scispace - formally typeset
Search or ask a question

Showing papers on "Lead acetate published in 2014"


Journal ArticleDOI
TL;DR: The administration of Omega-3 provided significant protection against lead acetate toxicity and induced hyperlipidemia via increasing of lipid profiles associated with decline in HDL-c level.
Abstract: The present study was conducted to investigate the protective role of Omega-3 polyunsaturated fatty acids against lead acetate-induced toxicity in liver and kidney of female rats. Animals were divided into four equal groups; group 1 served as control while groups 2 and 3 were treated orally with Omega-3 fatty acids at doses of 125 and 260 mg/kg body weight, respectively, for 10 days. These groups were also injected with lead acetate (25 mg/kg body weight) during the last 5 days. Group 4 was treated only with lead acetate for 5 days and served as positive control group. Lead acetate increased oxidative stress through an elevation in MDA associated with depletion in antioxidant enzymes activities in the tissues. Moreover, the elevation of serum enzymes activities (ALT, AST, ALP, and LDH) and the levels of urea and creatinine were estimated but total proteins were decreased. Also, lead acetate-treatment induced hyperlipidemia via increasing of lipid profiles associated with decline in HDL-c level. Significant changes of Hb, PCV, RBCs, PLT, and WBCs in group 4 were recorded. The biochemical alterations of lead acetate were confirmed by histopathological changes and DNA damage. The administration of Omega-3 provided significant protection against lead acetate toxicity.

99 citations


Journal ArticleDOI
TL;DR: Cinnamon exhibited protective effect on reproductive system by inhibiting lead acetate induced oxidative stress and excessive cell apoptosis and improved the level of SOD and catalase activities in male rats.
Abstract: The aim of this study was to investigate the protective effects of cinnamon on lead acetate induced reproductive toxicities in rats. Thirty-two male rats were randomly divided into 4 groups, 8 rats in each. Control rats received distilled water, while treated rats received lead acetate (30 mg/kg), cinnamon (250 mg/kg) and lead acetate and cinnamon (30 mg/kg and 250 mg/kg) for 60 days by gavage tube. In cinnamon treated rats, the relative weights of testes, epididymis, seminal and prostate glands were significantly (P < 0.05) increased compared with that in lead acetate treated rats. Sperm cell concentration and viability were significantly (P < 0.05) reduced, while sperm abnormalities were significantly (P < 0.05) increased in lead treated rats. The superoxide dismutase (SOD) and catalase activities were significantly reduced (P < 0.001) in lead acetate treated rats compared to the other groups, while the addition of cinnamon to lead acetate improved the level of SOD compared to the lead treated group. There was a marked reduction (P < 0.001) in the expression of androgen receptor and significant (P < 0.001) increase in the level of caspase-3 protein expression in the testis of lead treated rats. In conclusion, cinnamon exhibited protective effect on reproductive system by inhibiting lead acetate induced oxidative stress and excessive cell apoptosis.

92 citations


Journal Article
TL;DR: Results suggested that low-dose exposure to Pb and Cd can cause significant hepatic and renal apoptosis and finally impair their function.
Abstract: The combined subchronic effects of exposure to lead acetate and cadmium chloride on apoptosis protein expression were detected in the liver and kidney of rats to investigate the hazards of environmentally relevant, low-dose exposure to these compounds. The TUNEL assay showed that there were increased numbers of apoptotic cells. Immunohistochemical tests showed increased numbers of positive cells under Bax and caspase-3 protein detection and decreased Bcl-2 protein. Furthermore, mitochondrial injury and increased numbers of apoptotic cells with condensed nuclei were observed by TEM. These results suggested that low-dose exposure to Pb and Cd can cause significant hepatic and renal apoptosis and finally impair their function. Hepatic and renal apoptosis induced by low-dose exposure is associated with mitochondrial injury and changes in levels of apoptogenic proteins, such as Bcl-2, Bax, and caspase-3.

74 citations


Journal ArticleDOI
TL;DR: It is concluded that lead affects the general immune status of C. punctatus and renders the fish immunocompromised and susceptible to pathogens.

71 citations


Journal ArticleDOI
TL;DR: Experimental animals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyte antioxidant defence system via free radical generation and oxidative stress.

65 citations


Journal ArticleDOI
TL;DR: Critical involvement of microglial activation in mediating the neurotoxicity associated with lead exposure is brought forth.
Abstract: Lead is one of the major pollutants of environment and is highly toxic to the functioning of central nervous system (CNS). The chronic exposure of this heavy metal is debilitating to the functional behavior of an organism. Studies have shown that acute exposure to Pb can lead to glial activation and secretion of cyto-chemokines in both in vitro and in vivo models. However, the cellular source of secretion of these cyto-chemokines remains to be identified. Microglia are monocytes of the brain, and are primary source of cytokine secretion in the CNS. We hypothesized that microglia exposed to Pb can secrete cyto-chemokines, thereby resulting in subsequent neuronal death. Our studies show that stimulation of BV-2 mouse microglia with 10μМ dose of Pb resulted in up-regulation of extracellular signal-regulated kinase (ERK) and protein kinase B (Akt) pathways, along with activation of an important transcription factor, nuclear factor-κB (NF-κB). Further, we found that the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), and cyclooxygenase-2 (COX-2) pro-inflammatory enzyme were increased in response to Pb exposure. Furthermore, treatment with conditioned media from Pb treated BV-2 cells lead to neuronal death in neuroblastoma cells, which potentially involved the activation of caspase-3 enzyme. In all, the current study brings forth critical involvement of microglial activation in mediating the neurotoxicity associated with lead exposure.

63 citations


Journal Article
TL;DR: Exposure to sodium arsenite and mercuric chloride lead to more pronounced oxidative stress and hepatotoxicity while lead acetate caused significant alterations in haem synthesis pathway compared to two other thiol binding metal/metalloid.
Abstract: Globally, arsenic, mercury and lead constitutes as the three most hazardous environmental toxicants perturbing imbalance in pro—oxidant and antioxidant homeostasis. Individual toxicity of these environmental toxicants is well known but there is lack of comparative data on variables indicative of oxidative stress. We thus investigated the effects of chronic exposure to sodium arsenite, mercuric chloride and lead acetate on blood and tissue oxidative stress, metal concentration and metallothionein (MT) contents. Male rats were exposed to sodium arsenite, mercuric chloride and lead acetate (0.05 mg/kg each, orally, once daily) for 6 months. Arsenic, mercury and lead exposure led to a significant inhibition of blood δ—aminolevulinic acid dehydratase (ALAD) activity and glutathione level supported by increased thiobarbituric acid reactive substance (TBARS). The level of inhibition was more pronounced in case of lead followed by mercury and arsenic. These metals/ metalloid significantly increased reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS) and glutathione peroxidase (GPx) activity accompanied by a decreased superoxide dismutase (SOD), catalase and reduced and oxidized glutathione (GSH and GSSG) levels in blood and tissues. Mercury alone produced a significant induction of hepatic and renal MT concentrations. Serum transaminases, lactate dehydrogenase and alkaline phosphatase activities increased significantly on exposure to arsenic and mercury exposure suggesting liver injury which was less pronounced in case of lead exposure. These biochemical alterations were supported by increased arsenic, mercury and lead concentrations in blood and soft tissues. The present study suggests that exposure to sodium arsenite and mercuric chloride lead to more pronounced oxidative stress and hepatotoxicity while lead acetate caused significant alterations in haem synthesis pathway compared to two other thiol binding metal/metalloid.

54 citations


Journal ArticleDOI
TL;DR: This is the first demonstration that blood Pb(2+) (12µg/dl) concentrations below the WHO-established values increased systolic blood pressure and vascular phenylephrine reactivity.

52 citations


Journal ArticleDOI
TL;DR: Treatment of rats with lead acetate was shown to produce degeneration of endothelial lining of brain blood vessels with peri-vascular cuffing of mononuclear cells consistent to lymphocytes, congestion of choroid plexus blood vessels, ischemic brain infarction, chromatolysis and neuronal degeneration, microglial reaction and neuronophagia, degenerations of hippocampal and cerebellar neurons, and axonal demyelination.

52 citations


Journal ArticleDOI
TL;DR: In this article, a green recycling process was investigated to prepare lead acetate trihydrate precursors and novel ultrafine lead oxide from spent lead acid battery pastes, which showed good reversibility and cycle stability.

50 citations


Journal ArticleDOI
TL;DR: The results indicated that ethanolic extract of F. parviflora leaves has a potential to restore the suppressed reproduction associated with lead exposure and prevented lead‐induced testicular toxicity in male Wistar rats.
Abstract: Summary In recent years, the clinical importance of herbal drugs has received considerable attention in reducing free radical-induced tissue injury. Oxidative stress has been proposed as a possible mechanism involved in lead toxicity that causes reproductive system failure in both human and animals. Fumaria parviflora L., a traditional herb, has been used to cure various ailments in Persian folk medicine. This study was carried out to investigate whether ethanolic extract of F. parviflora leaves could protect the male rats against lead-induced testicular oxidative stress. Adult Wistar rats were treated with 0.1% lead acetate in drinking water with or without 200 mg kg day−1 F. parviflora extract via gavage for 70 days. Lead acetate treatment resulted in significant reduction in testis weight, seminiferous tubules diameter, epididymal sperm count, serum testosterone level, testicular content of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Moreover, significant elevation was observed in content of malondialdehyde (MDA) in lead-treated rats. However, co-administration of F. parviflora extract showed a significant increase in selected reproductive parameters in lead-treated rats. The results indicated that ethanolic extract of F. parviflora leaves has a potential to restore the suppressed reproduction associated with lead exposure and prevented lead-induced testicular toxicity in male Wistar rats.

Journal ArticleDOI
07 Jul 2014-PLOS ONE
TL;DR: It is suggested that lead has a negative impact on spine outgrowth in the developing hippocampus through altering the canonical Wnt pathway.
Abstract: Lead (Pb) exposure has been implicated in the impairment of synaptic plasticity in the developing hippocampus, but the mechanism remains unclear. Here, we investigated whether developmental lead exposure affects the dendritic spine formation through Wnt signaling pathway in vivo and in vitro. Sprague–Dawley rats were exposed to lead throughout the lactation period and Golgi-Cox staining method was used to examine the spine density of pyramidal neurons in the hippocampal CA1 area of rats. We found that lead exposure significantly decreased the spine density in both 14 and 21 days-old pups, accompanied by a significant age-dependent decline of the Wnt7a expression and stability of its downstream protein (β-catenin). Furthermore, in cultured hippocampal neurons, lead (0.1 and 1 µM lead acetate) significantly decreased the spine density in a dose-dependent manner. Exogenous Wnt7a application attenuated the decrease of spine density and increased the stability of the downstream molecules in Wnt signaling pathway. Together, our results suggest that lead has a negative impact on spine outgrowth in the developing hippocampus through altering the canonical Wnt pathway.

Journal ArticleDOI
Yi Liu1, Pengran Gao1, Xianfu Bu1, Guizhi Kuang1, Wei Liu1, Lixu Lei1 
TL;DR: In this paper, a nanocrystalline lead sulphate can be used as excellent negative active material in lead acid batteries, which can be obtained by a facile chemical precipitation of aqueous lead acetate and sodium sulphate in a few minutes, look like crosses with diameter of each arm being 100nm to 3μm.

Journal Article
TL;DR: Results indicate that combining Pb with Cd induces bone damage and increases the risk of osteoporosis, and co-induction of Pb and Cd results in bone microstructure damage, especially to trabecular bone, marrow cavity, collagen fiber, and osteoblast.
Abstract: This study aims to investigate the effects of low-dose subchronic exposure to lead acetate (Pb(NO3)2) and cadmium chloride (CdCl2·2.5H2O) on bone in rats. The rats were assigned randomly to a control group and three experimental groups that were given the mixture of Pb(NO3)2 and CdCl2·2.5H2O by gastric gavage at doses of 0 mg/kg body weight (b.w.) (Group I, to serve as a control), 29.96 mg/kg b.w. (Group II, 29.25+0.71), 89.88 mg/kg b.w. (Group III, 87.74+2.14), and 269.65 mg/kg b.w. (Group IV, 263.23+6.42) for at least 90 consecutive days. Calcium (Ca) and phosphorus (Pi) contents in the bone were determined. Bone mineral density (BMD) was measured at the tibia and femur region by dual-energy X-ray absorbsiometry. The histopathology of bone was evaluated by light microscope, scanning electron microscope, and transmission electron microscope. The BMD of rats in the experimental group was significantly lower and the contents of Ca and Pi were decreased than those in the control group. The histopathological evaluation showed that co-induction of Pb and Cd results in bone microstructure damage, especially to trabecular bone, marrow cavity, collagen fiber, and osteoblast. In general, results indicate that combining Pb with Cd induces bone damage and increases the risk of osteoporosis.

Journal ArticleDOI
TL;DR: The findings in the PP model allow us to hypothesize that ingestion of common phenolics such as FA may significantly alleviate the neurotoxic effects of Pb which may be largely attributed to its ability to abrogate oxidative stress.
Abstract: Epidemiological evidence has shown higher susceptibility of Children to the adverse effects of lead (Pb) exposure. However, experimental studies on Pb-induced neurotoxicity in prepubertal (PP) rats are limited. The present study aimed to examine the propensity of ferulic acid (FA), a commonly occurring phenolic acid in staple foods (fruits, vegetables, cereals, coffee etc.) to abrogate Pb-induced toxicity. Initially, we characterized Pb-induced adverse effects among PP rats exposed to Pb acetate (1,000–3,000 ppm in drinking water) for 5 weeks in terms of locomotor phenotype, activity of 5-aminolevulinic acid dehydratase (ALAD) in the blood, blood Pb levels and oxidative stress in brain regions. Further, the ameliorative effects of oral supplements of FA (25 mg/kg bw/day) were investigated in PP rats exposed to Pb (3,000 ppm). Pb intoxication increased the locomotor activity and FA supplements partially reversed the phenotype, while the reduced ALAD activity was also restored. FA significantly abrogated the enhanced oxidative stress in cerebellum (Cb) and hippocampus (Hc) as evidenced in terms of ROS generation, lipid peroxidation and protein carbonyls. Further, Pb-mediated perturbations in the glutathione levels and activity of enzymic antioxidants were also markedly restored. Furthermore, the protective effect of FA was discernible in striatum in terms of reduced oxidative stress, restored cholinergic activity and dopamine levels. Interestingly, reduced activity levels of mitochondrial complex I in Cb and enhanced levels in Hc among Pb-intoxicated rats were ameliorated by FA supplements. FA also decreased the number of damaged cells in cornu ammonis area CA1 and dentate gyrus as reflected by the histoarchitecture of Hc among Pb intoxicated rats. Collectively, our findings in the PP model allow us to hypothesize that ingestion of common phenolics such as FA may significantly alleviate the neurotoxic effects of Pb which may be largely attributed to its ability to abrogate oxidative stress.

Journal ArticleDOI
TL;DR: Investigation of the efficacy of quercetin against lead-induced neurotoxicity in Wistar rats found it mitigates the toxic effect of lead effectively and thus, may be an important compound for developing effective therapeutic intervention against metal toxicity.

Journal ArticleDOI
TL;DR: Treatment with the hydroalcoholic seed extract of C. sativum resulted in a tissue-specific amelioration of oxidative stress produced by lead, indicating lead-induced oxidative stress.
Abstract: Lead exposure is known to cause apoptotic neurodegeneration and neurobehavioral abnormalities in developing and adult brain by impairing cognition and memory. Coriandrum sativum is an herb belonging to Umbelliferae and is reported to have a protective effect against lead toxicity. In the present investigation, an attempt has been made to evaluate the protective activity of the hydroalcoholic extract of C. sativum seed against lead-induced oxidative stress. Male Wistar strain rats (100–120 g) were divided into four groups: control group: 1,000 mg/L of sodium acetate; exposed group: 1,000 mg/L lead acetate for 4 weeks; C. sativum treated 1 (CST1) group: 250 mg/kg body weight/day for seven consecutive days after 4 weeks of lead exposure; C. sativum treated 2 (CST2) group: 500 mg/kg body weight/day for seven consecutive days after 4 weeks of lead exposure. After the exposure and treatment periods, rats were sacrificed by cervical dislocation, and the whole brain was immediately isolated and separated into four regions: cerebellum, hippocampus, frontal cortex, and brain stem along with the control group. After sacrifice, blood was immediately collected into heparinized vials and stored at 4 °C. In all the tissues, reactive oxygen species (ROS), lipid peroxidation products (LPP), and total protein carbonyl content (TPCC) were estimated following standard protocols. An indicator enzyme for lead toxicity namely delta-amino levulinic acid dehydratase (δ-ALAD) activity was determined in the blood. A significant (p < 0.05) increase in ROS, LPP, and TPCC levels was observed in exposed rat brain regions, while δ-ALAD showed a decrease indicating lead-induced oxidative stress. Treatment with the hydroalcoholic seed extract of C. sativum resulted in a tissue-specific amelioration of oxidative stress produced by lead.

Journal ArticleDOI
TL;DR: Tunel assay showed that TUNEL assay can be used to determinate DNA fragmentation in somatic cells of rat liver and concluded that lead acetate may be considered as a strong hepatotoxic and genotoxic agent.
Abstract: Lead toxicity is probably the most common form of heavy metal intoxication. The present study was conducted to assess the histopathological and cytotoxic effects of lead exposure on rat liver. Adult male Wistar rats were randomly divided in 2 groups. The first was exposed to 2 g of lead acetate in distilled water during 35 days, while the second served as a control group and was given distilled water. The structural damage in the liver was investigated by histological study and supplemented by biochemical assay of liver enzyme levels. DNA fragmentation in somatic cells was determined using terminal desoxynucleotidyl transferase mediated dUTP nick end-labeling (TUNEL) assay. The results obtained show increase in liver enzyme levels in treated rats compared to controls. The histological study showed that lead can induce several alterations such as hypertrophy of hepatocytes, portal space and central vein dilatation, vacuolation and lymphocytic infiltration. Tunel assay revealed significant DNA fragmentation in rats exposed to lead. This study showed that TUNEL assay can be used to determinate DNA fragmentation in somatic cells of rat liver. Moreover, we conclude that lead acetate may be considered as a strong hepatotoxic and genotoxic agent.

Journal ArticleDOI
TL;DR: Direct interactions of lead with sex hormones are presented and a possible mechanism on lead induced reproductive toxicity at the molecular level is obtained.
Abstract: Lead exposure could induce endocrine disruption and hormonal imbalance of humans, resulting in detrimental effects on the reproductive system even at low doses. However, mechanisms of lead actions remain unknown. This article investigated lead interactions with human chorionic gonadotropin (HCG) as a conceivable mechanism of its reproductive toxicity by spectroscopic technique, isothermal titration calorimetry (ITC), molecular docking study, and enzyme-linked immunosorbent assay (ELISA). Fluorescence measurements showed that lead acetate dynamically quenched intrinsic fluorescence of HCG through collisional mechanism with the association constant (KSV) in the magnitude of 103 L/mol at the detected temperatures (298, 303, and 310 K). ITC and molecular docking results revealed lead acetate could bind into 5 binding sites of HCG through electrostatic effects (ΔH 0) and hydrophobic forces (ΔH > 0, ΔS > 0). The conformational investigation of HCG by UV–vis absorption spectroscopy, circular dichroism ...

Journal ArticleDOI
TL;DR: Administration of M. oleifera restored all the parameters back to control, tissue-specifically, and also showed improvement in restoration better than DMSA treatment, indicating reduction of the negative effects of lead-induced oxidative stress.
Abstract: Moringa oleifera is a tree belonging to Moringaceae family and its leaves and seeds are reported to have ameliorative effects against metal toxicity. In the present investigation, M. oleifera seed powder was tested against lead-induced oxidative stress and compared against meso-2, 3-dimercaptosuccinic acid (DMSA) treatment. Male Wistar rats (100-120 g) were divided into four groups: control (2000 ppm of sodium acetate for 2 weeks), exposed (2000 ppm of lead acetate for 2 weeks), Moringa treated (500 mg/kg for 7 days after lead exposure), and DMSA treated (90 mg/kg for 7 days after lead exposure). After exposure and treatment periods, rats were sacrificed and the brain was separated into cerebellum, hippocampus, frontal cortex, and brain stem; liver, kidney, and blood were also collected. The data indicated a significant (p<0.05) increase in reactive oxygen species (ROS), lipid perioxidation products (LPP), total protein carbonyl content (TPCC), and metal content of brain regions, liver, and kidney in the exposed group compared with their respective controls. In the blood, delta-amino levulinic acid dehydratase (ALAD) activity, RBC, WBC, hemoglobin, and hematocrit showed significant (p<0.05) decrease on lead exposure. However, administration of M. oleifera restored all the parameters back to control, tissue-specifically, and also showed improvement in restoration better than DMSA treatment, indicating reduction of the negative effects of lead-induced oxidative stress.

Journal ArticleDOI
TL;DR: It is suggested that Bacopa monniera can mitigate the lead induced-oxidative stress tissue specifically by pharmacologic interventions which encompass both chelation as well as antioxidant functions.
Abstract: Bacopa monniera is a rejuvenating herb for brain cells enhancing learning and cognitive ability. In the present investigation, the ameliorative effects of Bacopa monniera were examined against lead-induced oxidative stress in different regions of rat brain. Male rats were divided into five groups: control (1000 ppm sodium acetate) and exposed (1000 ppm lead acetate) for 4 weeks; DMSA (Meso-2,3-Dimercaptosuccinic acid)-treated (90 mg/kg body weight/day); Bacopa monniera-treated (BM) (10 mg/kg body weight/day) and a combination of BM + DMSA for seven consecutive days after 4 weeks of lead exposure. After treatment, the whole brain was isolated by sacrificing rats and four regions were separated namely cerebellum, hippocampus, frontal cortex and brain stem. Results indicated a significant (p < 0.05) increase in reactive oxygen species (ROS), lipid peroxidation products (LPP) and total protein carbonyl content (TPCC) in association with tissue metal content in all the four regions of brain for exposed...

Journal ArticleDOI
TL;DR: Taurine mitigated perturbations in the activities of the antioxidant enzymes and acetylcholinesterase, counteracted oxidative stress and brain lipoperoxidation and attenuated neuronal degeneration induced by joint CPF and LA-induced neurotoxicity, suggesting that TA is neuroprotective following chronic co-exposure of rats to CPF.

Journal ArticleDOI
TL;DR: Sesame oil showed effective hepatoprotective action against lead acetate induced hepatotoxicity in albino mice and populations of high risk to lead should be advised to take sesame oil.
Abstract: The liver performs many vital functions to eliminate toxins and harmful substances from the body. Hepatotoxic agents can react with the basic cellular components and consequently induce almost all types of liver lesions. The aim of this study was to investigate the possible hepatoprotective role of sesame oil against lead acetate induced hepatotoxicity in albino mice from the histological and biochemical aspects. In this study, thirty two adult male albino mice were used for this study and divided into four groups. The first group was control group, the 2nd was the sesame oil group orally received sesame oil (5 ml/kg body wt.), the 3rd group was the experimental and received lead acetate (500 mg /kg diet), the 4th one co-administered lead acetate (500 mg/kg diet) with sesame oil (5 ml/kg body wt.) daily for 30 days. The livers were dissected out, weighted and specimens were taken and processed for light microscopic examinations. Blood samples were obtained for assessment of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and γ- glutamyltransferase activities, serum total proteins and albumin. Results indicate that, in lead treated animals, there were severe structural damage in the liver. The hepatocytes appeared irregularly arranged with disorganization of hepatic architecture. The hepatocytes appeared large with light and foamy cytoplasm filled with numerous vacuole-like spaces. The nuclei appeared with pyknotic nuclei. The central vein appeared dilated and congested with massive hemorrhage extending to the nearby cells. Also, there were focal degenerative and necrotic changes along with inflammatory cell infiltration. Decrease in body weight and increase in liver weight were observed. Biochemically, the serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and γ- glutamyltransferase activities were increased and serum total proteins and albumin were decreased. Co-administration of sesame oil significantly improved the structural changes in the liver and also the serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and γ- glutamyltransferase activities were significantly declined and serum total proteins and albumin were elevated. Conclusion: It can be concluded that, the lead had adverse effects on the liver. Sesame oil showed effective hepatoprotective action against lead acetate induced hepatotoxicity in albino mice. So, the populations of high risk to lead should be advised to take sesame oil.

Journal ArticleDOI
TL;DR: The data suggest that supplementation of Se with NAC can improve the lead-induced biochemical oxidative stress in blood and tissue, the burden of lead on the body, and molecular alterations by recoupment in mean DNA damage.
Abstract: This study was carried out to investigate the in vivo protective role of N-acetylcysteine (NAC) per se, along with selenium (Se), against lead-induced hepatic, nephritic-oxidative, and neuronal-oxidative damage in rats. Lead acetate at a dose of 50 mg/kg body weight administered intraperitoneally for 3 days was preferred as the source of lead. Various oxidative stress markers such as reduced glutathione content, lipid peroxidation, superoxide dismutase, and catalase were measured to determine the degree of oxidative damage and healing due to NAC (50 mg/kg body weight administered orally) and Se (0.5 mg/kg body weight administered orally) and were studied along with the activities of enzymes such as transaminases (aspartate aminotransferase/alanine aminotransferase), δ-aminolevulinic acid dehydratase, δ-aminolevulinic acid synthase, and acetyl cholinesterase activity. The genotoxic effect of lead also was studied in terms of DNA damage using comet assay. The effect of lead was studied in blood biochemical variables such as cholesterol, triglycerides, urea, uric acid, and creatinine. Our data suggest that supplementation of Se with NAC can improve the lead-induced biochemical oxidative stress in blood and tissue, the burden of lead on the body, and molecular alterations by recoupment in mean DNA damage.

Journal ArticleDOI
TL;DR: It is concluded that 65% CR may prevent lead-induced oxidative stress and inflammation in rat liver and reduce liver SOD and GPx and increased MDA and TNF-α in AL animals, but in the CR animals lead injections did not significantly change the measured parameters.
Abstract: The aim of the present study is to investigate the effects of caloric restriction on liver of lead-administered rat. Male Sprague-Dawley rats were randomly divided into two groups: Ad libitum fed group (AL, free access to normal rat chow) and caloric restriction group (CR, fed 65% of AL animals' food intake). After 6 weeks, half of the animals of each group were injected lead acetate and the other half were injected saline. Liver tissue samples were collected at the end of the experiments. Glutathione peroxidase (GPx), superoxide dismutase (SOD), malondialdehyde (MDA), and tumor necrosis factor (TNF-α) were measured in the tissue extracts. Histological studies were also performed. Our results showed that lead administrations (not saline injections) reduced liver SOD and GPx and increased MDA and TNF-α in AL animals, but in the CR animals lead injections did not significantly change the measured parameters. The histological studies supported the biochemical findings. We concluded that 65% CR may prevent lead-induced oxidative stress and inflammation in rat liver.

Journal ArticleDOI
TL;DR: While A. caroliniana removes lead from aqueous solution, the heavy metal causes physiological and biochemical changes by impairing photosynthesis, changing mineral nutrition, and impeding the growth and formation of heterocysts of the symbiotic cyanobacteria that live within leaf cavities of the fronds.

Journal Article
TL;DR: Treatments with simvastatin caused protective effects on renal tissue of mice exposed to lead, however, there was no significant effect on urea and creatinine levels.
Abstract: Background: Lead is known to be a highly toxic heavy metal. There are a limited number of studies investigating the effects of antioxidants on lead-induced kidney damage. Statins are widely used drugs for the treatment of hypercholesterolaemia, but they also have other pleiotropic effects. The aim of this study was to determine the effect of different doses of simvastatin on biochemical and histopathological parameters in mice exposed to lead. Methods: Forty eight adult male mice were randomised into six groups. The control group received no lead. Group II was injected interaperitoneally with 60 mg/kg lead acetate and groups III-VI received intraperitoneally 5-10-20-40 mg/kg simvastatin plus 60 mg/kg lead. After 14 days, a stereological study was done in accordance with the principle of Cavalieri and serum concentrations of urea and creatinine were measured. Data were analyzed using SPSS software and ANOVA. Results: Lead acetate treatment caused collapse of glomeruli, glumerulosclerosis, necrosis and vacuolization in renal tubules. Administration of 20 mg of simvastatin reduced the severity of kidney damage. Glomerular volume in the groups treated with 40 mg of simvastatin was significantly different from the group treated with lead alone (P =0.001). The number of renal glomeruli in the group treated with 5 mg of simvastatin were significantly difference compared to the lead treated group (P =0.027). Serum concentrations of urea and creatinine were not significantly different in the groups treated with simvastatin compared to the group treated with lead alone. Conclusions: Treatments with simvastatin Caused protective effects on renal tissue of mice exposed to lead. However, there was no significant effect on urea and creatinine levels.

Journal ArticleDOI
21 Jul 2014
TL;DR: It could be concluded that chronic exposure to lead imposes a potent toxic effect on liver cells manifested as glycogen depletion, cellular infiltration and liver architecture in the form of initiation of periportal fibrosis that may progress to liver cirrhosis.
Abstract: Lead is one of the most well-known naturally occurring environmental heavy metals. This experimental study was designed to evaluate lead induced toxic effects on hepatocytes and lobular architecture as judged microscopically. Material and Methods: This study was conducted in anatomy department, Benha faculty of medicine, Benha University, Egypt from May to October 2013 on 30 normal adult albino rats divided into 3 groups; one control and 2 experimental groups. The experimental groups were given 0.13% lead acetate solution in drinking water for 4 and 8 weeks, respectively. Animals were scarified and livers were removed and used to identify microscopic changes. Specimens were stained with Hematoxylin and eosin, with Masson trichrome stain for study of fibrous tissue and with periodic acid shiff's (PAS) to study the glycogen content. Other specimens were prepared for ultrastructural study. Results: Mild lymphocytic infiltration, vacuolar degeneration and mild increase of periportal fibrosis with mild depletion of glycogen content and partial disappearance of glycogen vacuoles were reported in animals received contaminated water for 4 weeks. Animals maintained for 8 weeks on contaminated water showed hepatic changes in the form of abundant lymphocytic infiltration, increased cellular polymorphism, pyknotic nuclei and areas of cell necrosis with evident moderate periportal fibrosis and marked vacuolar degeneration associated with marked depletion of glycogen content. Ultrastructural study revealed mitochondrial edema, appearance of interstitial inflammatory cells, and appearance of scattered variable sized lead electron-dense inclusion bodies. Conclusion: It could be concluded that chronic exposure to lead imposes a potent toxic effect on liver cells manifested as glycogen depletion, cellular infiltration and liver architecture in the form of initiation of periportal fibrosis that may progress to liver cirrhosis.

Journal ArticleDOI
TL;DR: It could be concluded that selenium (Se) and alpha-tocopherol (alpha-toc) may be useful tool to minimize the toxic effects of lead toxicity by its potent antioxidant activity.
Abstract: Lead is a serious poison causing serious injury or death Current study was designed to investigate the potential protective effect of selenium (Se) and alpha-tocopherol (alpha-toc) against the hepatic and renal toxicity of lead acetate in Oreochromis niloticus Two hundred and twenty five O niloticus were divided into five groups; control, lead acetate treated (7340 mg/liter), Se treated (4 mg sodium selenite/ kg diet), alpha-toc treated (200 mg/kg diet) plus Se + alpha-toc co-treated groups for 10 weeks Levels of aspartate aminotransferase (AST), alanine transaminase (ALT), total protein, urea, creatinine, calcium (Ca), inorganic phosphate (P), magnesium (Mg), superoxide dismutase (SOD), reduced glutathione (GSH) and the lipid peroxidation index (MDA) were determined The results revealed an increase in the levels of liver enzymes, urea, creatinine and MDA; meanwhile, the total protein, Ca, P, Mg, SOD and GSH were decreased Therefore, it could be concluded that selenium (Se) and alpha-tocopherol (alpha-toc) may be useful tool to minimize the toxic effects of lead toxicity by its potent antioxidant activity

Journal ArticleDOI
TL;DR: The findings suggest that the methanolic extract of the rind of Citrullus lanatus exerts a possible beneficial effect on male reproductive parameters in albino Wistar rats and validates anecdotal reports of the beneficial effect of watermelon consumption from the authors' environment.
Abstract: Aims: The present study investigated the effects of the methanolic extract of the rind of Citrullus lanatus on lead acetate induced toxicity on semen parameters, reproductive hormone assay and testicular histology in male albino Wistar rats. Study Design: Controlled experimental study using randomly assigned laboratory animals. Place and Duration of Study: Department of Human Physiology, College of Health Sciences, University of Port Harcourt, PMB 5323, Port Harcourt, Nigeria and Department of Physiology, Madonna University, Elele Campus, Rivers State, Nigeria between January 2013 and February 2014. Methodology: Twenty male rats were assigned into four groups: Group A to D of five rats each. Group A served as control and received 2ml/kg bw of 10% extract vehicle; Group B Original Research Article European Journal of Medicinal Plants, 4(9): 1125-1137, 2014 1126 received 200mg/kg bw of the methanolic extract of the rind of Citrullus lanatus; Group C received 2.25mg/kg bw of lead acetate; and Group Dwere co-administered with 2.25 mg/kg bw lead acetate and 200 mg/kg bw of the methanolic extract of the rind of Citrullus lanatus. The drugs and extracts were administered orally to the rats for 35days. On day 36, blood samples were collected from anaesthetized rats by cardiac puncture for reproductive hormone assay and the testes harvested for determination of semen parameters and histological studies. Semen parameters: count, motility, viability, and morphology were determined and assay for plasma levels of Follicle Stimulating Hormone (FSH), Luteinizing Hormone (LH) and testosterone done. Results: Results obtained showed that, compared to control rats, administration of the methanolic extract of the rind Citrullus lanatus significantly enhanced sperm count and all reproductive hormone levels (P<0.05); and also caused non-significant increases in sperm motility, percentage of spermatocytes with normal morphology and percentage of live spermatocytes, but decreased percentage of dead spermatocytes (P>0.05). Treatment with lead acetate caused a significant reduction in levels of all reproductive hormones and significant diminution of sperm motility, morphology, viability; with increases in percentage of dead spermatocytes (P<0.05). Expectedly, co-administration of the methanolic extract of the rind of Citrullus lanatus with lead acetate ameliorated the deleterious effects of lead acetate resulting in significant increases in sperm count and all reproductive hormones (P<0.05) and non-significant increases in motility, morphology and live spermatocytes (P>0.05): however, the percentage of spermatocytes with abnormal heads were significantly increased. The results suggest that the methanolic extract of the rind of Citrullus lanatus exerts a possible ameliorative effect on lead acetate induced toxicity on some reproductive parameters in male albino Wistar rats. Conclusion: The findings suggest that the methanolic extract of the rind of Citrullus lanatus exerts a possible beneficial effect on male reproductive parameters in albino Wistar rats and validates anecdotal reports of the beneficial effect of watermelon consumption from our environment. We however, recommend further studies in this regard.