Activated α2Macroglobulin Increases β-Amyloid (25–35)-Induced Toxicity in LAN5 Human Neuroblastoma Cells

1999 ◽  
Vol 155 (2) ◽  
pp. 252-259 ◽  
Author(s):  
C. Fabrizi ◽  
R. Businaro ◽  
G.M. Lauro ◽  
G. Starace ◽  
L. Fumagalli
Keyword(s):  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Β Amyloid

scholarly journals Deleterious effects of combination of lead and β-amyloid peptides in inducing apoptosis and altering cell cycle in human neuroblastoma cells

2017 ◽  
Vol 10 (3) ◽  
pp. 93-98 ◽  
Author(s):  
Ayyalasomayajula Neelima ◽  
Ajumeera Rajanna ◽  
Reddy G. Bhanuprakash ◽  
C.S. Chetty ◽  
Challa Suresh
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Human Brain ◽  
Neuroblastoma Cells ◽  
Brain Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Amyloid Peptides ◽  
Β Amyloid ◽  
The Brain

AbstractLead (Pb) is a toxic pollutant known to cause several abnormalities related to the brain, including cognitive dysfunction, and it is ubiquitous in nature. β-amyloid peptides (AP) are crucially involved in Alzheimer’s disease (AD). It has been reported that there is a connection between lead and amyloid peptides in exerting similar kinds of altered functions in the brain and long-term exposure to lead leads ultimately to increased beta amyloid formation in the brain, lethal to human brain cells. There is still a lack of information on the mechanism by which Pb affects AP formation, exerting combined toxicity in AD patients. To fill the gap, we have systematically analyzed the toxicity individually and in combination of Pb and AP in human brain cells. We found that the combination of Pb and AP exerted a higher toxicity than individual exposures in human neuroblastoma cells. The lower inhibitory concentration values were determined by both time and concentration dependent manner on using MTT assay. The data resulted in the development of enhanced toxicity on exposure to Pb with both the combinations of AP(1-40) or (25-35) and with all combinations in human brain cells compared to individual exposures to Pb (1-40) or AP(25-35). The severe apoptotic effect and alteration in cell cycle by arresting at the S-phase evidenced the increased toxicity of combinational exposure to Pb and AP on human neuroblastoma cells. Furthermore, the quantitative determination of LDH and caspase-3 activity indicated the induction of severe toxicity. We conclude that both are synergistically associated with effects such as arresting the cell cycle and triggering apoptosis during the progression of Alzheimer’s disease.

Cholesterol Potentiates β-Amyloid-Induced Toxicity in Human Neuroblastoma Cells: Involvement of Oxidative Stress

2008 ◽  
Vol 33 (8) ◽  
pp. 1509-1517 ◽  
Author(s):  
Patricia Ferrera ◽  
Octavio Mercado-Gómez ◽  
Martín Silva-Aguilar ◽  
Mahara Valverde ◽  
Clorinda Arias
Keyword(s):  
Oxidative Stress ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Β Amyloid

Clerodane diterpenes from Polyalthia longifolia var. pendula protect SK-N-MC human neuroblastoma cells from β-amyloid insult

RSC Advances ◽  
2014 ◽  
Vol 4 (45) ◽  
pp. 23707-23712 ◽  
Author(s):  
Tung-Ho Wu ◽  
Yung-Yi Cheng ◽  
Jing-Ru Liou ◽  
Tzong-Der Way ◽  
Chao-Jung Chen ◽  
...  
Keyword(s):  
Methanolic Extract ◽  
Neuroblastoma Cells ◽  
Neuroprotective Activity ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Hexane Layer ◽  
Clerodane Diterpenes ◽  
Β Amyloid ◽  
Polyalthia Longifolia

The n-hexane layer of Polyalthia longifolia methanolic extract showed neuroprotective activity, resulting in the isolation of three new clerodane diterpenes.

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

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