Showing papers on "Lead acetate published in 2018"

Grape seed procyanidin extract ameliorates lead-induced liver injury via miRNA153 and AKT/GSK-3β/Fyn-mediated Nrf2 activation

Abstract: Lead-induced hepatotoxicity is characterized by an extensive oxidative stress. Grape seed procyanidin extract (GSPE) possesses abundant biological activities. Herein, we investigated the protective role of GSPE against lead-induced liver injury and determined the potential molecular mechanisms. In vivo, rats were treated with/without lead acetate (PbAc) (0.05%, w/v) in the presence/absence of GSPE (200 mg/kg). In vitro, hepatocytes were pretreated with/without GSPE (100 μg/ml) in the presence/absence of PbAc (100 μM). PbAc administration to rats resulted in anemia, liver dysfunction, lead accumulation in the bone and liver, oxidative stress, DNA damage and apoptosis. GSPE significantly attenuated these adverse effects, except lead accumulation in liver. GSPE also decreased the expression of miRNA153 and increased the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and levels of its downstream protein, and protein kinase B (AKT) phosphorylation in PbAc-induced liver injury. In primary hepatocytes treated with PbAc, GSPE increased hepatocyte viability and decreased lactate dehydrogenase release and reactive oxygen species levels. Dietary GSPE attenuated PbAc-induced liver injury in rats via an integrated mechanism associated with the miRNA153 and AKT/glycogen synthase kinase 3 beta/Fyn-mediated Nrf2 activation.

Lead exposure reduces sperm quality and DNA integrity in mice.

Abstract: Toxicity of lead on male reproductive functions has raised wide public concern as environmental lead contamination remains common worldwide. Conflicting and controversial data are available regarding effects of lead on male fertility. More importantly, our knowledge on effects of lead on sperm DNA integrity is significantly limited. Thus, further studies should focus on this issue. In the current study, adult male mice were exposed to a series of lead acetate concentrations in drinking water for six weeks. Following administration, lead levels in blood, testicles, and epididymis were measured, and potential changes in morphology of testis and epididymis due to lead exposure were identified. We also analyzed sperm parameters, including sperm density, viability, motility, and morphology, to evaluate quality of sperm collected from epididymis. Especially, hypothetical influence of lead on sperm DNA integrity was also evaluated by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling, alkaline comet assay, and sperm chromatin structure assay. Lead exposure possibly exerted no effect on growth of mice because these animals acquired similar body weight gain during the experimental period. However, high lead concentrations (0.5% and 1%) in drinking water affected sperm motility and increased percentage of spermatozoa with abnormal morphology. In groups treated with 0.25%, 0.5%, and 1% lead acetate, percentages of sperm cells showing DNA breaks and chromatin structure damage significantly increased. Altogether, lead exposure not only exhibits adverse effects on sperm physiological parameters, but also impairs DNA structure and integrity. These effects may lead to significant decline in male fertility.

Vitamin D alleviates lead induced renal and testicular injuries by immunomodulatory and antioxidant mechanisms in rats.

Abstract: This study measured the effects of vitamin D (VD) supplementation on the underlying molecular pathways involved in renal and testicular damage induced by lead (Pb) toxicity. Thirty two adult male Wistar rats were divided equally into four groups that were treated individually or simultaneously, except the negative control, for four weeks with lead acetate in drinking water (1,000 mg/L) and/or intramuscular VD (1,000 IU/kg; 3 days/week). Pb toxicity markedly reduced serum VD and Ca2+, induced substantial renal and testicular injuries with concomitant significant alterations in the expression of VD metabolising enzymes, its receptor and binding protein, and the calcium sensing receptor. Pb also significantly promoted lipid peroxidation and pro-inflammatory cytokines (IL-4 and TNF-α) in the organs of interest concomitantly with declines in several anti-oxidative markers (glutathione, glutathione peroxidase and catalase) and the anti-inflammatory cytokine, IL-10. The co-administration of VD with Pb markedly mitigated renal and testicular injuries compared with positive controls. This was associated with restoration of the expression of VD related molecules, promotion of anti-oxidative and anti-inflammatory markers, but tissue Pb concentrations were unaffected. In conclusion, this report is the first to reveal potential protective effects for VD against Pb-induced renal and testicular injuries via anti-inflammatory and anti-oxidative mechanisms.

Ferulic acid prevents lead-induced testicular oxidative stress and suppressed spermatogenesis in rats.

Abstract: Summary Lead affects multiple organ systems including testis. We investigated the effects of ferulic acid (FA) on lead-induced oxidative stress and spermatogenesis suppression in rats. Animals received lead acetate (500 mg/L in drinking water) and/or FA (50 mg/kg, i.g.) for eight weeks. Lead increased testicular malondialdehyde (MDA) and nitrite levels and decreased glutathione (GSH) content and catalase (CAT) activity. Lead decreased testis weight and testosterone level. Sperm parameters decreased in lead group. FA ameliorated the decreased testis weight, serum testosterone as well as sperm count, viability, motility and normal morphology in lead group. FA improved antioxidant capacity as well as sperm count, viability, motility and normal morphology. FA decreased Johnsen's mean testicular biopsy score (MTBS) criteria by restoring degeneration, atrophy and tubular disarrangement. FA also normalised spermatogonia, spermatocytes and spermatids numbers in lead group and led to increases in number of Leydig and Sertoli cells. FA showed beneficial effects in lead-induced testicular oxidative stress and spermatological disorders, through inhibiting lipid peroxidation and enhancing antioxidant defence systems. The positive effects of FA on Leydig cells may be involved in restoring testosterone levels in lead group. FA can be considered a potential candidate to protect testis against the deleterious effect of lead intoxication.

Intermittent low-level lead exposure provokes anxiety, hypertension, autonomic dysfunction and neuroinflammation.

Abstract: Background Exposures to lead (Pb) during developmental phases can alter the normal course of development, with lifelong health consequences. Permanent Pb exposure leads to behavioral changes, cognitive impairment, sympathoexcitation, tachycardia, hypertension and autonomic dysfunction. However, the effects of an intermittent lead exposure are not yet studied. This pattern of exposure has been recently increasing due to migrations, implementation of school exchange programs and/or residential changes. Objective To determine and compare lead effects on mammal’s behavior and physiology, using a rat model of intermittent and permanent Pb exposures. Methods Fetuses were intermittently (PbI) or permanently (PbP) exposed to water containing lead acetate (0.2% w/v) throughout life until adulthood (28 weeks of age). A control group (CTL) without any exposure to lead was also used. Anxiety was assessed by elevated plus maze (EPM) and locomotor activity and exploration by open field test (OFT). Blood pressure (BP), electrocardiogram (ECG), heart rate (HR), respiratory frequency (RF), sympathetic and parasympathetic activity and baro- and chemoreceptor reflex profiles were evaluated. Immunohistochemistry protocol for the assessment of neuroinflammation, neuronal loss (NeuN), gliosis and synaptic alterations (Iba-1, GFAP, Syn), were performed at the hippocampus. One-way ANOVA with Tukey’s multiple comparison between means were used (significance p Results The intermittent lead exposure produced a significant increase in diastolic and mean BP values, concomitant with a tendency to sympathetic overactivity (estimated by increased low-frequency power) and without significant changes in systolic BP, HR and RF. A chemoreceptor hypersensitivity and a baroreflex impairment were also observed, however, less pronounced when compared to the permanent exposure. Regarding behavioral changes, both lead exposure profiles showed an anxiety-like behavior without changes in locomotor and exploratory activity. Increase in GFAP and Iba-1 positive cells, without changes in NeuN positive cells were found in both exposed groups. Syn staining suffered a significant decrease in PbI group and a significant increase in PbP group. Conclusion This study is the first to show that developmental Pb exposure since fetal period can cause lasting impairments in physiological parameters. The intermittent lead exposure causes adverse health effects, i.e, hypertension, increased respiratory frequency and chemoreflex sensitivity, baroreflex impairment, anxiety, decreased synaptic activity, neuroinflammation and reactive gliosis, in some ways similar to a permanent exposure, however some are lower-grade, due to the shorter duration of exposure. This study brings new insights on the environmental factors that influence autonomic and cardiovascular systems during development, which can help in creating public policy strategies to prevent and control the adverse effects of Pb toxicity.

Role of geraniol against lead acetate-mediated hepatic damage and their interaction with liver carboxylesterase activity in rats

Abstract: In this study, the effect of geraniol (50 mg/kg for 30 d), a natural antioxidant and repellent/antifeedant monoterpene, in a rat model of lead acetate-induced (500 ppm for 30 d) liver damage was evaluated. Hepatic malondialdehyde increased in the lead acetate group. Reduced glutathione unchanged, but glutathione S-transferase, glutathione reductase, as well as carboxylesterase activities decreased in geraniol, lead acetate and geraniol + lead acetate groups. 8-OhDG immunoreactivity, mononuclear cell infiltrations and hepatic lead concentration were lower in the geraniol + lead acetate group than the lead acetate group. Serum aspartate aminotransferase and alanine aminotransferase activities increased in the Pb acetate group. In conclusion, lead acetate causes oxidative and toxic damage in the liver and this effect can reduce with geraniol treatment. However, we first observed that lead acetate, as well as geraniol, can affect liver carboxylesterase activity.

Dietary grape seed procyanidin extract protects against lead-induced heart injury in rats involving endoplasmic reticulum stress inhibition and AKT activation.

Abstract: To investigate the protective role of grape seed procyanidin extract (GSPE) against lead-induced heart injury and the possible molecular mechanism associated with this event, Wistar rats were orally given GSPE (200 mg/kg) daily with or without lead acetate (PbA) (0.5 g/L) in drinking water for 56 d. GSPE attenuated oxidative stress, heart dysfunction, and lead accumulation in lead-exposed rat hearts. Meanwhile, GSPE inhibited the protein kinase RNA-like endoplasmic reticulum (ER) kinase/eukaryotic initiation factor 2α signaling pathway, and promoted protein kinase B (AKT) and glycogen synthase kinase 3β phosphorylation altered by lead, and regulated lead-activated apoptosis and its related signaling pathway. This study suggests that dietary GSPE ameliorates lead-induced heart injury associated with ER stress inhibition and AKT activation. Dietary GSPE may be a protector against lead-induced heart injury and a novel therapy for lead exposure.

Effects of Orally Administered Lead acetate II on Rat Femur Histology, Mineralization Properties and Expression of Osteocalcin Gene

Abstract: Lead is one of the harmful heavy metals that may be produced from human activities, and have deleterious effects on many tissues such as bone. In this research, the effects of oral administration of lead acetate II on histology of rat femur, and expression level of osteocaclcin gene were investigated. Twenty male Wistar rats were randomly divided into 2 groups. The rats in tested group were fed with 100 ppm of lead acetate II during 2 months. The femur samples were removed, fixed and then stained by alizarin red S for mineralization ratio assessment, and Hematoxylin-Eosin for histological studies. Also, real-time PCR was performed to determine the expression level of osteocalcin gene. The dose of 100 ppm of lead acetate II reduced mineralization and bone density, and decreased the relative density of osteoblasts. Also, the diameter of the bone marrow increased while the expression of osteocalcin gene decreased in tested group in comparison with the control group (P < 0.05). The present study suggests that 100 ppm oral doses of lead acetate II might have strong destructive effects on femur histology and osteocalcin expression.

Exposure to low level of lead during preweaning period increases metallothionein-3 expression and dysregulates divalent cation levels in the brain of young rats.

Abstract: Lead (Pb) is a neurotoxic heavy metal, but the mechanism of its neurotoxicity is not clearly understood. Expression of metallothioneins (MTs) is induced in response to heavy metal exposure as a protective mechanism against heavy metal toxicity. There are several isoforms of MTs (MT-1 to 4), of which MT-3 is the neuron specific isoform, which also has neurite growth inhibitory effects. Whereas, the induction of MT-1 and 2 in response to Pb has been reported, the effect of Pb on the expression of MT-3 in the brain has not been documented. This study aimed at investigating the effect of Pb exposure on the expression of MT-3 in the cerebrum and hippocampus. Wistar rat pups were exposed to Pb via their dams’ drinking water (0.2% lead acetate in deionized water) from postnatal day (PND) 0 to 21 and directly via drinking water until PND30. Expression of MT-3 was measured by Western blot and quantitative RT-PCR. MT-3 localization was done by immunohistochemistry. Divalent metal ions were analysed by atomic absorption spectrophotometry. Levels of Pb in blood and cerebrum were significantly increased, while that of copper (Cu), zinc (Zn) and manganese (Mn) were significantly decreased in the Pb-exposed rats at both PND21 and PND30. MT-3 protein was significantly increased in the cerebrum (by 2.5-fold) and in hippocampus (1.4 to 3.2-fold) in both PND21 and PND30 Pb-exposed rats over controls. MT-3 gene expression also increased in the cerebrum (by 42%), and in the hippocampus (by 65% and 43% in the PND21 and PND30 rats, respectively), in the Pb-exposed rats over controls, but the increase was statistically significant (p

Preventive use of berberine in inhibition of lead - induced renal injury in rats

Abstract: The kidney is one of the main organs affected by lead toxicity. We investigated the effects of berberine on lead-induced nephrotoxicity in adult male Wistar rats. Animals received an aqueous solution of lead acetate (500 mg Pb/L in the drinking water) and/or berberine (50 mg/kg, i.g.) for 8 weeks. Lead caused an increase in malondialdehyde (P < 0.001) and total oxidant status (P < 0.01), and a decrease in reduced glutathione (P < 0.001), catalase (P < 0.01), superoxide dismutase (P < 0.001), and total antioxidant capacity (P < 0.05). Berberine prevented the prooxidant and antioxidant imbalance induced by lead (P < 0.001). Berberine corrected the increased relative kidney weight (P < 0.05) and biomarkers of renal function (creatinine (P < 0.001), urea (P < 0.05), uric acid (P < 0.001), albumin (P < 0.01), and total protein (P < 0.05)) in lead group. It also attenuated lead-induced abnormal renal structure. The results confirmed renoprotective effects of berberine in an animal model of lead-induced nephrotoxicity by molecular, biochemical, and histopathological analysis through inhibiting lipid peroxidation and enhancing antioxidant defense system mechanisms. Therefore, berberine makes a good candidate to protect against the deleterious effect of chronic lead intoxication.

Behavioral and neurochemical consequences of perinatal exposure to lead in adult male Wistar rats: protective effect by Centella asiatica

Abstract: The present study evaluated the protective effects of Centella asiatica (CA) leaf extract on behavioral deficits and neurotoxicity in adult rat exposed to lead during perinatal period. Adult Wistar rats were exposed to 0.15% lead acetate (Pb) from gestation day 6 through drinking water and the pups were exposed lactationally to Pb till weaning. Significant perturbations in locomotor activity and exploratory behavior were observed in rats exposed to Pb during perinatal period. The levels of lipid peroxidation increased significantly with a reduction in levels of glutathione and activity levels of acetylcholinesterase and antioxidant enzymes in hippocampus, cerebrum, cerebellum, and medulla of brains excised from Pb-exposed rats. Oral supplementation of CA during postweaning period provided significant protection against Pb-induced behavioral impairments and neurotoxicity, without chelating tissue Pb levels. The possible neuroprotective efficacy of CA may be due to its antioxidant potential but not by lowering effects of brain Pb content.

Ameliorative effects of curcumin against lead induced toxicity in human peripheral blood lymphocytes culture.

Abstract: Lead, a heavy metal and multifaceted toxicant, is well studied for its distribution and toxicity in ecosystem, yet there is no consensus on its amelioration by any synthetic or phytochemical compounds. Curcumin, a known antioxidant and dietary element, is a well-known herb, for its therapeutic uses and having a wide spectrum of its beneficial properties against several adverse effects. Hence, the current study was taken into consideration to evaluate the ameliorative effects of curcumin (3.87 μM, i.e. 1.43 μg/ml) against lead acetate (doses: 10-6 M, i.e. 0.379 μg/ml and 10-4 M, i.e. 37.9 μg/ml, durations: 24 h and 69 h) induced genotoxicity and oxidative stress in human peripheral blood lymphocyte cultures (PBLC). On one hand, antigenotoxic and antioxidative potentials of curcumin against lead were simultaneously evaluated by the array of genotoxicity and oxidative stress indices. The result postulated that lead acetate showed dose- and duration-dependent increase in both genotoxicity and oxidative stress whereas curcumin, when added along with lead acetate, showed the significant amelioration in all genotoxic and oxidative stress-related indices. The study indicated that, due to alteration in antioxidant defense system, there is an adverse genotoxic effect of lead. On the other hand, curcumin, a potent antidote, can protect chromatin material against lead -mediated genotoxicity by balancing the activity of antioxidant defense system.

Expression of Collagen Type II and Osteocalcin Genes in Mesenchymal Stem Cells from Rats Treated with Lead acetate II

Abstract: Background: Lead is one of the sustainable metals with devastating effects on many tissues. This study, examined the adverse effect of lead poisoning on the gene expression of collagen type II and osteocalcin by mesenchymal stem cells (MSCs) cultured in chondrogenic and osteogenic media, respectively. Methods: We used 18 male Wistar rats, divided in 3 groups. In addition to libitum feed as the control, treatment I and treatment II groups were fed by distilled water, distilled water with a dose of 50 ppm lead acetate II and distilled water with a dose of 100 ppm lead acetate II, respectively, over a 2-month period. The MSCs of rat femur were isolated in DMEM medium. After the second passage, the media were replaced separately with chondrogenic and osteogenic media over another 21 days. Then, Collagen Type II and Osteocalcin genes expression were investigated by real time PCR. Results: Collagen Type II and Osteocalcin genes expression in treatments I and II groups showed meaningful decreases compared with that of the control group. Also, the concentration of collagen type II in treatment II group in chondrogenic medium was significantly reduced compared with Osteocalcin concentration in osteogenic medium. Conclusion: We found that poisoning with lead and its accumulation at doses of 50 and 100 ppm in femoral bone marrow of rats decreased the expression of the collagen type II and osteocalcin genes in MSCs and in the chondrogenic and osteogenic media, respectively.

The Effect of Chitosan on the Erythrocyte Antioxidant Potential of Lead Toxicity-Induced Rats

Abstract: In the present study, the effects of chitosan on erythrocyte malondialdehyde (MDA) and glutathione (GSH) levels and glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH) enzyme activities in lead toxicity-induced rats were investigated. Twenty-eight male Wistar albino rats were divided into four groups of control (C), lead group (Pb group), lead + chitosan group (Pb + CS group), and chitosan group (CS group). Lead groups were administered 50 mg/kg lead acetate intraperitoneally (ip) for 5 days and chitosan groups were administered 200 mg/kg chitosan for 28 days via gavage. At the end of the study, lead levels were measured in the blood; MDA and GSH levels and GPx, GR, and G6PDH activities were measured in the erythrocyte. It was determined that, in parallel with the increase of full blood lead levels in the Pb group, erythrocyte MDA levels increased significantly, while GSH levels and GSH-Px, GR, and G6PDH activities decreased when compared to those in the C and CS groups (p ˂ 0.05). There was a statistically significant decrease in lead and MDA levels and GSH level and GSH-Px activity increased (p ˂ 0.05) in the Pb + CS group, where chitosan was administered as a protective agent in addition to lead, when compared to the Pb group. There were no differences between the Pb + CS group and the other three groups based on GR and G6PDH activities (p ˃ 0.05). No statistically significant difference was found between the C and CS groups based on the parameters of analysis (p ˃ 0.05). The findings of the present study demonstrated that lead increased oxidative stress by increasing free radical production in erythrocytes, and chitosan was effective in removing the lead from the circulation and enforced the antioxidant defense system.

Histological Changes in the Liver and Biochemical Parameters of Chickens Treated with Lead Acetate II

Abstract: Background: Lead is one of the heavy metals that is persists in the environment and has destructive effects on various human tissues. We investigated the effects of lead on the histological features of liver and its enzymatic functions. Methods: Forty chickens were purchased and randomly divided into four groups. In addition to the normal feed, each group received different doses of lead acetate II in the feed. After preparing microscopic slides, the level of liver enzymes was measured. Results: It was demonstrated that the level of liver enzymes increases and devastating effects on the liver structures occurred. Conclusion: In according to the adverse effects of lead on the liver and due to the increase use of this harmful agent in the different parts and its increase in the air, especially in Iran, there is a need for considering a comprehensive plan for preventing of more outbreak of this agents and inhibiting the toxic effects of it on the birds.

Ascorbic Acid Ameliorates Gestational Lead Exposure-Induced Developmental Alteration in GAD67 and c-Kit Expression in the Rat Cerebellar Cortex.

Abstract: In the present study, we investigated the effects of ascorbic acid on lead-exposed developing cerebellum. Female rats were divided into the following three groups: control (distilled water), lead (0.2% lead acetate), and lead plus ascorbic acid (100 mg/kg/day, 10% solution). To evaluate the effect of lead exposure and ascorbic acid treatment accurately on the cerebellar development for the gestational period, we halted further treatment with lead and ascorbic acid in the dams after delivery of the pups. Although the ascorbic acid slightly decreased the lead level in pups, lead level was still high in the group treated with lead plus ascorbic acid group compared with the control group. The blood lead levels indicated that the ascorbic acid could facilitate both the excretion and transfer of lead from a dam to its pups via milk. At postnatal day 21, lead exposure significantly reduced the number of Purkinje cells in the cerebellar cortex of pups. Additionally, lead treatment induced degenerative changes such as reduction of glutamic acid decarboxylase (GAD67) and c-kit expressions are observed in the developing cerebellar cortex. In the cerebellum of the pups from the lead plus ascorbic acid group, reduction of the number of Purkinje cells, GAD67 expression, and c-kit immunopositivity were remarkably restored compared with the lead group. Our present results suggested that ascorbic acid treatment to lead-exposed dam exerted protective effects on the developing cerebellum against lead-induced neurotoxicity.

Lead-induced changes of cytoskeletal protein is involved in the pathological basis in mice brain.

Abstract: Lead poisoning is a geochemical disease. On the other hand, lead is highly carcinogenic and exhibits liver and kidney toxicity. This element can also cross the blood-brain barrier, reduce learning and memory ability and damage the structure of the cerebral cortex and hippocampus. To further investigate the mechanism of lead neurotoxicity, 4-week-old Kunming mice were used to explore the effects of different concentrations of Pb2+ (0, 2.4, 4.8 and 9.6 mM) for 9 days. In this study, pathological and ultrastructural changes in brain cells of the treated group were related to damages to mitochondria, chromatin and the nucleus. Lead content in blood was tested by atomic absorption spectroscopy, which showed high lead concentrations in the blood with increasing doses of lead. Distribution of lead in nerve cells was analysed by transmission electron microscopy with energy dispersive spectroscopy. Data showed the presence of lead in nucleopores, chromatin and nuclear membrane of nerve cells in the treatment groups, whereas lead content increased with increasing doses of lead acetate. Finally, microtubule-associated protein 2 (MAP2) mRNA and protein expression levels were detected by real-time PCR and Western blotting, which showed a reduction in MAP2 expression with increasing lead doses in the mouse brain. These findings suggest that acute lead poisoning can cause significant dose-dependent toxic effects on mouse brain function and can contribute to better understanding of lead-induced toxicity.

Chronic lead exposure enhances the sympathoexcitatory response associated with P2X4 receptor in rat stellate ganglia.

Abstract: Chronic lead exposure causes peripheral sympathetic nerve stimulation, including increased blood pressure and heart rate. Purinergic receptors are involved in the sympathoexcitatory response induced by myocardial ischemia injury. However, whether P2X4 receptor participates in sympathoexcitatory response induced by chronic lead exposure and the possible mechanisms are still unknown. The aim of this study was to explore the change of the sympathoexcitatory response induced by chronic lead exposure via the P2X4 receptor in the stellate ganglion (SG). Rats were given lead acetate through drinking water freely at doses of 0 g/L (control group), 0.5 g/L (low lead group), and 2 g/L (high lead group) for 1 year. Our results demonstrated that lead exposure caused autonomic nervous dysfunction, including blood pressure and heart rate increased and heart rate variability (HRV) decreased. Western blotting results indicated that after lead exposure, the protein expression levels in the SG of P2X4 receptor, IL-1β and Cx43 were up-regulated, the phosphorylation of p38 mitogen-activated protein kinase (MAPK) was activated. Real-time PCR results showed that the mRNA expression of P2X4 receptor in the SG was higher in lead exposure group than that in the control group. Double-labeled immunofluorescence results showed that P2X4 receptor was co-expressed with glutamine synthetase (GS), the marker of satellite glial cells (SGCs). These changes were positively correlated with the dose of lead exposure. The up-regulated expression of P2X4 receptor in SGCs of the SG maybe enhance the sympathoexcitatory response induced by chronic lead exposure.

Downregulation of Osteocalcin Gene in Chickens Treated with Lead Acetate II

Abstract: Lead is one of the persistent agents found extensively in the environment and has destructive impacts on the tissues. Regarding the high spread of lead, particularly in Iran, we investigated the effects of lead acetate II on the expression level of osteocalcin gene and histological changes of bone. 40 chickens were randomly divided into four groups. As well as the libitum, the control group was fed with distilled water, while treatment 1, 2, and 3 groups were fed with distilled water and 50, 100, and 200 ppm of lead acetate II, respectively. Alterations in the histological profile of bone including decreased level of bone and pyknosis in the nuclei of osteocytes, and decreased expression of osteocalcin gene are the results of exposing to the lead. Regarding the adverse effects of lead on the bone, the spread of this toxic metal must be limited to decrease its adverse impacts on the birds, especially chickens.

Testicular toxic effect of lead acetate on adult male rats and the potential protective role of alcoholic extract of ginseng (histological, histomorphometrical and physiological)

Abstract: Corresponding author: Sawsan A. Ali Email: sawsanalhasoon@yahoo.com Department of Histology and Anatomy College of Veterinary Medicine University of Basrah Basrah Iraq ABSTRACT Objective: This work aims to evaluate the histological and histomorphometrical changes in the testicular oxidative stress in male rats post exposure to lead acetate and the possible protective role of Panax ginseng extract, which reducing heavy metal toxicities has raised worldwide. Methods: Animals were divided into five groups for 5 and 10 weeks. Each group (n=8). Group II, received (100 mg/kg b. wt/day) lead acetate for 5 weeks. Group III, received (100 mg/kg b.wt/day) lead acetate for 10 weeks. Group IV, received (100mg/kg b. wt/day) lead acetate with (200mg/kg b. wt/day) of P. ginseng extract, Group IIV, received (200mg/kg b. wt/day) ethanolic P. ginseng extract after exposure to lead acetate for 10 weeks. LH, FSH and testosterone level, body weight, genital organ weight and concentration of lipid peroxidation product (MDA) was estimated. Results: The result showed clearly impact of lead acetate on testicular tissue of male rats and degenerative changes in seminiferous tubules, vascular congestion, also alteration in spermatogenic layers in many tubules and necrosis dilation of interstitial spaces, leydig cell degeneration, while, the groups receiving P. ginseng extract after exposure for lead acetate (PbAc) were ameliorated the damaging effects, however body weight and testes weight, LH, FSH and testosterone level significantly increase in treated groups with P. ginseng extract. Conclusion: show that dose dependent P. ginseng extract significantly present adverse testicular toxicity and oxidative stress induced with lead acetate.