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Differential expression of metallothionein-l and cytochrome p450-2a5 (cyp2a5) in mice in response to lead acetate exposure and industrial effluents in Ibadan, Nigeria
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THE SOCIAL RELATIONS OF IMPORTED USED ELECTRONICS MERCHANDISE IN LAGOS, NIGERIA
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Page will reload when a filter is selected or excluded.- oxidative stress 7 results 7
- Oxidative stress 6 results 6
- rats 5 results 5
- Antioxidants 4 results 4
- Rats 4 results 4
- DNA damage 3 results 3
- Environmental Management 3 results 3
- Environmental Sciences 3 results 3
- Lead poisoning continues to pose a serious health challenge and more significantly so in developing countries with ineffective waste disposal systems. Recent efforts at solving lead poisoning issues have seen entire towns being resettled from lead-contaminated areas. This study was designed to investigate whether withdrawal of lead exposure results in a resolution of toxic effects of lead in cardiac tissues. Adult male Wistar rats were exposed orally to lead acetate (PbA) at doses of 0.25, 0.5, and 1.0 mg/ml for 6-week duration, after which one-half was sacrificed and the remaining left for a further 6 weeks without lead treatment. Exposure of rats to PbA produced significant decline (P < 0.05) in the activities of antioxidant parameters, including superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT), and reduced glutathione (GSH), whereas malondialdehyde (MDA) concentration was significantly elevated. Animals from the withdrawal period exhibited a similar pattern of alterations, with a significant (P < 0.05) reduction in GSH, GPx, and SOD and a significant elevation in MDA and H2O2 concentrations. However, GST activity was elevated, whereas CAT activity remained unaltered in the withdrawal period. The results of this study showed that cardiotoxicity indicated by induction of oxidative stress and reduction in antioxidant parameters failed to resolve upon withdrawal of lead exposure in male rats during the period of study. 3 results 3
- cardiotoxicity 3 results 3
- lead acetate 3 results 3
- — — — — — Environmental Studies 3 results 3
- Agriculture & Life Systems 2 results 2
- Agriculture & Life Systems — Food Systems 2 results 2
- Antioxidant 2 results 2
- Antioxidant enzymes 2 results 2
- Brain 2 results 2
- Cardiotoxicity 2 results 2
- Cholinergic System 2 results 2
- Clarias gariepinus 2 results 2
- Cobalt (Co) toxicity has been reported to produce central nervous system and gastrointestinal abnormalities. This study assessed the therapeutic effect of cholecalciferol (Cho) supplementation against damages caused by sub-acute (14-day) cobalt chloride (CoCl2) exposure in the brain and intestines. Thirty-five male Wistar rats were divided equally into five groups: Group I (control) received no treatment; Group II received oral CoCl2 (100 mg/kg) only; Groups III, IV, and V received 1000, 3000 and 6000 IU/kg of cholecalciferol, respectively by oral gavage, and concurrently with CoCl2. Cobalt-treated rats showed neuronal vacuolation and presence of pyknotic nuclei in the cerebral cortex and hippocampus, depletion of Purkinje cells in the cerebellum, as well as inflammation and congestion in the intestinal mucosa. Cobalt also increased brain and intestinal hydrogen peroxide (H2O2) and malondialdehyde (MDA) concentrations, while simultaneously reducing glutathione (GSH) content, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities. Further, CoCl2 induced increases in brain acetylcholinesterase (AchE) activity and serum zonulin (ZO-1) levels. Conversely, Cho administration suppressed CoCl2-induced damages in the brain and intestines by reducing lipid peroxidation and increasing the activities of antioxidant enzymes. Remarkably, Cho produced stimulation of brain choline acetyltransferase (ChAT) and suppression of AchE activity, along with dose-dependent reduction in serum levels of ZO-1, intestinal fatty acid-binding protein (iFABP) and nitric oxide. In conclusion, the protective role of cholecalciferol against cobalt-induced toxicity occurred via modulation of cholinergic, intestinal permeability and antioxidant pathways. The results may prove significant in the context of the role of gut-brain connections in neuroprotection. 2 results 2
- Cobalt chloride 2 results 2
- Germ and somatic cell mutation 2 results 2
- Intestinal Fatty Acid-Binding Protein 2 results 2
- Intestines 2 results 2
- Kolaviron 2 results 2
- Metal oxide nanoparticles 2 results 2
- Quercetin 2 results 2
- Titanium dioxide (TiO2) and zinc oxide (ZnO) nanoparticles are components of personal care products whose continuous release into the environment may enhance co-exposure, with potential risks to the ecosystem. In vitro studies have shown their potential to induce genetic damage. However, there is dearth of information on in vivo induction of DNA and systemic damage, alongside their interactive effects. This study was designed to investigate genetic and systemic toxicity and mechanism of DNA damage by TiO2 and ZnO nanoparticles and their mixture in mice. Male Swiss mice (=24.0±2.0g; n=80; 6-8 weeks old) were intraperitoneally exposed to distilled water (Control) and 9.4, 18.8, 37.5, 75.0 and 150.0 mg/kg concentrations of each of the nanoparticles and their mixture (1:1) for 5 days (5 mice/group) to assess micronucleus induction and cytomorphological abnormalities in the bone marrow of mice. Haematological parameters [Haemoglobin, Packed Cell Volume (PCV), Red Blood Cell (RBC) and White Blood Cell (WBC) counts] were assessed following standard procedures. Mechanism of DNA damage was evaluated by oxidative stress [Superoxide dismutase (SOD), reduced Glutathione and Malondialdehyde in the liver and kidney] parameters following standard methods. Sperm count, motility, abnormalities and concentrations of Luteinizing Hormone (LH), Follicle Stimulating Hormone (FSH) and Testosterone were evaluated in another group of mice (=30.0±2.0g; n=80; 11-15 weeks old), intraperitoneally exposed with the same nanoparticle concentrations (5 mice/group) at 35-day exposure. Liver, kidney and testis were sectioned for histopathological analysis. The Interaction Factor (IF) of nanoparticle mixture was calculated according to standard method. Data were analysed using descriptive statistics and ANOVA at α0.05. The nanoparticles and mixture induced micronuclei, but significant only for TiO2 (16.8±2.1-53.3±18.5) compared with the control (3.7±0.9). Blebbed, target, hyperchromic and hypochromic erythrocytes were the observed cytomorphological anomalies. The mixture exerted a significant reduction only in the WBC count. In the liver, there was a significant decrease in SOD (unit/mg protein) activities (1.3-1.5; 1.4-2.0; and 1.2-1.6 fold for TiO2, ZnO and mixture, respectively), with increase in Malondialdehyde (nmol/mg protein) levels (1.1-1.7; 1.2-1.8; and 1.7-1.7 fold for TiO2, ZnO and mixture, respectively). In the kidney, there were significant alterations in SOD: 1.2-1.3; and 1.1-1.4 fold decrease for TiO2 and ZnO, respectively; and 1.3-2.0 fold increase for the mixture. While Malondialdehyde levels increased (1.2-1.4; 1.4-1.6; and 1.7-1.9 fold for TiO2, ZnO and mixture, respectively). Both organs showed alterations in reduced Glutathione levels (1.0-1.5 fold decrease for TiO2; 1.0-1.1 fold increase for ZnO and mixture) indicating systemic toxicity. A significant decrease in sperm count and motility; and increase in abnormalities (1.3-8.0; 1.2-2.6; 4.6-12.1 fold for TiO2, ZnO and mixture, respectively), with a concomitant decrease in the serum level of LH and increase in FSH and Testosterone were observed. Hepatocellular and spermatogenic cell necrosis and degeneration of tubular epithelial cells were observed. The IF indicated synergism. Titanium dioxide and zinc oxide nanoparticles and their mixture induced genomic and systemic damage in somatic and germ cells of mice; with the mixture synergistically evoking the highest toxic response. Oxidative stress might be one of the mechanisms of cytogenotoxicity. 2 results 2
- Zonulin 2 results 2
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