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Showing papers on "Lead acetate published in 2007"


Journal ArticleDOI
TL;DR: Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach by affecting catalase and superoxide dismutase activities and the amount of nitrite in gastric mucosal samples.
Abstract: AIM: To investigate the role of reactive oxygen species in the ulcer-aggravating effect of lead in albino rats. METHODS: Albino Wistar rats were randomly divided into three groups and treated orally with 100 mg/L (low dose) or 5000 mg/L (high dose) of lead acetate for 15 wk. A third group received saline and served as control. At the end of wk 15, colorimetric assays were applied to determine the concentrations of total protein and nitrite, the activities of the oxidative enzymes catalase and superoxide dismutase, and lipid peroxidation in homogenized gastric mucosal samples. RESULTS: Exposure of rats to lead significantly increased the gastric mucosal damage caused by acidified ethanol. Although the basal gastric acid secretory rate was not significantly altered, the maximal response of the stomach to histamine was significantly higher in the lead-exposed animals than in the unexposed control group. Exposure to low and high levels of lead significantly increased gastric lipid peroxidation to 183.2% ± 12.7% and 226.1% ± 6.8% of control values respectively (P < 0.0). On the other hand, lead exposure significantly decreased catalase and superoxide dismutase (SOD) activities and the amount of nitrite in gastric mucosal samples. CONCLUSION: Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach.

94 citations


Journal ArticleDOI
TL;DR: In the group exposed to lead the concentration of lipid peroxide in homogenates of the reproductive system organs was significantly elevated versus control group and it can be assumed that the lower EPR signal was caused by decreased tissue concentrations of l-ascorbic acid.
Abstract: The hypothesis has been recently presented that lead may exert its negative effect at least partially through the increase of reactive oxygen species (ROS) level in tissues. However, little is known about the influence of lead intoxication on equilibrium between generation and elimination of ROS in the male reproductive system. Sexually mature male Wistar rats were given ad libitum 1% of aqueous solution of lead acetate (PbAc) for 9 months. Significantly higher lead concentrations were found in blood [median 7.03 (Q25-Q75: 2.99-7.65) versus 0.18 (0.12-0.99) microg dl-1, P < 0.01], caput epididymis [median 5.51 (Q25-Q75: 4.31-7.83) versus 0.51 (0.11-0.80) microg g-1 d.m., P < 0.001], cauda epididymis [median 5.88 (Q25-Q75: 4.06-8.37) versus 0.61 (0.2 - 1.08) microg g-1 d.m., P < 0.001] and testis [median 1.81 (Q25-Q75: 0.94-2.31) versus 0.17 (0.03-0.3) microg g-1 d.m., P < 0.01] of lead-intoxicated rats when compared to the control. The concentration of ascorbyl radical, generated in vitro from L: -ascorbic acid (present in tissues in vivo) was measured by means of Electron Paramagnetic Resonance (EPR) spectroscopy. The EPR signal of ascorbyl radical in caput epididymis, cauda epididymis, testis and liver of lead acetate-treated animals revealed a significant decrease by 53%, 45%, 40% and 69% versus control tissues, respectively. Plasma L: -ascorbic acid content measured by high performance liquid chromatography (HPLC) method and total antioxidant status (TAS) measured by means of spectrophotometry were also significantly lower in the intoxicated versus control animals (28% and 21%, respectively). In the group exposed to lead the concentration of lipid peroxide in homogenates of the reproductive system organs was significantly elevated versus control group. It can be assumed that the lower EPR signal was caused by decreased tissue concentrations of L: -ascorbic acid. The latter may have resulted from consumption of ascorbic acid for scavenging of ROS excess in tissues of animals chronically exposed to lead.

89 citations


Journal ArticleDOI
TL;DR: It is concluded that lead induces oxidative stress in a dose- dependent manner and no dose-dependent response was observed in blood GPx activity and liver MDA content.

83 citations


Journal ArticleDOI
TL;DR: Data from the present study indicates that lead and cadmium in isolation and in combination cause oxidative stress, indicating the competition between them due to similarity in electronic affinities.
Abstract: The effects of combined exposure to lead and cadmium on granulose cells were studied Adult female rats were treated ip with either lead acetate (LA) or cadmium acetate (CA) both, alone, or in combination at a dose of 005 mg/kg body weight on a daily basis for 15 days Both metals were accumulated in the ovary after metal exposure Metal exposure caused a decrease in reduced glutathione content along with elevated lipid peroxidation in all groups Granulose cells of both cadmium as well as combination group demonstrated a maximum increase in lipid peroxides and catalase activity, along with decreased glutathione status and superoxide dismutase activities Combined treated animals exhibited an intermediate effect in antioxidant status However, “in vitro" exposure showed no significant change in antioxidant enzymes in all metal exposed cells Data from the present study indicates that lead and cadmium in isolation and in combination cause oxidative stress Lead and cadmium in combination do not show additive or synergistic effect indicating the competition between them due to similarity in electronic affinities Present study highlights the effects of toxic metals that disturb membrane integrity of cells via ROS and thereby classifying mechanism for altered receptor binding, steroidogenesis, and hormone production

75 citations


Journal ArticleDOI
TL;DR: These findings strongly indicated that combination of VC and VB(1) can lessen the damage to liver cells from oxidative stress induce by lead, but the antioxidant effects are dependent on their concentrations.
Abstract: Objective: To investigate the effect of ascorbic acid [vitamin C (VC)] on liver damage parameters in the lead-exposed mice, when given in combination with thiamine [vitamin B1 (VB1)] at different concentrations. Methods: Sixty-six male mice were randomly assigned into 11 groups (n 5 6). Mice in Group I were supplied with only the tap water as the drinking water; mice in Group II were provided with a tap water containing 0.2% lead acetate; mice in Group III–XI were given different dose of VC (140, 420, 1260 mg kg 21 bw) and VB1 (10, 30, 90 mg kg 21 bw) according to 3 3 3 factorial design by oral gavages, along with ingestion of 0.2% lead acetate. After 42 test days, DNA damage of liver cells was assessed using single-cell gel electrophoresis. The apoptosis rate of liver cells was determined by flow cytometry. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in blood and the level of reduced glutathione (GSH) in liver cells were measured based on individual biochemical reactions. Results: Compared with the Group I, sub-chronic lead ingestion (Group II) resulted in a significant decrease of Hb, GSH-PX, SOD in blood and GSH level in liver cells; lead exposure induced also a significant increase in DNA damage and apoptosis of liver cells (P < 0.05). Supplementation with VC and VB1, however, reversed these effects. The best effective combination was VC (420 mg kg 21 bw) and VB1 (10 mg kg 21 bw), followed by the combination of VC (420 mg kg 21 bw) and VB1 (30 mg kg 21 bw). But no reversion was shown in the combination of the highest combination of VC (1260 mg kg 21 ) and VB1 (90 mg kg 21 ). Conclusions: These findings strongly indicated that combination of VC and VB1 can lessen the damage to liver cells from oxidative stress induce by lead, but the antioxidant effects are dependent on their concentrations.

71 citations


Journal ArticleDOI
TL;DR: It seems that ascorbic acid may potentially be beneficial in treating lead-induced brain injury in the developing rat brain.

54 citations


Journal Article
TL;DR: Garlic or olive oils alleviated the previous changes in blood, serum glucose and renal parameters, whereas DMSA, calcium disodium ethylenediaminetetraacetic acid and CaNa2-EDTA reversed such changes to near the control levels.
Abstract: This study investigated lead impact on blood, serum glucose and kidney function and the efficacy of treatment with chelating agents meso-2,3-dimercaptosuccinic acid (DMSA), calcium disodium ethylenediaminetetraacetic acid (CaNa2-EDTA) and natural olive and garlic oils to reduce lead toxicity in albino rats. Oral administration of 1000 or 2000 ppm lead acetate significantly decreased red blood cell count, hemoglobin level and hematocrit value at 20, 40 and 60 days compared with control groups (rats administered deionized water and 1000 or 2000 ppm sodium acetate). Serum glucose was also decreased significantly with both doses of lead acetate administration. In contrast, serum urea, uric acid and creatinine were significantly increased. Garlic or olive oils (1 ml/kg body weight/day, each) alleviated the previous changes in blood, serum glucose and renal parameters, whereas DMSA (50 mg/kg body weight/day) or CaNa2-EDTA (100 mg/kg body weight/day) reversed such changes to near the control levels. Although chemical therapy is more efficient in reducing lead toxicity, natural products with their fewer side effects are still preferable.

52 citations


Journal ArticleDOI
TL;DR: Combined treatment of lead-exposed animals with Nigella sativa showed marked improvement in both biochemical and histopathological findings as well as reduction in the damaged areas of lead acetate-induced rats' toxicity in particularly on liver and kidney.
Abstract: Heavy metals are widely distributed in the environment and some of them occur in food, water, air and tissues even in the absence of occupational exposure. Among of these lead, (Pb) is a hazardous substance to human and animals. The present study was carried out to investigate the possible protective effect of co-administered Nigella sativa seeds on lead acetate-induced rats' toxicity in particularly on liver and kidney. Thirty-six male rats were divided into six groups, 6 rats each. The first group was served as a control, while the second group was fed on the basal diet with Nigella sativa addition, whereas the other groups contained lead acetate (10 and 20% of LD50) with and without Nigella sativa supplementation for six weeks. At the end of the feeding period, rats were fasted over night and anesthetized and blood and tissue samples were taken for biochemical and histopathological studies. The results of this study revealed that lead acetate caused significant elevations in AST, urea, creatinine, total cholesterol and triglycerides in serum. Lead treatment also produced significant decrease in serum total protein and albumin. Histopathological observations showed severe damage in the liver and kidneys. Its damaged areas were measured using Image analyzer. Combined treatment of lead-exposed animals with Nigella sativa showed marked improvement in both biochemical and histopathological findings as well as reduction in the damaged areas. These experimental results strongly indicate the protective effect of Nigella sativa against toxic effect of lead on liver and kidney tissues.

51 citations


Journal ArticleDOI
TL;DR: The data indicated a region-specific oxidative stress in the brain exposed to lead, which was more in the cerebellum and the hippocampus compared to other regions of the brain.
Abstract: The objective of this study is to determine the effect of lead (pb) on antioxidant enzymes and lipid peroxidation products in different regions of rat brain. Wistar male rats were treated with lead acetate (500 ppm) through drinking water for a period of 8 weeks. Control animals were maintained on sodium acetate. Treated and control rats were sacrificed at intervals of 1st, 4th and 8th week and the whole brains were dissected on ice into four regions namely the cerebellum, the hippocampus, the frontal cortex and the brain stem. Antioxidant enzymes namely catalase and superoxide dismutase in all the four regions of brain were determined. In addition, lipid peroxidation products were also estimated. The results indicated a gradual increase in the activity of antioxidant enzymes in different regions of the brain and this response was time-dependent. However, the increase was more in the cerebellum and the hippocampus compared to other regions of the brain. The lipid peroxidation products also showed a similar trend suggesting increased effect of lead in these two regions of the brain. The data indicated a region-specific oxidative stress in the brain exposed to lead.

49 citations


Journal ArticleDOI
TL;DR: Lead acetate (300 mg Pb/L) and/or cadmium acetate(10mg Cd/L), were administered as drinking water to pregnant Wistar rats from day 1 of pregnancy to parturition (day 0) or until weaning (day 21), to investigate the toxic effects in blood and in the liver as discussed by the authors.

41 citations


Journal ArticleDOI
TL;DR: The results suggest that thioredoxin reductase-1 may be an early indicator of acute exposure to low lead doses, as well as on indicators of renal function commonly used to assess lead poisoning.
Abstract: Oxidative stress has been suggested to be an important molecular mechanism of toxic effects of lead in the kidney. Thioredoxin reductase-1 is a selenoprotein involved in many cellular redox processes. This study evaluated the effect of acute and chronic exposure intraperitoneally to lead acetate on thioredoxin reductase-1 activity and on other oxidative stress parameters in the rat kidney, as well as on indicators of renal function commonly used to assess lead poisoning. Acute exposure to 25 mg/kg lead acetate increased superoxide dismutase and thioredoxin reductase-1 activity (after 6, 24 and 48 hr), while exposure to 50 mg/kg lead acetate increased catalase activity (after 48 hr) and inhibited delta-aminolevulinate dehydratase activity (after 6, 24 and 48 hr) in the kidney (P < 0.05). Chronic exposure (30 days) to 5 mg/kg lead acetate inhibited delta-aminolevulinate dehydratase and increased glutathione S-transferase, non-protein thiol groups, catalase, thioredoxin reductase-1 and uric acid plasma levels, while exposure to 25 mg/kg lead acetate reduced body weight and delta-aminolevulinate dehydratase, but increased glutathione S-transferase, non-protein thiol groups and uric acid plasma levels (P < 0.05). No changes were observed in thiobarbituric acid reactive substances, glutathione peroxidase, creatinine or inorganic phosphate levels after either acute or chronic exposure. Our results suggest that thioredoxin reductase-1 may be an early indicator of acute exposure to low lead doses.

Journal ArticleDOI
TL;DR: It is indicated that ontogenetic exposure to lead can have consequences on monoaminergic neuronal function at an adult stage of life, generally promoting accentuated behavioral effects of direct and indirect monoaminerential agonists, and related to increased dopamine turnover in basal ganglia.
Abstract: To determine the effect of prenatal lead exposure on brain monoaminergic systems, pregnant rats were given tap water containing 250 ppm lead acetate, for the duration of pregnancy, while tap water without lead (Pb(2+)) was substituted at birth. Control rats were derived from dams that consumed tap water during pregnancy, and had no exposure to lead afterwards. At 12 weeks after birth, Pb(2+) content of brain cortex was increased 3- to 4-fold (P < 0.05). At this time the endogenous striatal levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid were 19% lower in Pb(2+) exposed rats (P < 0.05), while there was no change in the striatal level of dopamine (DA), noradrenaline, 3,4-dihydroxyphenylglycol, serotonin (5-HT) and 5-hydroxyindoleacetic acid (HPLC/ED). Also there was no change in these monoamines and metabolites in the prefrontal cortex of Pb(2+) exposed rats. However, turnover of 5-HT in prefrontal cortex, as indicated by 5-hydroxytryptophan accumulation 30 min after acute treatment with the decarboxylase inhibitor NSD-1015 (100 mg/kg IP), was lower in the Pb(2+) exposed rats. In the striatum AMPH-induced (1 mg/kg IP) turnover of DA, evidenced as L-DOPA accumulation after NSD-1015, was increased to a lesser extent in the Pb(2+) exposed rats (P < 0.05). The nitric oxide synthase inhibitor 7-nitroindazole (10 mg/kg IP) attenuated the latter effect, indicating that neuronal NO mediates this AMPH effect, at least in part. Moreover, DA D(2) receptor sensitivity developed in Pb(2+) exposed rats, as evidenced by enhanced quinpirole-induced yawning activity and enhanced quinpirole-induced locomotor activity (each, P < 0.05). These findings indicate that ontogenetic exposure to lead can have consequences on monoaminergic neuronal function at an adult stage of life, generally promoting accentuated behavioral effects of direct and indirect monoaminergic agonists, and related to increased dopamine turnover in basal ganglia.

Journal ArticleDOI
TL;DR: The results suggest a brain region‐ and time‐specific response following lead acetate exposure, with the region most vulnerable to alterations occurs in the hippocampus with alterations beginning at PND 12, in which caspase 3, bcl‐x, BDNF increase with lead exposure.
Abstract: Previous reports have recently shown the prototypic neurotoxicant, lead, to induce apoptosis in the brains of developing organisms. In the current study, timed-pregnant rats were exposed to lead acetate (0.2% in the drinking water) 24 hrs following birth at postnatal day 1 (PND 1). Dams and pups were continuously exposed to lead through the drinking water of the dam until PND 20. Postnatal exposure in the pups resulted in altered mRNA levels of the following apoptotic and neurotrophic factors: caspase 2 and 3, bax, bcl-x, and brain-derived neurotrophic factor (BDNF). Ribonuclease protection assays were conducted to measure the factors simultaneously at the following postnatal time points: 9, 12, 15, 20, and 25 days. Our results suggest a brain region- and time-specific response following lead acetate exposure. The region most vulnerable to alterations occurs in the hippocampus with alterations beginning at PND 12 in which caspase 3, bcl-x, and BDNF increase with lead exposure. Significant treatment effects were not observed for both the cortex and cerebellum.

Journal ArticleDOI
TL;DR: It is suggested that Zn coadministration might alleviate toxic effects of Pb on the male reproductive system, whereas it could enhance the toxicity on thyroid function.
Abstract: In order to investigate the effects of Zn on Pb toxicities. Proportion of abnormal sperm, percentage of micronucleated polychromatic erythrocyte (MPCE), serum thyroid hormones (T3, T4) and cortisol were measured. Rats received intraperitoneal injection of 25 mg/kg Pb acetate, 4 mg/kg Zn acetate, both Pb acetate and Zn acetate, or normal saline as controls, once every two days, 7 times in total. No significant differences in whole blood Pb were detected between groups received Pb alone or both Pb and Zn. On the contrary, the concentration of whole blood Zn in the group given Zn alone was significantly higher than that in the group that received both Pb and Zn. In the groups given Pb alone or both Pb and Zn, proportion of abnormal sperm, frequency of MPCE and serum cortisol were significantly higher than those in controls, whereas serum T3 and T4 were significantly lower than in controls. In the group given both Pb and Zn, T4 was decreased most obviously among the four groups. While the proportion of abnormal sperm was less in the group given both Pb and Zn than in the group given Pb alone. These findings suggest that Zn coadministration might alleviate toxic effects of Pb on the male reproductive system, whereas it could enhance the toxicity on thyroid function. Zn did not affect the toxicities of Pb on cytogenetic systems as indicated by MPCE percentage, and on serum cortisol levels under the dose of the present study. Our results suggested the double-edged effects of Zn on Pb toxicities in different organs. Therefore, the effects of Zn on Pb toxicities should be evaluated systematically.

Journal Article
TL;DR: Data imply that synbiotic fermented milk containing honey, garlic, ginseng, cod liver oil and chicory inulin may play a role in protection against lead acetate contamination in rats by increasing the activity of the enzyme GST that requires the antioxidant glutathione as substrate, thus protecting the liver against the oxidative damage.
Abstract: The present study investigated some biological effects of synbiotic fermented milk in rats receiving lead acetate in drinking water. Synbiotic fermented milk was prepared by mixing probiotic fermented milk with honey, garlic, ginseng, cod liver oil and chicory inulin. Glutathione-S-transferase (GST), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were estimated in rats receiving lead acetate alone and in rats receiving lead acetate and synbiotic milk, in addition to the negative control group. The obtained results showed a significant increase in the activities of ALT and AST in sera of rats receiving lead acetate compared with the negative control. The activities of ALT and AST increased from an average of 23.0 to 37.3 and from 160 to 220 IU/L, respectively. The activities of these enzymes in rats receiving lead together with the synbiotic milk were almost similar to the activities of the enzymes of rats fed basal diet (negative control). The mean values of ALT and AST in lead-treated group fed synbiotic fermented milk were 25±3.6 and 156±21.36 IU/L compared with the positive control 37.33±2.51 and 220.66±28.88 IU/L respectively. The obtained results showed that GST activity in sera of rat fed on synbiotic fermented milk was increased with mean value of 23.438 M/min compared with negative and positive controls with mean values of 12.01 and 13.95 M/min respectively. Data imply that synbiotic fermented milk containing honey, garlic, ginseng, cod liver oil and chicory inulin may play a role in protection against lead acetate contamination in rats by increasing the activity of the enzyme GST that requires the antioxidant glutathione as substrate, thus protecting the liver against the oxidative damage.

Journal ArticleDOI
TL;DR: Results show that lead exposure affects the serotonergic innervation of the SCO, and the enhancement of SCO secretion suggests a role of this gland in neuroprotection and lead detoxification of the brain in Meriones shawi.

Journal Article
TL;DR: Airways are the primary target of lead exposure from atmospheric pollution, its effect on airway smooth muscle and their responsiveness to bronchoactive agents is not clearly understood and the involvement of airway epithelium was examined.
Abstract: Airways are the primary target of lead exposure from atmospheric pollution, its effect on airway smooth muscle and their responsiveness to bronchoactive agents is not clearly understood. In the present investigation the effect of lead on the isolated airway smooth muscle activity was studied in organ bath set-up. Further the involvement of airway epithelium was examined and the responsiveness of airway smooth muscle to adenosine, acetylcholine (bronchoconstrictors) and isoproterenol (bronchodilator) was also investigated. Lead in concentration of 10(-12) M to 10(-4) M produced concentration-dependant contractile response in rat tracheal rings. Acetylcholine and adenosine induced concentration-dependent contractile response was slightly inhibited after lead exposure. The relaxant response to isoproterenol was also inhibited in lead exposed tissues. Epithelium removal did not significantly change the contractile response to lead suggesting that the lead induced contraction of airway smooth muscle is epithelium independent.

Journal ArticleDOI
TL;DR: Results showed that fresh garlic extract and garlic tablet had almost same effects on lead reduction in tissues.
Abstract: Garlic ability to reduce lead burden in body tissues before and during chronic lead toxicity was studied. Eighty mice were divided into 8 groups. Group D received placebo. Groups A1, A2 and A3, respectively received 500, 250 and 125 mg kg(-1) day garlic and Groups B1, B2 and B3, respectively 1/4, 1/8 and 1/16 garlic tablet kg(-1) day in first four weeks and in second four weeks they received 5 mg kg(-1) day lead acetate plus garlic or garlic tablet. Group C received placebo in first four weeks and in second four weeks they received 5 mg kg(-1) day lead acetate and placebo. Reduction in lead burden of kidney, liver, bone and blood (except for group A3) in experimental groups was significant compared with group C (p<0.05). Results showed that fresh garlic extract and garlic tablet had almost same effects on lead reduction in tissues.

Journal ArticleDOI
TL;DR: The results of the present study suggested the antioxidant and protective efficacy of spirulina and L iv-52 against lead induced toxicity in albino rats.
Abstract: Objective: The present study was carried out to evaluate the antioxidant property of spirulina and L i v-52 against lead induced toxicity in albino rats. Materials and methods: The antioxidant property of spirulina and L iv-52 was investigated by using lead acetate to induce toxicity in albino rats. The extent of lipid peroxidaiton in terms of thiobarbituric acid reactive susbstances (TBARS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and reduced glutathine (GSH) were assayed in the liver and kidney homogenate. Results: Oral administration of lead (10mg/kg body weight/day) as lead acetate for 30 days resulted in a significant increase (P<0.01) in the level thiobarbituric acid reactive substances (TBARS) and a decrease in the level of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) when compared to normal control. Administration of both spirulina and L iv-52 produced a pronounced protective effect (P<0.01) in respect to these parameters when compared to their individual administration in lead intoxicated rats. Conclusion: The results of the present study suggested the antioxidant and protective efficacy of spirulina and L iv-52 against lead induced toxicity in albino rats.

Journal ArticleDOI
01 Jun 2007
TL;DR: In conclusion, the results of different parameters studied in rats received orally vitamin C or selenium showed improvement compared with the rats orally received lead.
Abstract: The objective of this study was to explore whether Vitamin C or selenium could be protective against the toxic effect of lead acetate. To achieve this purpose, certain hematological and biochemical parameters were studied. Twenty male albino rats (Rattus norvegicus), weighing about 130-150 gram were used. The rats were divided into four groups, each group included five rats. The first group was the control, the second group was administrated orally lead acetate (20 mg / kg of the body weight / day/four weeks), the third group was administrated orally with the same dose of lead acetate plus vitamin C (50 mg/kg body weight/ day/four weeks), the fourth group was given the same dose of lead acetate as the second group and plus sodium selenate in a dose of (0.1 mg /kg body weight/ day/four weeks). Food and water were allowed adlibitum for all the groups. The experimental period was four weeks. The results showed that there was a significant decrease in hematological indices studied in the second group (red blood count, white blood count, and hemoglobin concentration and haematocrit value) after the administration of lead acetate. Moreover, there were higher significantly increase in serum glucose, total lipids, cholesterol, urea and creatinine compared with the control group. The third group showed improvement in the hematological parameters,(red blood& white blood count ,hemoglobin concentration and haematocrit value ).Also improvement in the biochemical parameters of serum glucose ,total lipids ,cholesterol ,urea and creatinine compared to second group. The fourth group showed significant improvement compared with the second group. In addition, a significant decrease in serum glucose, total lipids, total cholesterol, urea and creatinine were found of this group. In conclusion, the results of different parameters studied in rats received orally vitamin C or selenium showed improvement compared with the rats orally received lead.

Journal ArticleDOI
TL;DR: The increased MAO activity by lead intoxication may contribute to the neurobehavioral changes such as cognitive and attention deficit as well as hyperactivity, which is commonly observed both in lead intoxication and perturbed monoaminergic neurotransmission.

Journal Article
TL;DR: Results show that cerebral oligemic hypoxia combined with acute lead exposure may cause selective and long-lasting impairment in memory function.

Journal ArticleDOI
TL;DR: Pectin treatment promoted the decrease in lead content in the liver, reduction of LPO activity, and recovery of parameters of lipid metabolism in mice treated with enteral treatment with lead acetate.
Abstract: Study of the effects of low-esterified pectin in toxic damage to the liver caused by enteral treatment with lead acetate showed that pectin treatment promoted the decrease in lead content in the liver, reduction of LPO activity, and recovery of parameters of lipid metabolism.

Journal ArticleDOI
TL;DR: It is suggested that Zn plays an important role in regulating the liver marker enzymes and essential elements under conditions of Pb toxicity and protein deficiency.
Abstract: This study was designed to determine the protective effects of zinc (Zn) using liver marker enzymes in the serum and liver along with hepatic elemental profile in lead (Pb)-treated protein-deficient (PD) Sprague–Dawley male rats. Zn in the form of zinc sulfate at a dose of 227 mg L−1 in drinking water was administrated to control, PD as well as Pb-treated PD rats for 8 weeks. Pb treatment was given orally as lead acetate at a dose level of 100 mg kg−1 body weight to control and PD rats. The effects of different treatments were studied on the activities of enzymes that included alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum. The status of different elements (Cl, K, Mn, Fe, Cu, Zn, Se, Rb, Pb) in liver was also studied. Rats given PD diet and Pb showed significant inhibition in serum ALP activity associated with significant elevation in both AST and ALT activities. Serum ALP activity showed a significant inhibition week 1 until week 8 in Pb-treated P...

Journal Article
TL;DR: Lead has an effect on thyroid hormones, causing damage to thyroid function by inhibiting deiodination of T4 and increasing the activity of MAO and acetylcholineasterase and in this way changes the pattern of releasing TSH.
Abstract: Introduction: Lead is a heavy metal that could be an environmental pollutant. It is a natural metal that exists in water and soil, enters the body through digestive or respiratory systems. The researches showed that various amounts of lead has some effects on the endocrine glands and metabolic activities of the body. So, in this research, we studied and compared the effects of different amounts of lead on thyroid gland and liver enzymes in adult male rats. Methods: 40 adult male wistar rats were studied in the from of experimental, sham and control groups. Experimental group was in divided into three subgroups and received lead acetate 25, 50, 100 (mg/kg) by oral rate, in fifteen days. Sham groups received distilled water and control group received nothing. At the end of the fifteenth day, blood samples were taken and concentrations of T3, T4, TSH, AST, ALT and ALP were measured. Results: The assessed results using Tukey test were studied. The findings after statistical analysis showed that concentration of T3 hormone and enzymes of AST, ALT by receiving various amounts of lead acetate in comparison with control group show no significant difference, but concentration of TSH and ALP showed a significant reduction. Conclusion: According to above results and to findings and studies made by other researchers, lead has an effect on thyroid hormones, causing damage to thyroid function by inhibiting deiodination of T4. Lead decreases the activity of MAO and acetylcholineasterase and in this way changes the pattern of releasing TSH. It decreases the release of TSH hormone by inhibition of dopamine uptake. We may conclude that lead has some toxic effect on thyroid function and the liver as well.

Journal Article
TL;DR: In this article, the authors evaluated the lead discharging effects of apple polyphenol (AP) on male Kunming mice given lead by intraperitoneal injection for 10 days.
Abstract: The purpose of this paper was to evaluate the lead discharging effects of apple polyphenol (AP) on male Kunming mice given lead. Lead acetate was administered by intraperitoneal injection for 10 days. Administration of AP to mice by gastric incubation was performed for 15 days from the end of lead exposure up to the end of the experiment. Then, the mice were sacrificed for comparison of lead distribution. Concentrations of lead in the specimens were determinated by graphite furnace atomic absorption spectrophotometry. It was observed that the blood lead, the liver lead and the femur level significantly decreased, but urinates lead elimination significantly increased. The results illustrated that AP could discharge lead .

Journal ArticleDOI
TL;DR: It is suggested that exposure to lead causes spatial memory deficits in male rats and a significant reduction in cyclooxygenase‐2 immunoreactivity in the CA1 and dentate gyrus areas of the hippocampus.
Abstract: Chronic lead exposure during development is known to produce learning deficits. In the present study, we investigated the effects of developmental exposure to lead on spatial memory, as shown in the Morris water maze, and on expression of inducible cyclooxygenase-2 protein in the hippocampi of male rats. Rats were separated into four groups according to which concentration of lead acetate at which developmental stage they were exposed. One group was exposed maternally to lead acetate at a concentration of 250 parts per million (ppm), one group was exposed continuously to 250 ppm lead, one group was exposed maternally to 750 ppm lead, and one group was exposed continuously to 750 ppm lead. Increases were observed in both average escape latency and traveled distance of the rats in the maternally and continuously 750 ppm lead-exposed groups, indicating significant impairment of spatial memory. Quantitative immunostaining analysis by optical density measurement of brain sections from rats in all lead-exposed groups revealed a significant reduction (P < 0.001) in the intensity of cyclooxygenase-2 immunoreactivity in the Ammon's horn region 1 (CA1) and the dentate gyrus areas of the hippocampus. This reduction was concentration-dependent, with the maximum reduction observed in rats exposed to 750 ppm lead. Taken together, these findings suggest that exposure to lead causes spatial memory deficits in male rats and a significant reduction in cyclooxygenase-2 immunoreactivity in the CA1 and dentate gyrus areas.

Journal ArticleDOI
TL;DR: The results show that pectin helps to rapidly reduce lead concentration in liver, to decrease lipid peroxidation, and to normalize the levels of total cholesterol and triglycerides in blood serum and liver.
Abstract: The effects of pectin from the eelgrass Zostera marina on toxic liver injury induced by enteral administration of lead acetate are examined in experiments on rats. The results show that pectin helps to rapidly reduce lead concentration in liver, to decrease lipid peroxidation, and to normalize the levels of total cholesterol and triglycerides in blood serum and liver.

14 Dec 2007
TL;DR: In this article, the authors focused on the activity of superoxide dismutase (SOD) in Mona and Syrena cultivars plantlets of Lactuca sativa L. obtained from seeds treated with lead acetate.
Abstract: Our study is focused on the activity of superoxide dismutase (SOD) in Mona and Syrena cultivars plantlets of Lactuca sativa L. obtained from seeds treated with lead acetate. Total activity of SOD in Mona cultivar show an inhibition at all tested concentrations of lead acetate. For Syrena cultivar, the lead acetate shows a slowly stimulative effect of activity SOD only in the first two concentration of the three used.

Journal Article
TL;DR: It was observed that the nut milk extract contains flavanoids, phenols and carbohydrates and the drug was effective against lead acetate induced toxicity and after the treatment of Semecarpus anacardium the liver damage decreased.
Abstract: The present study was carried out to understand the antioxidant and protective effect of Semecarpus anacardium against lead acetate induced toxicity. This was done by analyzing the phytochemicals (Flavanoids, alkaloids, resins, tannins, carbohydrates, proteins, etc.) present in the plant and by assessing the hepatoprotective efficacy of the plant against lead acetate induced albino rats. Histopathological examination was also carried out to have a supporting evidence for the study. It was observed that the nut milk extract contains flavanoids, phenols and carbohydrates and the drug was effective against lead acetate induced toxicity. The levels of the marker enzymes were increased in the lead acetate induced rats and after the treatment of Semecarpus anacardium the liver damage decreased.