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Introduction: Aluminium, a ubiquitous metal implicated in some neurodegenerative diseases is linked to activation of free oxygen species. The antioxidant-rich plants, Moringa oleifera (MO) is reported to protect against Aluminium activities. This study investigated the actions of MO leaf extract (MOLE) against Aluminium chloride (AlCl3)- induced hippocampal cellular changes and serum levels of alkaline phosphatase (ALP), aspartate transaminase (AST) and alanine transaminase (ALT) in adult Wistar rats.Materials and Methods: Thirty Wistar rats weighing between 150 g and 220 g were grouped (n=5) into; 1-control (5 mL/kg distilled water), 2-AlCl3 (100 mg/kg), 3-low dose MOLE (250 mg/kg), 4-high dose MOLE (1,000 mg/kg), 5-concurrent AlCl3 and low dose MOLE, and 6-concurrent AlCl3 and high dose MOLE. All administrations were by oral gavages for 21 days. On day 22, following deep anaesthesia and cardiac puncture, blood was obtained for serum enzyme analysis, and the brain perfusion fixed, harvested and processed for histological study.Results: Results showed significantly (p < 0.05) higher ALP level in the AlCl3 group compared with the control, as well as the other test groups. However, there was no significant (p > 0.05) AST and ALT levels. The hippocampal CA3 of the AlCl3 group showed hypertrophic cells, with some of the cells having karyorrhectic features. The concurrent AlCl3 and low and high doses, MOLE groups showed less of these adverse features.Conclusion: These results suggest that MOLE may protect enzymatic activities against Aluminium chloride. However, its action on hippocampus is still subject to further investigation.
Introducción: El aluminio, un metal presente en diversos lugares implicado en algunas enfermedades neurodegenerativas, está relacionado con la activación de especies reactivas de oxígeno. Se informa que las plantas ricas en antioxidantes, Moringa oleifera (MO) protegen contra la acción del aluminio. Este estudio investigó las acciones del extracto de hoja de MO (MOLE) en los cambios celulares del hipocampo inducidos por el cloruro de aluminio (AlCl3) y los niveles séricos de fosfatasa alcalina (ALP), aspartato transaminasa (AST) y alanina transaminasa (ALT) en ratas Wistar adultas.Materiales y métodos: SE utilizaron treinta ratas Wistar divididas en 5 grupos, los animales pesaban entre 150 gy 220 g; 1 control (5 ml / kg de agua destilada), 2-AlCl3 (100 mg / kg), 3 MOLE de dosis baja (250 mg / kg), 4 MOLE de dosis alta (1000 mg / kg), 5 AlCl3 concurrente y MOLE de dosis baja, y MOLE 6-concurrente y MOLE de dosis alta. Todas las administraciones fueron por sonda oral durante 21 días. El día 22, después de la anestesia profunda y la punción cardíaca, se obtuvo sangre para el análisis de las enzimas séricas y la perfusión cerebral se fijó, recogió y procesó para el estudio histológico.Resultados: Los resultados mostraron un nivel de ALP significativamente (p <0.05) más alto en el grupo AlCl3 en comparación con el control, así como en los otros grupos de prueba. Sin embargo, no hubo niveles significativos (p> 0.05) de AST y ALT. El hipocampo CA3 del grupo AlCl3 mostró células hipertróficas, y algunas de las células tenían características cariorrecticas. Los grupos de AlCl3 concurrentes y dosis bajas y altas, MOLE mostraron menos de estas características adversas.Conclusión: Estos resultados sugieren que MOLE puede proteger las actividades enzimáticas contra el cloruro de aluminio. Sin embargo, su acción sobre el hipocampo aún está sujeta a más investigaciones.
Subject(s)
Animals , Rats , Moringa oleifera/anatomy & histology , Aluminum Chloride/administration & dosage , Hippocampus/anatomy & histology , Rats, WistarABSTRACT
Aims: It has been shown that aluminium and its compounds accumulate in some tissues causing metabolic dysfunctions. This study investigated the effects of vitamin E administration on certain biochemical and antioxidants indices in rat tissues treated with aluminium chloride (AlCl3). Study Design: Twenty four male Wistar rats with average weight of 160 g were randomly selected into four groups and treated as follows; group A(distilled water), group B (vitamin E only,100 mg/kg. bw/day), group C (AlCl3 only,40 mg/kg. bw/day) and group D (vitamin E and AlCl3), all administered orally in 0.2 ml solution for 21 days. Methodology: Biochemical and antioxidant indices were evaluated using standard methods. Results: Results showed that treatment with AlCl3 only (group C) caused significant (P=.05) decreases in Red Blood Cell (WBC) count, Packed Cell Volume (PCV), serum total protein and High Density Lipoprotein-Cholesterol ( HDL-C) with increases in White Blood Cell (WBC) count, triglyceride and total cholesterol. It also elicits significant (P=.05) increases in some liver and kidney indices such as Alanine Aminotransferase (ALT), Gamma Glutamyl Transferase (GGT), alkaline phosphatase (ALP) activities, serum urea and creatinine concentrations. Analysis of antioxidant indices of the liver, kidney, brain and testis also revealed decreases in activities of Superoxide Dismutase (SOD), Catalase (CAT) and Reduced Glutathione (GSH) concentration with corresponding significant (P=.05) increases in Malondialdehyde (MDA) level by AlCl3 administration. In contrast, treatment with vitamin E and AlCl3 (group D) showed improved in metabolic alterations observed in AlCl3 intoxication as these indices were reversed with greater effects observed in group B. Conclusion: Results obtained are indication of antioxidative and tissue protective effects of vitamin E against dyslipidemia and heamatological disorder induced by (AlCl3).
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Objective@#To investigate the influence of aluminum chloride (AlCl3) solution on the embryon-ic development of zebrafish and neurobehavior of juvenile fish.@*Methods@#The embryos of zebrafishat 6 hours after fertilization were exposed to AlCl3 solution at a concentration of 0, 55.0, 60.5, 66.6, 73.5, 80.5, or 100.0 mg/L, and embryonic hatching rates at 48 and 72 hours after fertilization were calculated. The embryos of zebrafishat 6 hours after fertilization were exposed to AlCl3 solution at a concentration of 0, 60.0, 72.0, 86.4, 103.7, or 124.4 mg/L, and the embryonic mortality rates at 12, 24, 48, 72, and 96 hours after fertilization were calculat-ed. The embryos of zebrafish at 6 hours after fertilization were exposed to AlCl3 solution at a concentration of 0, 50, 100, 200, 400, or 800 μg/L, and the changes in the neurobehavior of juvenile fish were observed after hatching, including touch-escape reaction at 72 hours after fertilization and autonomic movement and panic es-cape reflex at 7 days after fertilization.@*Results@#Compared with the 0 mg/L group, the≥66.6 mg/L group had a sig-nificant reduction in embryonic hatching rate at 48 and 72 hours after fertilization, and the ≥72.0 mg/L group had a significant increase in embryonic mortality rate at 96 hours after fertilization (P<0.05) . Compared with the 0 μg/L group, the≥100 μg/L group had a significant reduction in the number of times of touch-escape reaction (P<0.05) .Compared with the 0 and 50 μg/L groups, the 100-800 μg/L groups had significant reductions in total movement distance and average speed (P<0.05) . Compared with the dark period before illumination, all groups had a significant increase in movement speed during the light period of the panic escape reflex test (i.e., the third minute) (P<0.05) ; within 2 minutes after the light was turned off, there was no significant change in movement speed in the 0-200 μg/L groups (P>0.05) ; the 400 and 800 μg/L groups had a significant increase in movement speed (P<0.05) .@*Conclusion@#AlCl3 exposure may cause embryonic developmental disorder in zebrafish and ab-normal neurobehavior in juvenile fish.
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Aluminium is presents in many manufactured foods and medicines and is also added to drinking water for purification purposes. The lungs consist essentially of; the spongy respiratory tissue in which gaseous exchange occurs between blood and air, and a branching system of air tubes called bronchioles and bronchi which “pipe” air into and from the pockets and passageways of the spongy respiratory tissue. The purpose of this study was to evaluate the possible effects that aluminium chloride exposure could have on the histology of lungs of wistar rats. Twenty wistar rats were used for this study. They were well fed with grower mash, provided with adequate water and kept under good ventilation. The wistar rats were divided into five groups as follows: Group I was the control, group II was given 475mg/Kg, group III received 950mg/kg, group IV received 1,425mg/kg and group V received 1,900mg/kg of aluminium chloride through oral intubation for period of eight weeks. The wistar rats were humanely sacrificed, the lungs removed, fixed, processed and stained with Haematoxylin and eosin. Photomicrographs of the lungs showed congested blood vessels in the aluminium treated groups. Based on our observations, we therefore conclude that aluminium chloride exposure was detrimental to the histology of lungs.
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The present experiments were done to determine the effectiveness of a non-specific nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on oxidative stress parameters induced by aluminium chloride (AlCl3) intrahippocampal injections in Wistar rats. Animals were sacrificed 3 h and 30 d after treatments, heads were immediately frozen in liquid nitrogen and forebrain cortices were removed. Crude mitochondrial fraction preparations of forebrain cortices were used for the biochemical analyses: nitrite levels, superoxide production, malondialdehyde concentrations, superoxide dismutase (SOD) activities and reduced glutathione contents. AlCl3 injection resulted in increased nitrite concentrations, superoxide anion production, malondialdehyde concentrations and reduced glutathione contents in the forebrain cortex, suggesting that AlCl3 exposure promoted oxidative stress in this brain structure. The biochemical changes observed in neuronal tissues showed that aluminium acted as a pro-oxidant. However, the non-specific nitric oxide synthase (NOS) inhibitor, L-NAME, exerted anti-oxidant actions in AlCl3-treated animals. These results revealed that NO-mediated neurotoxicity due to intrahippocampal AlCl3 injection spread temporally and spatially to the forebrain cortex, and suggested a potentially neuroprotective effect for L-NAME.
Subject(s)
Animals , Male , Rats , Aluminum Compounds/toxicity , Chlorides/toxicity , Glutathione/metabolism , Malondialdehyde , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide Synthase/antagonists & inhibitors , Nitrites/chemistry , Prosencephalon/drug effects , Rats, Wistar , Superoxide Dismutase/metabolism , Superoxides/metabolismABSTRACT
Objective To develop a complete set of medical water processing and supply system to meet the needs of water in field operations for emergency rescues and disaster relief work, filed advance drill, etc. Methods A complete set of medical water processing and supply system was composed of two parts, including water processing system and water supply system. The means of filtrating, precipitating, sterilizing, adsorbing and ion regulating were adopted in water processing system to purify the water from primitive and to pure state for living or medical treatment. The techniques and equipments such as pressurizing, buffering, current regulating and special pipes, valves, fast joints, etc, were adopted in water supply system, and high performance water-pipe network were established. Results The water processing and supply system has some disadvantages, such as water quality guarantee, water quantity abundance, water flow stabilization, water pressure qualification, and system safety, credibility, low failure-ratio, energy saving etc, and can meet the needs of medical water in field operations. Conclusion The water system can be carried out by design optimizing and can realize mobile and emergencies.
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The toxic and teratogenic effect of AlCl_3 on leghorn chick embryos were studied. Different concentrations of AlCl_3 dissolved in redistilled water were injected into the air sac of the eggs (0.2 ml per egg) on the third day of incubation. It was identified that the maximal permissible dosage was 1.708 ?mol/egg, the minimal lethal dosage was 2.25 ?mol/egg, the absolute lethal dose was 35.34 ?mol/egg, and LD_(50) was 8.09 ?mol/egg. The mortality of the embryos raised with the increase of the dose of AlCl_3. AlCl_3 also retarded the development of chick embryos and showed apparent tetratogenic effects.