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1.
Biocell ; 33(3): 187-197, Dec. 2009. ilus
Article in English | LILACS | ID: lil-595016

ABSTRACT

The effect of manganese toxicity on the ultrastructure of the olfactory bulb was evaluated. Male albino mice were injected intraperitoneally with MnCl2 (5 mg/Kg/day) five days per week during nine weeks. The control group received NaCl (0.9%). The olfactory bulbs of five mice from each group were processed for transmission electron microscopy after 2, 4, 6 and 9 weeks of manganese treatment. On week 2, some disorganization of the myelin sheaths was observed. After 4 weeks, degenerated neurons with dilated cisternae of rough endoplasmic reticulum and swollen mitochondria appeared. A certain degree of gliosis with a predominance of astrocytes with swollen mitochondria, disorganization of the endomembrane system, dilation of the perinuclear cisternae and irregularly shaped nuclei with abnormal chromatin distribution were observed after 6 weeks. Some glial cells showed disorganization of the Golgi apparatus. On week 9, an increase in the number of astrocytes, whose mitochondrial cristae were partially or totally erased, and a dilation of the rough endoplasmic reticulum were found. Neurons appear degenerated, with swollen mitochondria and a vacuolated, electron dense cytoplasm. These changes seem to indicate that the olfactory bulb is sensitive to the toxic effects of manganese.


Subject(s)
Male , Animals , Mice , Golgi Apparatus , Golgi Apparatus/ultrastructure , Astrocytes , Astrocytes/ultrastructure , Chlorides/toxicity , Endoplasmic Reticulum, Rough , Endoplasmic Reticulum, Rough/ultrastructure , Olfactory Bulb , Olfactory Bulb/ultrastructure , Manganese Compounds , Microscopy, Electron, Transmission , Mitochondria , Mitochondria/ultrastructure , Neuroglia , Neuroglia/ultrastructure , Neurons , Neurons/ultrastructure
2.
West Indian med. j ; 58(5): 422-427, Nov. 2009. ilus, tab
Article in English | LILACS | ID: lil-672514

ABSTRACT

Aluminium has a unique combination of physical and chemical properties which has enabled man to put this metal to very wide and varied use. However, prolonged exposure to aluminium ions may lead to adverse health effects. In this study, we evaluated the effects of dietary aluminium on the protein composition and the intrinsic activity of cytochrome oxidase (COX) for brain mitochondria. New Zealand white rabbits were maintained on a diet of commercial rabbit pellets and distilled water for a period of 12 weeks. For the experimental group, AlCl3, 330mg/kg/L was added to the drinking water. When compared to the control, mitochondria isolated from the brains of the AlCl3 fed rabbits showed no change in Km but an approximate 35% decrease in both the low and high affinity Vmax values. Also, whereas the protein composition of the mitochondria from both sources appeared to be normal, isolation of highly purified COX proved to be difficult and for the AICI3 fed rabbits, a number of the enzyme's low molecular weight subunits were absent. These results appear to confirm a relationship between long term aluminium consumption and low brain COX activity; they further suggest that an altered COX structure may be the cause of the low enzymic activity.


El aluminio posee una combinación única de las propiedades físicas y químicas que ha permitido al ser humano hacer un uso amplio y variado de este metal. Sin embargo, un número de estudios recientes, sugiere que la exposición prolongada a los iones de aluminio puede tener efectos nocivos sobre la salud. En el presente estudio, evaluamos los efectos del aluminio dietético sobre la composición proteínica y la actividad intrínseca de la oxidasa citocrómica (COX) para la mitocondria cerebral. Conejos blancos de Nueva Zelanda, fueron mantenidos con una dieta de alimento para conejos y agua destilada por un período de 12 semanas. Para el grupo experimental AlCl3, 330mg/kg/L fueron añadidos al agua potable. En comparación con el grupo de control, las mitocondrias aisladas de los cerebros de los conejos alimentados con AlCl3 no mostraron cambios en Km pero hubo una disminución de aproximadamente 35% tanto en los valores Vmax de baja y alta afinidad. Por otro lado, mientras que la composición proteica de las mitocondrias de ambas fuentes parecía ser normal, resultó difícil aislar el COX altamente purificado y un número de enzimas de subunidades de bajo peso molecular MMMM estuvieron ausentes. Estos resultados parecen confirmar una relación entre el consumo de aluminio a largo plazo y la baja actividad del COX del cerebro. Asimismo, sugieren que una alteración de la estructura del COX puede ser la causa de una baja actividad enzimática.


Subject(s)
Animals , Rabbits , Aluminum Compounds/toxicity , Brain/metabolism , Chlorides/toxicity , Electron Transport Complex IV/drug effects , Electron Transport Complex IV/metabolism , Mitochondria/enzymology , Administration, Oral , Aluminum Compounds/administration & dosage , Astringents/administration & dosage , Astringents/toxicity , Brain Chemistry/drug effects , Brain/enzymology , Chlorides/administration & dosage , Mitochondria/chemistry
3.
Journal of Veterinary Science ; : 15-22, 2009.
Article in English | WPRIM | ID: wpr-151239

ABSTRACT

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/metabolism
4.
J Environ Biol ; 2005 Jun; 26(2 Suppl): 349-53
Article in English | IMSEAR | ID: sea-113807

ABSTRACT

The effect of aluminium on shoot-root fresh weight and water relations [water potential (psiw), osmotic potential (psis), turgor potential (psip), and relative water content (RWC)] was studied in cowpea. The 3 microg g(-1) Al showed slight enhancement in psiw and psip in test plants. Concentrations beyond 3 microg g(-1) Al significantly decreased psiw (less negative) and psip. Relative water content (RWC) vis a vis the fresh weight was also affected adversely at higher Al concentrations.


Subject(s)
Aluminum Compounds/toxicity , Chlorides/toxicity , Dose-Response Relationship, Drug , Fabaceae/drug effects , Toxicity Tests , Water/metabolism
5.
Indian J Exp Biol ; 2000 Sep; 38(9): 948-50
Article in English | IMSEAR | ID: sea-60347

ABSTRACT

Aluminium (Al; 50 mg AlCl3/kg body wt/day) treatment caused a marked change in histological picture of normal brain as indicated by an increased number of vacuolated spaces. These changes returned to normal partially by simultaneous treatment with nifedipine (0.7 mg/kg body wt/day) and completely by similar treatment with 50 ppm calcium (CaCl2; 12.5 mg/kg body wt./day). Neither nifedipine nor calcium treatment alone altered the normal histological condition. The histological changes could not be correlated with the decrease in calcineurin activities in brain as nifedipine decreases calcineurin activity without any histological changes. Hence the histological changes may be considered as specific for Al and not due to a general decrease in calcineurin activity.


Subject(s)
Aluminum Compounds/toxicity , Animals , Brain/drug effects , Brain Diseases/chemically induced , Calcineurin/metabolism , Calcium/therapeutic use , Calcium Channel Blockers/therapeutic use , Calcium Channels/drug effects , Chlorides/toxicity , Homeostasis/drug effects , Male , Nifedipine/therapeutic use , Rats , Rats, Sprague-Dawley
6.
Indian Heart J ; 1992 May-Jun; 44(3): 177-80
Article in English | IMSEAR | ID: sea-3094

ABSTRACT

Experiments were carried out in rabbits to determine the effects of prolonged treatment of cadmium (8 mg/kg/day) for a period of 6 months on histopathological changes and biochemical alterations of lipid profiles in various tissues compared to normal rabbits. No ECG changes were observed before and at the end of cadmium treatment. Histopathological studies of the coronary artery revealed atherosclerotic changes. Total lipids, cholesterol, free fatty acids and phospholipids were significantly increased in heart and kidney, but decreased in serum and liver. Triglyceride content was increased significantly in heart and kidney with a significant depletion in liver and serum. It is postulated that atherosclerotic changes in rabbits probably occurred through toxic effects of cadmium but the exact mechanism needs to be elucidated.


Subject(s)
Animals , Arteriosclerosis/chemically induced , Cadmium/toxicity , Cadmium Chloride , Cadmium Poisoning/pathology , Chlorides/toxicity , Coronary Artery Disease/chemically induced , Coronary Vessels/pathology , Kidney/pathology , Lipids/blood , Liver/pathology , Male , Muscle, Smooth, Vascular/pathology , Rabbits
7.
Indian J Exp Biol ; 1992 Mar; 30(3): 241-3
Article in English | IMSEAR | ID: sea-58245

ABSTRACT

Daily administration of cadmium salt for 25 days (2.5 mg per Kg body weight) in the male domestic fowl caused the end of treatment period. An increased incidences of concentration. Fertility dropped to zero at the end of the treatment period. Activity of acid and alkaline phosphomonoesterases were also drastically reduced by the end of treatment period. An increased incidences of morphological abnormalities of spermatozoa were noticed in the treated birds. After 46 days cessation of the treatment, full recovery of the above measures was found. These alterations suggest the reversible type of effect of cadmium chloride on the spermatozoa of male domestic fowl.


Subject(s)
Animals , Cadmium/toxicity , Cadmium Chloride , Chickens , Chlorides/toxicity , Fertility/drug effects , Male , Phosphoric Monoester Hydrolases/metabolism , Semen/drug effects , Sperm Count/drug effects , Spermatozoa/drug effects
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