with delayed recovery was observed in the animals of combination group (i.e., chlorpyrifos plus lead). Chlorpyrifos in presence of lead increases the inhibition of both serum and RBC cholinesterase enzymes. The long lasting or persistence effects of CPF along with and lead may result in impaired cognitive functions of brain considering the role of cholinesterases in neuronal architecture of brain and other normal functioning of nervous system. Therefore, simultaneous exposure to a combination of chlorpyrifos and lead is considered to be more dangerous than to an exposure of either alone. In addition, serum chemistry revealed changes in concentrations of glucose and sodium owing to lead treatment.
01 Jan 2009
TL;DR: Using antox, (an antioxidant contains three supplementary nutritional vitamins A, C and E with rare element selenium) with lead or arsenic led to an improvement of serum cholinesterase activity in rats and also relative brain weight, which proved the effectiveness of antox that attributed to its antioxidant properties.
Abstract: Adult male albino rats were exposed to 100 mg/L of lead acetate or 100 mg/L sodium arsenate in drinking water for 3 and 6 weeks, lead and arsenic inhibit cholinesterase activity after both time intervals, with percentage reached 23% and 25% in lead and arsenic after 6 weeks, respectively. The results revealed that lead or arsenic leading to increase in relative brain weight in most of the experimental period. Using antox, (an antioxidant contains three supplementary nutritional vitamins A, C and E with rare element selenium) with lead or arsenic led to an improvement of serum cholinesterase activity in rats and also relative brain weight. Histological studies showed that lead and arsenic treated rats induced neuron injuries and change in brain cells. Rats treated with antox during administration of lead or arsenic repair some injuries of brain cells and neuron induced by lead or arsenic. Rats treated with both lead or arsenic and antox revealed an improvement in histopathological alteration induced by lead or by arsenic after 3 weeks and 6 weeks. This proved the effectiveness of antox that attributed to its antioxidant properties. In conclusion, heavy metals i.e. lead and arsenic proved severely neurotoxic and antox reduces the resulting damage probably due to its ability to neutralize free radicals that are generated by lead and arsenic.
Journal Article•
TL;DR: It is concluded that the combined EMF and lead acetate- exposure produced severe changes in the hemato-biochemical and immune parameters which were both real and inconsistent.
Abstract: The present study was carried out to investigate the potential effects of extremely low-frequency electromagnetic fields (ELF-EMF) and lead acetate on some hemato-biochemical, immune and pathologic variables in mice. A total 120 female mice were equally divided into eight groups. Gp. 1 kept as control. Gp. 2 exposed to EMF of 2 millitesla intensity and 50 Hz frequency (4h/day) for 30 days. Gps. 3, 4 and 5 were administered lead acetate orally at various doses (1, 5 and 10 mg/kg BW) for 30 days. The last 3 groups (6, 7 and 8) were exposed to EMF- lead combination for the same period. EMF- exposure, for 4h/day during 30 consecutive days, induced a significant increase in the erythrogram, leukogram and platelet counts, compared to control. Anemia, leucopenia, neutropenia, lymphopenia and monocytopenia were recorded with oral administration of lead acetate at various doses. The severity of changes was dose related. The phagocytosis % and phagocytic index were significantly (P<0.05) increased in mice exposed to EMF for 30 days (gp.2) but decreased in those given high doses of lead acetate. However, the immune parameters were insignificantly changed in groups 3, 7 and 8. Comparing to unexposed mice, significant variations in biochemical parameters (glucose, enzymes, and protein profiles) were noticed. Lead-EMF combination had synergistic effect on some previous parameters, whereas mice given the highest dose of lead with EMF aggravated hematobiochemical and pathological findings. We concluded that the combined EMF and lead acetate- exposure produced severe changes in the hemato-biochemical and immune parameters which were both real and inconsistent.
TL;DR: Results suggest that early developmental exposure to lead and cadmium both alone and in combination can suppress the hepatic xenobiotic‐metabolizing enzyme activities in the liver of F1 generation male and female rats in a sex‐dependent manner.
Abstract: Liver has evolved complex enzymatic mechanisms to detoxify a wide array of xenobiotic substances, ranging from dietary components to environmental toxins to pharmaceuticals. Activities of many steroid-metabolizing enzymes in adult rat liver microsomes are sexually differentiated. Toxic effects of lead and cadmium on hepatic tissue have been well established in our earlier studies. We thus monitored the effects of gestational and lactational coexposure to lead and cadmium on hepatic phase I and phase II xenobiotic- and steroid-metabolizing enzyme activities in both male and female F1 generation postnatal day (PND) 56 rats. Adult pregnant female rats were treated subcutaneously [0.05 mg/(kg body wt. day)] with sodium acetate (control group), lead acetate, and cadmium acetate separately and in combination throughout the gestational and lactational period. Hepatic phase I xenobiotic-metabolizing enzymes (NADPH- and NADH-cytochrome c reductase) activities significantly decreased significantly in all the metal-treated groups in both PND 56 male and female rats as compared with the control group. Hepatic phase II enzymes (uridine diphosphate-glucuronosyl transferase, γ-glutamyl transpeptidase, glutathione-S-transferase, 17-β-hydroxysteroid oxidoreductase) were also highly susceptible to all the metal-treated groups. The observed alterations in the oxidative stress and biochemical parameters in the liver of F1 generation male and female rats resulted from an independent effect of lead and/or cadmium and also from their interaction. Results suggest that early developmental exposure to lead and cadmium both alone and in combination can suppress the hepatic xenobiotic-metabolizing enzyme activities in the liver of F1 generation male and female rats in a sex-dependent manner. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:419–431, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20305
TL;DR: Results showed the bone to produce a significant level of lead in bone, brain, muscle, liver and kidney tissues of female rats as well as Allium sativum and ascorbic acid.
Abstract: The effects of Ascorbic acid (vitamin C) and Allium sativum (garlic) on the lead levels in bone, brain, muscle, liver and kidney tissues of female rats (Rattus navigicus) were investigated. Group I was Control, rats in Groups II – IV were injected intraperitoneally with 100µmol/kg body weight of lead acetate for 7 days. In addition, groups III and IV rats were fed with Allium sativum (200 g/kg diet) and ascorbic acid (500 mg/kg body weight) for 7 days respectively. Results showed the bone to produce a significant (p Keywords : Lead level, Allium sativum, ascorbic acid, tissue Nigerian Journal of Health and Biomedical Sciences Vol. 7 (2) 2008: pp. 38-41