Effect of aluminum on regional brain antioxidant defense status in Wistar rats

Julka, Deepinder; Gill, Kiran Dip

doi:10.1007/bf02576841

Cited by 37 publications

(17 citation statements)

References 24 publications

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“…This finding was in agreement with the results achieved by Agrawal et al [8]. The ability of melatonin to inhibit AchE activity and improve cognitive functions is related to its effect in balancing oxidant/antioxidant status and regulating the generation of inflammatory mediators particularly TNF-a and IL-1b [9].…”

Section: Discussionsupporting

confidence: 93%

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Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

et al. 2012

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This study aimed to elucidate the mechanisms of melatonin to manage neurological damage in Alzheimer's disease (AD) induced in ovariectomized rats. Forty adult female rats were enrolled in our study and were classified as; gonad intact control, ovariectomized control group, ovariectomized rats received melatonin, ovariectomized rats injected with AlCl 3 to induce AD and ADinduced rats treated with melatonin. Hydrogen peroxide (H 2 O 2 ), malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT), B cell lymphoma 2 (Bcl-2), brain derived neurotrophic factor (BDNF), acetylcholinesterase (AchE) and acetylcholine (Ach) were estimated in the brain tissues of the different groups. Treatment of AD-induced rats with melatonin produced marked improvement in the most studied biomarkers which was confirmed by histological investigation of the brain. In Conclusion, melatonin significantly ameliorates the neurodegeneration characteristic of AD in experimental animal model due to its antioxidant, antiapoptotic, neurotrophic and anti-amyloidogenic activities.

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Section: Discussionsupporting

confidence: 93%

“…with aluminum chloride (AlCl 3 ) dissolved in distilled water daily for 3 months in a dose of 4.2 mg/Kg b wt [9], after 3 months of surgical operation and served as Al-intoxicated control group.…”

Section: Experimental Designmentioning

confidence: 99%

Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

et al. 2012

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“…The observed reduction in the level of GSH, that is a major source of reducing power in the aqueous compartment of the cell, further suggests increased prooxidant status in these cells. This finding is similar to a study which demonstrated that chronic exposure of rats to aluminum leads to a decrease in glutathione peroxidase which parallels an increase in lipid peroxidation [20]. Although our previous work demonstrated that aluminum promotes iron-dependent oxidative processes in subcellular systems [10], in the intact animal, exogenous iron did not interact with aluminum [21].…”

Section: Discussionsupporting

confidence: 90%

Aluminum-induced oxidative events in cell lines: glioma are more responsive than neuroblastoma

Campbell

Prasad²,

Bondy

1999

Free Radical Biology and Medicine

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Abstract-Aluminum, a trivalent cation unable to undergo redox reactions, has been linked to many diseases such as dialysis dementia and microcytic anemia without iron deficiency. It has also been implicated in Alzheimer's disease although this is controversial. Because cell death due to oxidative injury is suspected to be a contributory factor in many neurological diseases and aluminum neurotoxicity, glioma (C-6) and neuroblastoma (NBP 2 ) cells were utilized to assess early changes in oxidative parameters consequent to a 48-h exposure to aluminum sulfate. A 500-M concentration of this salt produced a significant increase in reactive oxygen species (ROS) production and a significant decrease in glutathione (GSH) content in glioma cells. However, the same concentration of the aluminum salt did not lead to any significant changes in the neuroblastoma cells. Mitochondrial respiratory activity in glioma cells was also found to be significantly higher in the aluminum treated cells. As judged by morin-metal complex formation, aluminum can enter glioma cells much more readily than neuroblastoma cells. Thus, it is possible that the cerebral target following an acute exposure to aluminum may be glial rather than neuronal.

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“…Furthermore, neurologic disorders are often accompanied by increased rates of lipid peroxidation in the brain and aluminum appears able to enhance the intracellular oxidative phenomena [46] through an enhancement of the iron catalyzed, oxygen-derived free radical production [47] which in turn can affect both proteins oxidation (and then their turnover) or membrane lipid peroxidation [48] (and then membrane integrity and efficiency). Similar conclusions can be achieved from 'in vivo' experiments showing that increased levels of lipid peroxidation in animals treated with aluminum are paralleled by a decrease of the activity of antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase [49]. Moreover, it has been reported that several proteases are induced by the presence of oxidatively damaged proteins [50,51] and that aluminum promotes prooxidant events in the brain [52].…”

Section: Discussionsupporting

confidence: 68%

Aluminum modulation of proteolytic activities

Lupidi

Angeletti

Eleuteri

et al. 2002

Coordination Chemistry Reviews

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The effect of aluminum ions on the activity of proteolyic activities, mainly serine proteases and calpains, has been examined. Aluminum affects the biological activity of proteolytic activities either through a direct effect on the enzyme molecule or through a deregulation of the control mechanisms acting on them. Binding of the ion, most likely results in molecular rearrangements affecting both the substrates binding site and the site involved in the recognition of macromolecular inhibitors. As whole, the data reported clearly indicate that aluminum significatively affects the intracellular protein turnover, most likely triggering catastrophic events for the cellular life. The physiopathological significance of these effects has been discussed, in particular for neurological disorders (the Alzheimer's disease included) where an imbalance of proteolytic as well as antiproteolytic systems appears a crucial event both for the formation of neuritic plaques and neurofibrillary tangles which are the major hallmarks of the disease. #

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Effect of aluminum on regional brain antioxidant defense status in Wistar rats

Cited by 37 publications

References 24 publications

Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

Aluminum-induced oxidative events in cell lines: glioma are more responsive than neuroblastoma

Aluminum modulation of proteolytic activities

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