Differential toxicity of nitric oxide, aluminum, and amyloid β-peptide in SN56 cholinergic cells from mouse septum

Bielarczyk, Hanna; Jankowska, Agnieszka; Madziar, Beata; Matecki, Andrzej; Michno, Anna; Szutowicz, Andrzej

doi:10.1016/s0197-0186(02)00097-9

Cited by 57 publications

(52 citation statements)

References 43 publications

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“…It has been demonstrated that aluminium interferes with the metabolism of acetyl-CoA, leading to a decrease in mitochondrial acetyl-CoA content [110]. As elevated cholinergic activity stimulates acetyl-CoA synthesis in order to supply it for synthesis of acetylcholine, the deleterious effects of aluminium on this metabolic pathway are more prominent in cholinergic nerve terminals [111][112][113]. The choline used for the synthesis of acetylcholine is either transported from the synaptic cleft (see Section 6) to the presynaptic nerve terminal or is derived from phosphatidylcholine.…”

Section: Neurotransmitter Synthesis and Storagementioning

confidence: 99%

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Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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Section: Neurotransmitter Synthesis and Storagementioning

confidence: 99%

“…In actual fact, the number of perforated synapses, which are known to occur transiently after the induction of long-term potentiation, decreased to a greater extent in the hippocampus. Accordingly, aluminium brings some loss of cell extensions and intercellular connections to differentiated SN56 cholinergic cells in culture [112].…”

Section: Synaptic Strengthmentioning

confidence: 99%

Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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“…Aluminum is considered a potential etiological factor in Alzheimer's disease because Al might induce characteristic brain neurofi brillary of the disease (ElRahman, 2003). The administration of Al compounds causes neuroanatomical and neurochemical alterations in the brain such as neurofi lament accumulation (Simpson et al, 1985), neuron loss (Ghetti et al, 1985) and suppression of the cholinergic system (Julka et al, 1995;Bielarczyk et al, 2003). In addition, Al exposure was found to cause glutamate system impairment such as decreases of glutamate contents in brain (Exley, 1999;Nayak and Chatterjee, 2001).…”

Section: Introductionmentioning

confidence: 99%

Memory performance, brain excitatory amino acid and acetylcholinesterase activity of chronically aluminum exposed mice in response to soy isoflavones treatment

Liu

Xin

Liang

et al. 2010

Phytotherapy Research

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Memory performance, brain excitatory amino acid and acetylcholinesterase activity of chronically aluminum (Al) exposed mice in response to soy isoflavones (SI) treatment was investigated in the study. Forty eight mice were allotted randomly into a control group, an Al exposed group (100 mg/kg Al) and an Al exposed group treated with SI (100 mg/kg Al + 60 mg/kg SI) for 60 days. Chronic Al exposure significantly impaired long memory performance in mice as assessed using a passive avoidance task test (χ(2) analysis, p < 0.05). Interestingly, SI treatment markedly improved the memory performance score in the Al exposed mice. This improvement was associated with a total reversal of Al-induced increases in acetylcholinesterase activity in the cerebral cortex and hippocampus of mice. The Al exposure also led to significant decreases in brain levels of aspartic and glutamic acids, two excitatory amino acid neurotransmitters; whereas SI treatment partially reversed the decreased aspartic and glutamic acid contents in the hippocampus. The results suggest that SI can improve long memory performance in the Al exposed mice, possibly by modulating the metabolism of brain acetylcholine and amino acid neurotransmitters.

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“…[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.…”

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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Differential toxicity of nitric oxide, aluminum, and amyloid β-peptide in SN56 cholinergic cells from mouse septum

Cited by 57 publications

References 43 publications

Does neurotransmission impairment accompany aluminium neurotoxicity?

Does neurotransmission impairment accompany aluminium neurotoxicity?

Memory performance, brain excitatory amino acid and acetylcholinesterase activity of chronically aluminum exposed mice in response to soy isoflavones treatment

Involvement of NO Generation in Aluminum-Induced Cell Death

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