Vitamin E, γ-tocotrienol, Protects Against Buthionine Sulfoximine-Induced Cell Death by Scavenging Free Radicals in SH-SY5Y Neuroblastoma Cells

2016 ◽  
Vol 68 (3) ◽  
pp. 507-517 ◽  
Author(s):  
Jen-Kit Tan ◽  
Sue-Mian Then ◽  
Musalmah Mazlan ◽  
Rahman Jamal ◽  
Wan Zurinah Wan Ngah
Keyword(s):  
Cell Death ◽  
Free Radicals ◽  
Vitamin E ◽  
Neuroblastoma Cells ◽  
Buthionine Sulfoximine

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.

scholarly journals Inhibition of autophagy by 3-methyladenine potentiates sulforaphane-induced cell death of BE(2)-C human neuroblastoma cells

2012 ◽  
Vol 12 (1) ◽  
pp. 535-542 ◽  
Author(s):  
IRENA HORWACIK ◽  
MONIKA GAIK ◽  
MAŁGORZATA DURBAS ◽  
ELŻBIETA BORATYN ◽  
GRZEGORZ ZAJĄC ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Tissue transglutaminase and apoptosis: sense and antisense transfection studies with human neuroblastoma cells

1994 ◽  
Vol 14 (10) ◽  
pp. 6584-6596
Author(s):  
G Melino ◽  
M Annicchiarico-Petruzzelli ◽  
L Piredda ◽  
E Candi ◽  
V Gentile ◽  
...  
Keyword(s):  
Cell Death ◽  
Structural Changes ◽  
Tissue Transglutaminase ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Neuroblastoma Cell Line ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Transfected Cells ◽  
Protein Levels

In this report, we show that the overexpression of tissue transglutaminase (tTG) in the human neuroblastoma cell line SK-N-BE(2) renders these neural crest-derived cells highly susceptible to death by apoptosis. Cells transfected with a full-length tTG cDNA, under the control of a constitutive promoter, show a drastic reduction in proliferative capacity paralleled by a large increase in cell death rate. The dying tTG-transfected cells exhibit both cytoplasmic and nuclear changes characteristic of cells undergoing apoptosis. The tTG-transfected cells express high Bcl-2 protein levels as well as phenotypic neural cell adhesion molecule markers (NCAM and neurofilaments) of cells differentiating along the neuronal pathway. In keeping with these findings, transfection of neuroblastoma cells with an expression vector containing segments of the human tTG cDNA in antisense orientation resulted in a pronounced decrease of both spontaneous and retinoic acid (RA)-induced apoptosis. We also present evidence that (i) the apoptotic program of these neuroectodermal cells is strictly regulated by RA and (ii) cell death by apoptosis in the human neuroblastoma SK-N-BE(2) cells preferentially occurs in the substrate-adherent phenotype. For the first time, we report here a direct effect of tTG in the phenotypic maturation toward apoptosis. These results indicate that the tTG-dependent irreversible cross-linking of intracellular protein represents an important biochemical event in the induction of the structural changes featuring cells dying by apoptosis.

scholarly journals Protective Effect of Matricaria chamomilla Ethanolic Extract on Hippocampal Neuron Damage in Rats Exposed to Formaldehyde

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Zahra Sayyar ◽  
Alireza Yazdinezhad ◽  
Maryam Hassan ◽  
Iraj Jafari Anarkooli
Keyword(s):  
Cell Death ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Passive Avoidance ◽  
Avoidance Learning ◽  
Total Antioxidant Capacity ◽  
Ethanolic Extract ◽  
Passive Avoidance Learning ◽  
Matricaria Chamomilla ◽  
Total Antioxidant

Formaldehyde, as a frequently used compound in many applications, crosses the blood-brain barrier and leads to hippocampal cell death and memory impairment. This study investigates the effects of ethanolic extract of Matricaria chamomilla (MC) on passive avoidance learning induced by damaged hippocampal cells and evaluates the antioxidant traits of MC. The male Wistar rats were divided into six (6 in each) groups: control (10 mg/kg normal saline), 200 (200 mg/kg MC extract), 500 (500 mg/kg MC extract), F (10 mg/kg formaldehyde), F200 (10 mg/kg formaldehyde and 200 mg/kg MC extract), and F500 (10 mg/kg formaldehyde and 500 mg/kg MC extract). Shuttle box assay was used for evaluation of passive avoidance learning. The apoptosis rate of hippocampal tissue, malondialdehyde (MDA) free radicals, and total antioxidant capacity was evaluated to determine the positive effect of the ethanolic extract of MC. We found that the ethanolic extract of MC reduced the cell death, time spent in a dark room, and MDA free radicals in the hippocampus, leading to increased total antioxidant capacity in this region. In conclusion, the ethanolic extract of MC could ameliorate formaldehyde-induced memory damage through decreasing cell death and MDA activity of the hippocampal region and increasing total antioxidant capacity.

Evaluation of the Local Effects of Vitamin E ( E-Mousse®) on Free Radicals in Diabetic Microangiopathy: A Randomized, Controlled Trial

Angiology ◽  
2003 ◽  
Vol 54 (4) ◽  
pp. 415-421 ◽  
Author(s):  
I. Ruffini ◽  
G. Belcaro ◽  
M.R. Cesarone ◽  
G. Geroulakos ◽  
A. Di Renzo ◽  
...  
Keyword(s):  
Randomized Controlled Trial ◽  
Free Radicals ◽  
Vitamin E ◽  
Controlled Trial ◽  
Diabetic Microangiopathy ◽  
Local Effects ◽  
Randomized Controlled

scholarly journals Effectiveness of Vitamin C and Vitamin E Antioxidant Combination on Caspase-3 Expression in Wistar White Rat Pulmonum Contusion

2020 ◽  
Vol 3 (1) ◽  
pp. 31-44
Author(s):  
Bermansyah ◽  
Gama Satria ◽  
Ahmad Umar
Keyword(s):  
Cell Death ◽  
Vitamin E ◽  
Vitamin C ◽  
Wistar Rats ◽  
Caspase 3 ◽  
Cell Function ◽  
Pulmonary Contusion ◽  
Tnf Α ◽  
Male Wistar Rats

Introduction.Pulmonary contusions can cause a progressive inflammatory response. Activation of TNF-α cytokines and reactive oxygen species (ROS) can cause pulmonary cell death. Antioxidants can have the potential to neutralize ROS. The purpose of this study is to determine the effectiveness of antioxidant administration in maintaining pulmonary cell function in wistar rats that have been induced to experience pulmonary contusions through caspase-3 levels. Methods.This study was an in vivo experimental study conducted on thirty male wistar rats and divided into five groups (n = 6): control, pulmonary contusion + asthaxanthine 5 mg/kgBW, pulmonary contusion + vitamin C and E 50 mg/kgBW, pulmonary contusion + vitamin C and E 100 mg/kgBW, pulmonary contusion + vitamin C and E 200 mg/kgBW. The value of Caspase-3 is evaluated by the IHC. All data analyzes used SPSS 18. Results. Low doses of antioxidants have the potential to reduce pulmonary cell death in wistar rats induced by pulmonary contusions.Conclussion. Vitamin C and E effective to reduce polmonary cell death in pulmonary contusion.Keywords: antioxidants, vitamin C, vitamin E, pulmonary contusions animal model, apoptosis, caspase-3

scholarly journals Mitochondrial Pathway of α-Tocopheryl Succinate-Induced Apoptosis in Human Epidermoid Carcinoma A431 Cells

Acta Naturae ◽  
2012 ◽  
Vol 4 (3) ◽  
pp. 88-94 ◽  
Author(s):  
M. A. Savitskaya ◽  
M. S. Vildanova ◽  
O. P. Kisurina-Evgenieva ◽  
E. A. Smirnova ◽  
G. E. Onischenko
Keyword(s):  
Cell Death ◽  
Vitamin E ◽  
Apoptotic Cell ◽  
Mitochondrial Pathway ◽  
Epidermoid Carcinoma ◽  
A431 Cells ◽  
Human Carcinoma ◽  
Tocopheryl Succinate ◽  
Induced Apoptosis ◽  
Human Epidermoid Carcinoma

Vitamin E derivatives are known to act as agents exhibiting cytotoxity against tumor cells. The effect of vitamin E succinate on human epidermoid carcinoma cell line A431 was investigated in this study using live imaging, immunocytochemistry, and transmission electron microscopy. -Tocopheryl succinate-induced apoptotic cell death in A431 cells was shown to be both dose- and time-dependent. The hyperproduction of reactive oxygen species, changes in size, shape and ultrastructural characteristics of mitochondria followed by the release of cytochrome c from mitochondria to cytosol were observed. These results suggest that -tocopheryl succinate induces apoptosis that occurs via the mitochondrial pathway. Mitochondria are shown to be crucial targets in -tocopheryl succinate-induced caspase-dependent cell death in human carcinoma A431 cells.

Sign in / Sign up

Export Citation Format

Share Document