Showing papers on "Lead acetate published in 2020"
TL;DR: Dietary supplementation of SP at different levels attenuated the cumulative effect of lead in rabbits in dose-dependent manner; this attenuation may be attributed to its anti-oxidative, anti-inflammatory, as well as its immune stimulant effect.
64 citations
TL;DR: CoQ10 reduces the deleterious cellular side effects of PbAc exposure due to its antioxidant, anti-inflammatory and anti-apoptotic effects.
Abstract: The kidney is among the metabolic organs most susceptible to injury, particularly following exposure to xenobiotics and heavy metals. We aimed to explore the potential protective impacts of coenzyme Q10 (CoQ10) on lead acetate (PbAc)-induced nephrotoxicity in rats. Four experimental groups (n = 7) were applied as follows: control group, CoQ10 alone (10 mg/kg), PbAc alone (20 mg/kg), and PbAc with CoQ10. Exposure to PbAc led to the accumulation of Pb in the kidney and increased urea and creatinine serum levels. The deposition of Pb coupled with the elevation of malondialdehyde and nitrate/nitrite levels along with the upregulation of inducible nitric oxide synthase. Additionally, upon PbAc poisoning, glutathione content and the antioxidant enzymes were depleted along with the downregulation of Nrf2 and HO-1 expression. Moreover, PbAc injection increased the protein and mRNA levels of pro-inflammatory cytokines namely, tumor necrosis factor-alpha and interleukin-1 beta, while decreased the levels of interleukin-10, an anti-inflammatory cytokine, in the kidney. Furthermore, exposure to PbAc correlated with increased levels of pro-apoptotic markers, Bax and caspase-3, and reduced levels of the anti-apoptotic marker Bcl-2. The administration of CoQ10 alleviated the molecular, biochemical and histological changes following PbAc intoxication. Thus, CoQ10 reduces the deleterious cellular side effects of PbAc exposure due to its antioxidant, anti-inflammatory and anti-apoptotic effects.
48 citations
TL;DR: The results showed that the extract is highly affluent in total flavonoids, total phenolic, and also has antioxidant activity, which indicates the antioxidant activity of Laurus leaves extract and assumes that it has a defensive role against the oxidative damage caused by lead in a rat's brain.
35 citations
TL;DR: Curcumin has antioxidant, anti-inflammatory, and immunomodulatory effects and is able to minimize the LA-induced oxidative damage in rats.
Abstract: Lead, toxic heavy metal of global concern, induces toxicity in various organs via oxidative stress. Thereby, in this study, the protective role of curcumin against lead acetate-induced toxicity was evaluated. Thirty-two male albino rats were allocated equally into four groups and orally administered with corn oil as a vehicle (Cont.), curcumin (CUR) (400 mg/kg bw), lead acetate (LA) (100 mg/kg bw), and lead acetate plus curcumin (LA + CUR). All rats had received their treatments daily for 4 weeks. The results revealed that LA toxicity induced normocytic normochromic anemia with significant leukocytosis and lymphocytosis. Moreover, LA-intoxicated rats showed a marked elevation in the liver enzyme activities, serum cholesterol, and triglyceride levels. In contrast, sero-immunological parameters, total protein, albumin, globulin, and testosterone levels were significantly reduced compared to the control rats. Additionally, LA-induced hepatic and testicular oxidative damage revealed by marked increased in MDA level with prominent reduction in the antioxidant system. The gene expression of the hepatic pro-inflammatory markers and testicular steroidogenic biomarkers including LHR and aromatase were significantly upregulated; meanwhile, the expressions of testicular StAR, CYP17a, 3B-HDS, SR-B1, and P450SCC were significantly downregulated in the LA-intoxicated group. Curcumin treatment could partially improve the hematological, biochemical, and histopathological alterations induced by LA. Also, it was observed that curcumin significantly restored hepatic pro-inflammatory markers and testicular steroidogenic enzymes. In conclusion, curcumin has antioxidant, anti-inflammatory, and immunomodulatory effects and is able to minimize the LA-induced oxidative damage in rats.
34 citations
TL;DR: Findings may suggest that LUT may be useful for attenuating neuronal damage induced by PbAc through inhibiting the oxidative damage, neuroinflammation, and the cortical cell death.
Abstract: Luteolin (LUT) is a glycosylated flavonoid compound that has multiple beneficial pharmacological and biological impacts. The current investigation was undertaken to evaluate the putative neuroprotective potency of LUT against neuronal damage induced by lead acetate (PbAc). Twenty-eight rats were placed into four equal groups. Group 1: served as the control group, group 2: rats were supplemented orally with LUT (50 mg kg-1), group 3: rats were intraperitoneally injected with PbAc (20 mg kg-1), and group 4: rats were pretreated with LUT before PbAc injection with the same doses. All animals were treated for 7 days. The exposure to PbAc increased the concentration of lead in the cortical tissue, neuronal lipid peroxidation, and nitric oxide (NO) production and decreased the antioxidant enzymes. Additionally, PbAc enhanced a neuroinflammatory response in the cortical tissue through increasing the pro-inflammatory cytokines secretion and inducible NO synthase expression. Moreover, cortical cell death was recorded following PbAc intoxication as evidenced by the enhancement of the proapoptotic and inhibiting the antiapoptotic markers. Interestingly, LUT supplementation reversed the cortical adverse reactions induced by PbAc. Taken together, these findings may suggest that LUT may be useful for attenuating neuronal damage induced by PbAc through inhibiting the oxidative damage, neuroinflammation, and the cortical cell death.
27 citations
TL;DR: In insight into the mechanism of preventing lead induced AD through cerebrovascular pathways, lead exposure increased blood lead concentration which revealed the internal exposure level, accelerated Aβ1-42 deposition in APP/PS1 mouse cortexes and abnormal change in Zonula Occludin-1 and Claudin-5 protein.
27 citations
TL;DR: In this paper, the authors successfully recovered lead from lead-acid battery and used it to fabricate normal planar heterojunction perovskite solar cells (PerSCs) with a power conversation efficiency reaching 17.83%.
26 citations
TL;DR: The factorial analysis demonstrated that synergistic interaction was responsible for the combined toxicity of c-BC and Pb co-exposure and could induce some unexpected toxicity, even beyond the known toxicities of the individual compounds in BEAS-2B cells at the NOAEL.
24 citations
TL;DR: It is pointed out that MOE could be used as an alternative remedy to overcome the adverse effects of Pb exposure, which may be due to its potent antioxidant, anti-inflammatory, and anti-apoptotic effects.
Abstract: Lead (Pb) is an environmental toxicant; its consumption can induce renal deficits. In this study, we explored the possible protective efficiency of Moringa oleifera extract (MOE) against lead acetate (PbAc)-mediated reprotoxicity. Four experimental groups of seven rats each were used: control, PbAc, MOE, and MOE+PbAc groups. All groups were given their respective treatment for 4 weeks. PbAc impaired the oxidative/antioxidative balance in the renal tissue, as shown by the decreased antioxidant proteins (glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase) and increased oxidants (lipid peroxidation and nitric oxide). Additionally, PbAc enhanced the progression of kidney inflammation by increasing tumor necrosis factor-alpha, interleukin-1 beta, and nuclear factor kappa B associated with upregulation of inducible nitric oxide synthase. Moreover, a dysregulation in the apoptotic-regulating proteins (Bax, caspase-3, and Bcl2) were recorded upon PbAc exposure. Remarkably, MOE oral administration restored redox homeostasis, suppressed the inflammatory and apoptotic responses in the kidney tissue. Our findings point out that MOE could be used as an alternative remedy to overcome the adverse effects of Pb exposure, which may be due to its potent antioxidant, anti-inflammatory, and anti-apoptotic effects.
24 citations
TL;DR: C. esculentus exhibited a dose-dependent mitigation of lead acetate-induced testicular dysfunction in Wistar rats via its antioxidant, anti-inflammatory and anti-apoptotic effects.
23 citations
TL;DR: The present study showed that the bodyweight of chickens was not affected significantly by lead acetate exposure, and the levels of MCHC, PCV, TEC, Hb, LDL, HDL, and total protein were found to be significantly decreased while WBC, LDC, and ALT profile were enhanced due to administration of Lead acetate.
Abstract: Lead is one of the utmost contaminated and dangerous heavy metals. This toxicant ultimately enters into the human body through the food chain and accumulated in the body because the animal/human body has not an appropriate mechanism to excrete it from the body. The main objective of the present research was to assess the toxicological effects of lead on body weights, biochemical, and hematological parameters of chickens and also to measure its bioaccumulation in the brain. Lead acetate was administrated orally at doses of 0, 71, 142, 213, and 284 mg/kg of body weight of chicken for groups A, B, C, D, and E, respectively. Along with determination of biometry of all experimental chicks, hematological [hemoglobin (Hb), packed cell volume (PCV), mean corpuscular hemoglobin concentration (MCHC), total erythrocyte count (TEC), white blood cells (WBCs), leukocyte differential count (LDC)] and biochemical [low density lipoprotein (LDL), total protein, high-density lipoprotein (HDL), and alanine aminotransferase (ALT)] parameters were measured. The present study showed that the bodyweight of chickens was not affected significantly by lead acetate exposure. The levels of MCHC, PCV, TEC, Hb, LDL, HDL, and total protein were found to be significantly decreased while WBC, LDC, and ALT profile were enhanced due to administration of lead acetate. Bioaccumulation of lead acetate was found to be higher in the brain. We conclude that the chronic administration of lead acetate affected the blood and biochemical profile of exposed chicken. These effects might be due to the accumulation of the chemical in certain vital organ(s). However, further studies in the future are suggested to refine such findings.
TL;DR: It is concluded that LUT may have a beneficial effect against PbAc‐induced testicular injury through preventing oxidative challenge, inflammation, and finally apoptosis.
Abstract: Lead (Pb) is a toxic heavy metal that is harmful to humans, especially male reproductive organs. Luteolin (LUT) is a naturally occurring flavonoid with numerous biological activities. Our aim was to investigate the possible reproprotective effect of LUT against testicular deficits induced by Pb intoxication. In the present study, 28 rats were distributed into 4 groups: control, LUT (50 mg/kg), lead acetate (PbAc, 20 mg/kg), and LUT + PbAc groups, in which rats were pre-treated with LUT 3 hr before PbAc injection. All animals were treated for 7 days. Oxidative stress, inflammatory and apoptotic markers along with histopathological changes have been examined using spectrophotometric, ELISA, real-time PCR, and histopathological methods. PbAc injection elevated Pb concentration in testicular tissue and decreased levels of sex hormones. PbAc intoxication exacerbated lipoperoxidation and nitric oxide formation, depleted superoxide dismutase, and catalase activities along with glutathione and its originated enzymes (glutathione peroxidase and glutathione reductase). At the molecular level, PbAc deactivated nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 in the testicular tissue. In addition, PbAc toxicity induced inflammatory and apoptotic cascades in testicular tissue as evidenced by the increased tumor necrosis factor-alpha, interleukin-1 beta, inducible nitric oxide synthase, Bax, and caspase 3, while Bcl-2 was declined. Histopathological examination of testicular tissue also revealed that PbAc caused degeneration alterations in spermatogenic cells, the spermatogenic epithelial cells were disconnected from the basement membrane, and the seminiferous tubules were vacuolated. Remarkably, pre-treatment with LUT minimized significantly the testicular damage induced by PbAc. Therefore, we conclude that LUT may have a beneficial effect against PbAc-induced testicular injury through preventing oxidative challenge, inflammation, and finally apoptosis.
TL;DR: It is suggested that CoQ10 can act as a natural therapeutic agent to protect against the reproductive impairments associated with lead acetate exposure and improve testicular function by inhibiting Pb accumulation, oxidative stress, inflammation, cell death, and histopathological changes following PbAc exposure.
Abstract: Exposure to lead (Pb) causes multiorgan dysfunction including reproductive impairments. Here, we examined the protective effects of coenzyme Q10 (CoQ10) administration on testicular injury induced by lead acetate (PbAc) exposure in rats. This study employed four experimental groups ( ) that underwent seven days of treatment as follows: control group intraperitoneally (i.p.) treated with 0.1 ml of 0.9% NaCl containing 1% Tween 80 ( ), CoQ10 group that was i.p. injected with 10 mg/kg CoQ10, PbAc group that was i.p. treated with PbAc (20 mg/kg), and PbAc+CoQ10 group that was i.p. injected with CoQ10 2 h after PbAc. PbAc injection resulted in increasing residual Pb levels in the testis and reducing testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Additionally, PbAc exposure resulted in significant oxidative damage to the tissues on the testes. PbAc raised the levels of prooxidants (malondialdehyde and nitric oxide) and reduced the amount of endogenous antioxidative proteins (glutathione and its derivative enzymes, catalase, and superoxide dismutase) available in the cell. Moreover, PbAc induced the inflammatory response as evidenced by the upregulation of inflammatory mediators (tumor necrosis factor-alpha and interleukin-1 beta). Further, PbAc treatment induced apoptosis in the testicular cells, as indicated by an increase in Bax and caspase 3 expression, and reduced Bcl2 expression. CoQ10 supplementation improved testicular function by inhibiting Pb accumulation, oxidative stress, inflammation, cell death, and histopathological changes following PbAc exposure. Our findings suggest that CoQ10 can act as a natural therapeutic agent to protect against the reproductive impairments associated with PbAc exposure.
TL;DR: It is shown once again that the systemic toxic effects of a metal combination, its in vivo genotoxicity included, can be more or less attenuated by background administration of a theoretically justified composition of biologically active agents.
TL;DR: Long-term exposure to low doses of lead can cause bone damage without inducing other obvious symptoms through decreasing bone density and the number of cancellous bone trabeculae, further suppressing bone formation, which suggests that lead may exacerbate bone loss and osteoporosis, especially in the elderly.
Abstract: The aim of this study was to investigate the long-term effects of low-dose lead exposure on bone microstructure in mice. Ten SPF 12-week-old male C57BL/6J mice were randomly divided into two groups: control (deionized water) and lead exposure (150 ppm of lead acetate in drinking water). After 24 weeks treatment, mice were weighed and the left femurs were collected and stored at − 80 °C. The right femurs of the mice were scanned by Micro-CT for three-dimensional reconstruction, and bone mineral density, bone volume fraction, trabeculae thickness, trabeculae number, and trabeculae separation were measured. The right tibia was collected to investigate histopathological changes in H&E-stained sections. The gene expression of osteoprotegerin (OPG), RANKL, and runt-related transcription factor 2 (Runx2) was determined using real-time PCR. The bone density of femoral cancellous bone and the number of cancellous bone trabeculae in the lead exposure group were both significantly decreased compared with the control group. Bone marrow stromal cell numbers were decreased following lead administration, and lipid droplet vacuoles were observed in the lead group. Levels of OPG were significantly decreased in the lead group, and lead also inhibited the expression of Runx2 compared with the control group. Long-term exposure to low doses of lead can cause bone damage without inducing other obvious symptoms through decreasing bone density and the number of cancellous bone trabeculae, further suppressing bone formation. It suggests that lead may exacerbate bone loss and osteoporosis, especially in the elderly.
TL;DR: The administration of APE ameliorated the lead-induced alterations in liver function and structure, exemplifying the benefits of Azolla’s phytochemical contents.
Abstract: The current study investigated the protective potential of Azolla pinnate ethanolic extract (APE) against lead-induced hepatotoxicity in rats. Sixty male Wistar albino rats were randomly allocated into six groups (n = 10). The control group was orally administrated with saline. The second group received lead acetate (100 mg/kg body weight (BW) orally for 60 days). The third group was fed with APE (10 mg/kg BW orally for 60 days). The fourth group was administrated with lead acetate like the second group and APE like the third group, concomitantly, for 60 days. The fifth group was administrated with APE like the third group for 30 days, then orally administrated with the lead acetate like the second group for another 30 days. The sixth group was administrated with lead acetate like the second group for 30 days, then with APE like the third group for a further 30 days. Phytochemical analysis of APE indicated the presence of peonidin 3-O-glucoside cation, vitexin, rutin, thiamine, choline, tamarixetin, hyperoside, astragalin, and quercetin. The latter has been elucidated using one- and two-dimensional nuclear magnetic resonance (1D and 2D NMR) and liquid chromatography-mass spectrometry (LC-MS-MS). Lead acetate increased the serum levels of alanine and aspartate aminotransferases and that of urea, creatinine, tumor necrosis factor alpha, and interleukin 1β, hepatic tissue malondialdehyde contents, and caspase 3 protein expression, as well as altering the hepatic tissue architecture. However, it decreased the serum levels of interleukin 10 and glutathione (GSH) contents, and the activities of catalase and superoxide dismutase in hepatic tissue. In contrast, the administration of APE ameliorated the lead-induced alterations in liver function and structure, exemplifying the benefits of Azolla's phytochemical contents. Collectively, A. pinnate extract is a protective and curative agent against lead-induced hepatotoxicity via its antioxidant, anti-inflammatory, and anti-apoptotic impacts.
TL;DR: In this paper, the solubility of flaxseed protein isolate (FPI) in the acidic media was exploited in preparation of lemon juice with FPI, which suppressed the elevation in kidney functions, lipid peroxidation of kidney tissues, urinary protein and creatinine as well as liver functions caused by lead intoxication.
Abstract: Finding renal and hepatoprotective agents preferably with antioxidant activities against environmental pollutants especially lead which can adversely affect liver and kidney is a great demand. In the current study, flaxseed protein isolate (FPI) was extracted from defatted flaxseed meal. Amino acids profile, antioxidant capacity and solubility of the extracted FPI were determined. The solubility of FPI in the acidic media was exploited in preparation of lemon juice with FPI. Twenty four male rats were assigned to four groups; normal control, lead intoxicated (oral daily dose of 60 mg/kg b.w. in distilled water for four weeks), lead intoxicated and orally administrated with daily dose equal 1 ml of lemon juice as well as lead intoxicated and orally administered with FPI (daily dose equal 100 mg/kg) in 1 ml of lemon juice. The oral administration of FPI incorporated in lemon juice suppressed the elevation in kidney functions, lipid peroxidation of kidney tissues, urinary protein and creatinine as well as liver functions caused by lead intoxication. Additionally, lemon juice with FPI combated the reduction of GSH of kidney tissues. It was revealed also that lemon juice without FPI suppressed the elevation in kidney and liver functions caused by lead. It can be concluded that flaxseed protein isolate is a good source of protein with potent antioxidant activity. Additionally, lemon juice and FPI are considered protective sources of kidney and liver against lead toxicity.
TL;DR: Results showed that Pb exposure led to disorders in cellular interactions that affect testicular function; however, simultaneous treatment with quercetin did not alleviate these effects.
Abstract: Environmental pollutant effects on fertility sometime are irretrievable. The aim of this study was to investigate the effect of lead acetate and quercetin on tight (claudin 11 and occludin) and gap junctional (connexin 43) proteins and the integrity of the blood-testis barrier status. Experimental groups, including the lead acetate (Pb), quercetin (QE), lead acetate with quercetin (Pb + QE), and control mice, were treated at least one spermatogenic cycle. Gene expression of claudin 11 and occludin decreased in Pb + QE, Pb, and QE compared with the control group. Connexin 43 (Cx43) expression in the control and Pb groups was lower than in Pb + QE and QE. The immunohistochemical data were generally in line with these findings. In conclusion, the results showed that Pb exposure led to disorders in cellular interactions that affect testicular function; however, simultaneous treatment with quercetin did not alleviate these effects. Graphical Abstract.
TL;DR: In this paper, the effects of repeated intraperitoneal injections of lead acetate and cadmium chloride, administered either alone or in combination, are shown to affect the biochemical, cytological and morphometric parameters of blood, liver, heart and kidneys.
Abstract: Subchronic intoxications induced in male rats by repeated intraperitoneal injections of lead acetate and cadmium chloride, administered either alone or in combination, are shown to affect the biochemical, cytological and morphometric parameters of blood, liver, heart and kidneys. The single twitch parameters of myocardial trabecular and papillary muscle preparations were measured in the isometric regime to identify changes in the heterometric (length-force) and chronoinotropic (frequency-force) contractility regulation systems. Differences in the responses of these systems in trabecules and papillary muscles to the above intoxications are shown. A number of myocardium mechanical characteristics changing in rats under the effect of a combined lead-cadmium intoxication and increased proportion of α-myosin heavy chains were observed to normalize fully or partially if such intoxication was induced against background administration of a proposed bioprotective complex. Based on the experimental results and literature data, some assumptions are suggested concerning the mechanisms of the cardiotoxic effects produced by lead and cadmium.
TL;DR: In this article, a closed-loop ammonium salt system is proposed for spent lead-acid battery paste recovery, where the spent lead paste is first leached by a mixed solution of ammonium acetate, acetic acid and hydrogen peroxide.
TL;DR: Co-administration of aqueous Moringa extract with lead significantly alleviated lead-induced adverse effects and restored the lead perturbations through reduction of oxidative stress–induced DNA damage via amelioration of NF-kB and TNF-α which kept hepatocyte integrity and reduced serum hepatic enzyme activities.
Abstract: Current research was performed to explore the hepatoprotective potential of Moringa oleifera leaves extract on lead acetate–induced hepatic injury. Twenty-four male Wistar rats were divided equally into 4 groups. The first group was control, while the second, third, and fourth groups were given 200 mg/kg aqueous Moringa extract only, 100 mg/kg lead only, and 100 mg/kg lead plus 200 mg/kg aqueous Moringa leaves extract, respectively, via oral gavage for 4 weeks. Weight gain and feed efficiency ratio were recorded. Serum lipid profiles, liver enzyme activities, and proteins beside hepatic superoxide dismutase activity, reduced glutathione, tumor necrosis factor alpha (TNF-α), and deoxyribonucleic acid fragmentation were assessed. Liver histopathological examination and nuclear factor kappa B (NF-kB) immunohistochemistry were performed. Administration of lead lowered (P < 0.05) weight gain, feed efficiency ratio, and perturbed lipid profile than control. Lead increased liver enzyme activities and TNF-α, while reduced serum proteins and hepatic antioxidant markers compared to control. Lead aggravated hepatic DNA fragmentation beside the presence of histopathological lesions. Co-administration of aqueous Moringa extract with lead significantly alleviated lead-induced adverse effects. The administration of aqueous Moringa extract with its antioxidant significantly restored the lead perturbations through reduction of oxidative stress–induced DNA damage via amelioration of NF-kB and TNF-α which kept hepatocyte integrity and reduced serum hepatic enzyme activities.
TL;DR: Evaluated the ameliorative effects of curcumin on Pb‐induced hepatorenal toxicity in a rat model and found it to have antioxidative properties.
Abstract: Introduction Lead (Pb) is a ubiquitous toxic heavy metal that inflicts numerous clinical consequences on humans. Curcumin is the principal component of turmeric, which is reported to have antioxidative properties. This study aimed at evaluating the ameliorative effects of curcumin on Pb-induced hepatorenal toxicity in a rat model. Methods Thirty-six male Sprague-Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and six rats each for the lead-treated group (LTG) (50 mg/kg lead acetate [Pb acetate] for 4 weeks), recovery group (50 mg/kg Pb acetate for 4 weeks and left with no treatment for another 4 weeks), treatment group 1 (Cur100) (50 mg/kg Pb acetate for 4 weeks, followed by 100 mg/kg curcumin for 4 weeks), and treatment group 2 (Cur200) (50 mg/kg Pb acetate for 4 weeks, followed by 200 mg/kg curcumin for 4 weeks). All the experimental groups received oral treatments via orogastric-tube on alternate days. Pb concentration in the liver and kidney of the rats were evaluated using inductive-coupled plasma mass spectrometry techniques. Results Pb-administered rats revealed significant alteration in oxidative status and increased Pb concentration in their liver and kidney with obvious reduction of hemogram and increased in leukogram as well as aberration in histological architecture of the liver and kidney. However, treatment with curcumin reduces the tissue Pb concentrations and ameliorates the above mention alterations. Conclusions The results in this study suggested that curcumin attenuates Pb-induced hepatorenal toxicity via chelating activity and inhibition of oxidative stress.
TL;DR: Results provide a rationale for the inhibitory role of carvacrol in the attenuation of lead-induced neurotoxicity and ameliorated neurodegeneration, antioxidative capacity, and lipid peroxidation in the hippocampus of rats exposed to lead.
Abstract: Carvacrol is a monoterpene with neuroprotective effects in several animal models of neurodegeneration, including epilepsy, ischemia, and traumatic neuronal events. In this study, we aimed to examine the effects of carvacrol on neurodegeneration induced by lead acetate in rats. A total of 50 male Wistar rats were divided into five equal groups. The control group received drinking water, while the neurotoxic group was exposed to 500 ppm of lead acetate in drinking water for 40 days. The three remaining groups, which were also exposed to 500 ppm of lead acetate, received carvacrol at doses of 25, 50, and 100 mg/kg orally for 40 days. The Morris water maze test was employed to examine spatial learning and memory. Pathological damage to the hippocampus was determined by Nissl staining. The level of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were detected using biochemical analysis and the free radical scavenging activity as evaluated by the DPPH test. Administration of carvacrol significantly restored learning and memory impairment induced by lead acetate. Moreover, carvacrol ameliorated neurodegeneration, antioxidative capacity, and lipid peroxidation in the hippocampus of rats exposed to lead. The present results provide a rationale for the inhibitory role of carvacrol in the attenuation of lead-induced neurotoxicity.
TL;DR: It is indicated that the concentrations of essential elements could be used as sensitive toxicological indicators of Pb exposure and caused alterations in the Mg distribution pattern, and decreased the correlation of Mg, Ca and Zn in the brain.
TL;DR: It was observed that the values approached the values of the control group in the combination of lead and diosmin, and had a positive effect on the regression of tissue damage.
Abstract: In this study, the effect of diosmin against the adverse effects of lead exposure in rats was investigated. Wistar Albino race 40 male rats weighing 150-200 g 2-3 months were used. A total of 4 groups were assigned, one of which was control and the other 3 were trial groups. The rats in the control group were treated with dimethyl sulfoxide, which was used only as a vehicle in diosmin administration. Groups 2, 3, and 4 from the experimental group were given diosmin at a dose of 50 mg/kg.bw, lead acetate at the dose of 1000 ppm, lead acetate at the dose of 1000 ppm, and diosmin at a dose of 50 mg/kg.bw for 6 weeks, respectively. Application of lead acetate with drinking water and also diosmin was performed by oral catheter. At the end of the experimental period, blood was taken to dry and with heparin by puncture to the heart under light ether anesthesia. Following the blood samples, some organs of the rats (the liver, kidney, brain, heart, and testis) were removed. Some biochemical parameters (glucose, triglyceride, cholesterol, BUN, creatinine, uric acid, LDH, AST, ALT, ALP, total protein, albumin) were measured in serum. Some oxidative stress parameters in tissue samples and blood (MDA, NO, SOD, CAT, GSH-Px, GSH) were evaluated. Body and organ (the liver, kidney, brain, heart, and testis) weights were also evaluated at the end of the study. No significant change was observed in the parameters examined in the diosmin alone-treated group by comparison to control group. On the other hand, significant changes were found in the values of lead acetate-treated group comparing control group. It was observed that the values approached the values of the control group in the combination of lead and diosmin. Exposure to lead acetate at a dose of 1000 ppm for 6 weeks causes organ damage; however the diosmin application at a dose of 50 mg/kg.bw had a positive effect on the regression of tissue damage.
TL;DR: The results demonstrate that the F and SA are effective natural extracts for lead-eliminating, and that they can ameliorate oxidative damage induced by lead toxicity.
TL;DR: SLE supplemented after the establishment of lead acetate-toxicity also reduced the AST, ALT, and ALP activity and hepatic oxidative stress, indicating its ameliorative effect.
Abstract: The present study investigated the hepatoprotective effects of seabuckthorn (Hippophae rhamnoides) leaf-extract (SLE) supplementation in lead acetate-intoxicated Wistar rats. Adult male Wistar rats...
TL;DR: It is suggested that AT1 activation plays a role in AT2 upregulation, probably as a protective mechanism, and low-dose lead acetate exposure induces an increase of NO involving mainly AT2 receptor activation and the PI3K/Protein Kinase B/Akt pathway.
TL;DR: F fry from Nile tilapia was used to evaluate the effects of lead acetate by chronic exposure on the growth and the activities of the digestive enzymes after 30 and 60 days exposures, and the digestive enzyme response is discussed as a possible limited biomarker of exposure, to be used in biomonitoring.
Abstract: Lead is a metal capable of affecting physiology and metabolism in fish, including Nile tilapia (Oreochromis niloticus). However, few studies have evaluated the effects of lead on digestive enzyme activities in fry. At that stage, independent feeding begins, and there is increased demand and consumption of food, so chronic exposure to metal during this stage of development would cause null or minimal growth in organisms. In this study, fry from Nile tilapia was used to evaluate the effects of lead acetate by chronic exposure on the growth and the activities of the digestive enzymes after 30 and 60 days exposures. Four treatment groups 0.025, 0.050, 0.075 and 0.100 mg/L of lead acetate and a lead-free control were established. The activity of enzymes decreased, in the case of acidic proteases after 30 days and lipases after 60 days of exposure, from 0.025 and 0.050 mg/L of lead acetate, respectively. The amylase activity increased in metal-treated, while the chymotrypsin decreased partially at 60 days. Lipases decreasing activity might be causing an increase of triglycerides (lipids) and body mass observed during the first 30 days of exposure. Concentrations, equal to or above 0.075 mg Pb/L, cause significant effects on size and weight of fry, with nearly 54% lower than controls. At chronic exposure and early stage of development, the enzymatic activity is partially reduced along with body weight gain, which would affect subsequent growing and aquaculture production. The digestive enzyme response is discussed as a possible limited biomarker of exposure, to be used in biomonitoring.
25 Mar 2020
TL;DR: The results of this study reveal that methanol extract has a very strong antioxidant effect and can reduce the influence of toxicity induced by lead acetate in mice kidney.
Abstract: In this study, we determine the curative effects of okra pods (Abelmoschus esculentus L.) extract against lead acetate toxicity in mice kidney. n-Hexane, ethyl acetate, and methanol solvent were used for extracting okra pods. The role of the extract as an antioxidant was tested by DPPH and FRAP methods. The methanol extract was used for experiments in animals. A total of 30 male BALB/c mice were randomly divided into six equal groups: normal control, negative control (lead-induced), and treatment groups (lead-induced for 28 days and administration of methanol extract at doses of 50, 100, 200, and 400 mg/kg BW for the 28 days). The following were analyzed in all groups: activity of the antioxidant enzymes, namely, superoxide dismutase (SOD) and catalase (CAT); oxidant level, namely, malondialdehyde (MDA) and nitric oxide (NO); and markers of kidney injury, namely, blood urea nitrogen (BUN) and creatinine (Cre). Kidney histopathology was also evaluated. This study showed that the methanol extract showed the highest antioxidant activity (IC50 is 35.21 µg/mL, and FRAP is 57.58 µM Fe2+/g). The CAT and SOD activities increased significantly in okra-treated groups ( ). The okra administration groups experienced a significant decrease in MDA, NO, BUN, and Cre levels ( ). Thickness of the epithelial proximal tubule, diameter of the proximal tubule, and percentage of necrotic cells in proximal tubule decreased, but the diameter ratio of glomerular Bowman’s capsule in mice treated with okra was optimally improved and repaired like normal control ( ). The results of this study reveal that methanol extract has a very strong antioxidant effect and can reduce the influence of toxicity induced by lead acetate in mice kidney.