Aluminum Enhances Iron Uptake and Expression of Neurofibrillary Tangle Protein in Neuroblastoma Cells

Abreo, Kenneth; Abreo, Fleurette; Sella, M; Jain, Sushil K.

doi:10.1046/j.1471-4159.1999.0722059.x

Cited by 36 publications

(11 citation statements)

References 36 publications

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“…The neurotoxic effect of Al has also been related to the morphological and biochemical characteristics of beta-amyloid and neurofibrillary tangles and has often been related to oxidative stress [50]. The evidence in mouse neuroblastoma cells indicated that Al enhance Fe uptake and the expression of neurofibrillary tangle protein [51]. Apparently, this evidence supported that Al may still be a toxicant playing a pivotal role in the causation of uremic patients with dementia.…”

Section: Discussionmentioning

confidence: 96%

Alterations in Trace Elements and Oxidative Stress in Uremic Patients with Dementia

Guo¹,

Ko²,

Chen³

et al. 2009

Biol Trace Elem Res

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The present study was conducted to compare the trace elements and oxidative status between uremic patients with and without dementia. Chronic hemodialysis patients with dementia (n = 20) and without dementia (n = 25), and age-matched healthy volunteers (n = 20) were enrolled. The nutritional status, blood levels of trace elements aluminum (Al), zinc (Zn), copper (Cu), magnesium (Mg) and iron (Fe), malondialdehyde (MDA), and protein carbonyl production, antioxidant enzymes glutathione peroxidase (GPx), and glutathione reductase (GR) activities were measured. No significant difference in nutritional status or clinical characteristics was observed between nondementia and dementia patients. However, uremic patients with dementia have significantly higher Al, Cu, and Mg and lower Zn concentrations, as well as increased Cu/Zn ratio in comparison to nondementia patients. There were statistically significant increased MDA and carbonyl production and decreased GPx and GR activities in dementia patients. Furthermore, the significant associations of Al, Mg, and Cu/Zn ratio with oxidative status in patients with dementia were noted. The dementia may initially worsen with abnormal metabolism of trace elements and oxidative stress occurrence. Our results suggest that abnormalities in trace element levels are associated with oxidative stress and may be a major risk factor in the dementia development of uremic patients.

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Section: Discussionmentioning

confidence: 96%

Alterations in Trace Elements and Oxidative Stress in Uremic Patients with Dementia

Guo¹,

Ko²,

Chen³

et al. 2009

Biol Trace Elem Res

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“…Taking together the present and previous findings, it is conceivable that fucoidan-binding Al may move into the S-phase nucleus. A number of studies of a variety of cultured cell lines have shown that Al loading resulted in abnormal Fe accumulation and compartmentalization [31][32][33]. Co-localization of Al and Fe has been found in hepatocytes of dialysis patients [34].…”

Section: Discussionmentioning

confidence: 99%

Intracellular Changes of Metal Elements by Fucoidan Extracted from Brown Seaweed (Cladosiphon okamuranus)

Nagamine

Takada

Kusakabe

et al. 2008

Biol Trace Elem Res

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This study was undertaken to elucidate the intracellular changes of metal elements after the administration of fucoidan extracted from Cladosiphon okamuranus. TRL1215 cells (normal rat liver cell line) were treated with 0, 0.1, or 1.0 mg/ml fucoidan and incubated in 5% CO2 at 37 degrees C. The cellular levels of Mg, Al, Fe, and Zn were significantly increased in the 1.0 mg/ml fucoidan-treated cells compared to those of the 0.1 mg/ml fucoidan-treated cells and the control. Next, TRL1215 cells were cultured on Mylar film overnight. At 24 h after 5-bromo-2'-deoxyuridine dosing, 0, 0.1, or 1.0 mg/ml fucoidan was treated for 9 h. The cellular distribution of elements was analyzed using in-air micro-micro-particle induced X-ray emission. The X-ray spectra showed that yields of Al, Mg, and Zn were high in order of the 1.0 mg/ml fucoidan-treated sample, the 0.1 mg/ml fucoidan-treated sample, and the control. Fe yield was mildly increased by fucoidan administration. In fucoidan-treated cells, the focal accumulation of Br was correlated spatially with phosphorous-rich region, suggesting that Br was localized within the nucleus. Al distribution provided a spatial association with Br map. These data suggest that fucoidan increases the accumulations of Al, Mg, Fe, and Zn in normal rat hepatocytes, and fucoidan-binding Al is postulated to be transferred into the nucleus.

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“…Caspase Activity Assay The PC12 cells (1ϫ10 7 ) were washed twice with CMF-PBS and then suspended in an icecold 50-mM potassium phosphate buffer (pH 7.5). To prevent the non-specific cleavage of proteins, cell lysis was performed by two cycles of freezing and thawing at 4°C.…”

Section: )mentioning

confidence: 99%

“…6) Several lines of research that use cultured cells and the aluminum-maltolate complex (Al(maltol) 3 ), which is a membrane permeable, lipophilic complex of Al, also showed that the exposure of cells such as the Neuro-2a murine neuroblastoma cells, 7) human NT2 neuroblastoma cells, 8) and PC12 cells 9,10) to the Al complex results in a decrease in cell viability via the apoptotic cell death pathway. Recently, we have reported that the treatment of PC12 cells with Al(maltol) 3 causes a decrease in the levels of the intracellular reduced glutathione depending on the amount of Al(maltol) 3 accumulated in the cells.…”

mentioning

confidence: 99%

Involvement of NO Generation in Aluminum-Induced Cell Death

Satoh

Yasuda

Yamada

et al. 2007

Biological & Pharmaceutical Bulletin

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Aluminum (Al) is the third most abundant element in the earth's crust and has been implicated as an etiologic factor in neurological disorders including Alzheimer's disease, 1,2) Parkinson's dementia syndrome, and dialysis encephalopathy syndrome. 3,4) In fact, some evidence supports the selective accumulation of Al within neurons containing neurofibrillay tangles in patients with Alzheimer's disease and within the aging human brain. 1,5) Meiri et al., have also reported that brain Al concentrations reach submilimolar levels in some encephalopathies.6) Several lines of research that use cultured cells and the aluminum-maltolate complex (Al(maltol) 3 ), which is a membrane permeable, lipophilic complex of Al, also showed that the exposure of cells such as the Neuro-2a murine neuroblastoma cells, 7) human NT2 neuroblastoma cells, 8) and PC12 cells 9,10) to the Al complex results in a decrease in cell viability via the apoptotic cell death pathway. Recently, we have reported that the treatment of PC12 cells with Al(maltol) 3 causes a decrease in the levels of the intracellular reduced glutathione depending on the amount of Al(maltol) 3 accumulated in the cells. 11) These findings strongly suggested that Al accumulation in tissues is closely related to the development of neurodegenerative disorders although a causal relationship between Al and neurodegenerative disorders remains unclear.NO is considered to be a modulator and a simple and diffusible free radical.12) It is believed to play an important role in physiological and pathophysiological events in many cellular systems. [13][14][15] Furthermore, it has also been reported that NO concentration increased in the brain during the course of ischemia, Alzheimer's disease, and other degenerative conditions. [16][17][18] Numerous studies in several cell systems have demonstrated that NO is closely related to cell death mechanisms and plays the role of a mediator. [19][20][21][22][23] A recent study has reported that NO is produced in the mitochondria via Ca 2ϩ -dependent mitochondrial NO synthases (mtNOS). [24][25][26] The NO produced in the mitochondria by mtNOS plays the role of a modulator of mitochondrial oxygen consumption and transmembrane potential via a reversible reaction with cytochrome c oxidase. It is well-known that NO rapidly reacts with superoxide anion radicals to form peroxynitrite, which is an oxidant substance producing cytotoxic effects in many cells. 14,20) Previously, we have reported that accumulation of Al(maltol) 3 in PC12 cells results in apoptotic cell death depending on the intracellular generation of reactive oxygen species (ROS).10) Therefore, it would be interesting to determine if intracellular NO generation is involved in the onset mechanism of Al-mediated-cytotoxicity. Therefore, in the present study, we examined the effects of a NO generator and NO synthase inhibitors on Al(maltol) 3 -induced cell death. Our results suggest that intracellular NO generation may play an important role in the development of cell toxicity associated wit...

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Aluminum Enhances Iron Uptake and Expression of Neurofibrillary Tangle Protein in Neuroblastoma Cells

Cited by 36 publications

References 36 publications

Alterations in Trace Elements and Oxidative Stress in Uremic Patients with Dementia

Alterations in Trace Elements and Oxidative Stress in Uremic Patients with Dementia

Intracellular Changes of Metal Elements by Fucoidan Extracted from Brown Seaweed (Cladosiphon okamuranus)

Involvement of NO Generation in Aluminum-Induced Cell Death

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