NDLI: Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Please wait, while we are loading the content...

Activation of nicotinic acetylcholine receptor prevents the production of reactive oxygen species in fibrillar β amyloid peptide (1-42)-stimulated microglia

Cross talk between P2 purinergic receptors modulates extracellular ATP-mediated interleukin-10 production in rat microglial cells

Age-dependent dichotomous effect of superoxide dismutase Ala16Val polymorphism on oxidized LDL levels

Characterization of a novel anti-human TNF-α murine monoclonal antibody with high binding affinity and neutralizing activity

Etoposide-induced Smad6 expression is required for the G1 to S phase transition of the cell cycle in CMT-93 mouse intestinal epithelial cells

Rutin inhibits osteoclast formation by decreasing reactive oxygen species and TNF-α by inhibiting activation of NF-κB

RANKL stimulates proliferation, adhesion and IL-7 expression of thymic epithelial cells

Nur77 upregulates HIF-α by inhibiting pVHL-mediated degradation

Migration of human neural stem cells toward an intracranial glioma

Endothelin 1 protects HN33 cells from serum deprivation-induced neuronal apoptosis through Ca2+-PKCα-ERK pathway

Alterations of proliferative and differentiation potentials of human embryonic stem cells during long-term culture

Depletion of mitochondrial DNA up-regulates the expression of MDR1 gene via an increase in mRNA stability

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Anti-tumor immunostimulatory effect of heat-killed tumor cells

In vivo hepatitis B virus-neutralizing activity of an anti-HBsAg humanized antibody in chimpanzees

Erratum

Year: 2007, Volume: 39

Year: 2002, Volume: 34

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Content Provider	PubMed Central
Author	Lee, Kheun Byeol Lee, Jong-soo Park, Jin-woo Huh, Tae-lin Lee, You Mie
Copyright Year	2008
Abstract	Proton beam is useful to target tumor tissue sparing normal cells by allowing precise dose only into tumor cells. However, the cellular and molecular mechanisms by which proton beam induces tumor cell death are still undefined. We irradiated three different tumor cells (LLC, HepG2, and Molt-4) with low energy proton beam (35 MeV) with spread out Bragg peak (SOBP) in vitro, and investigated cell death by MTT or CCK-8 assay at 24 h after irradiation. LLC and HepG2 cells were sensitive to proton beam at over 10 Gy to induce apoptosis whereas Molt-4 showed rather low sensitivity. Relative biological effectiveness (RBE) values for the death rate relative to γ-ray were ranged from 1.1 to 2.3 in LLC and HepG2 but from 0.3 to 0.7 in Molt-4 at 11 d after irradiation by colony formation assay. The typical apoptotic nuclear DNA morphological pattern was observed by staining with 4'-6-diamidino-2-phenylindole (DAPI). Tiny fragmented DNA was observed in HepG2 but not in Molt-4 by the treatment of proton in apoptotic DNA fragment assay. By FACS analysis after stained with FITC-Annexin-V, early as well as median apoptotic fractions were clearly increased by proton treatment. Proton beam-irradiated tumor cells induced a cleavage of poly (ADP-ribose) polymerase-1 (PARP-1) and procaspases-3 and -9. Activity of caspases was highly enhanced after proton beam irradiation. Reactive oxygen species (ROS) were significantly increased and N-acetyl cysteine pretreatment restored the apoptotic cell death induced by proton beam. Furthermore, p38 and JNK but not ERK were activated by proton and dominant negative mutants of p38 and JNK revived proton-induced apoptosis, suggesting that p38 and JNK pathway may be activated through ROS to activate apoptosis. In conclusion, our data clearly showed that single treatment of low energy proton beam with SOBP increased ROS and induced cell death of solid tumor cells (LLC and HepG2) in an apoptotic cell death program by the induction of caspases activities.
Related Links	http://dx.doi.org/10.3858/emm.2008.40.1.118
Starting Page	118
File Format	PDF
ISSN	12263613
Journal	Experimental & Molecular Medicine
Issue Number	1
Volume Number	40
Language	English
Publisher	Korean Society of Medical Biochemistry and Molecular Biology
Publisher Date	2008-01-01
Access Restriction	Open
Rights Holder	Korean Society of Medical Biochemistry and Molecular Biology
Subject Keyword	Clinical Biochemistry Molecular Medicine Biochemistry Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Molecular Biology Clinical Biochemistry Molecular Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Proton beam radiation induces DNA damage and cell apoptosis in glioma stem cells through reactive oxygen species

Proton beam radiation induces DNA damage and cell apoptosis in glioma stem cells through reactive oxygen species

Soy soluble polysaccharide induces apoptosis in HCT116 human colon cancer cells via reactive oxygen species generation.

Apoptosis induction of U937 human leukemia cells by diallyl trisulfide induces through generation of reactive oxygen species

Panaxydol induces apoptosis through an increased intracellular calcium level, activation of JNK and p38 MAPK and NADPH oxidase-dependent generation of reactive oxygen species

H2O2-induced secretion of tumor necrosis factor-α evokes apoptosis of cardiac myocytes through reactive oxygen species-dependent activation of p38 MAPK

Hellebrigenin induces apoptosis in colorectal cancer Cells through induction of excessive reactive oxygen species

Carnosic Acid, a Rosemary Phenolic Compound, Induces Apoptosis Through Reactive Oxygen Species-Mediated p38 Activation in Human Neuroblastoma IMR-32 Cells

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Similar Documents

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Proton beam radiation induces DNA damage and cell apoptosis in glioma stem cells through reactive oxygen species

Proton beam radiation induces DNA damage and cell apoptosis in glioma stem cells through reactive oxygen species

Soy soluble polysaccharide induces apoptosis in HCT­116 human colon cancer cells via reactive oxygen species generation.

Apoptosis induction of U937 human leukemia cells by diallyl trisulfide induces through generation of reactive oxygen species

Panaxydol induces apoptosis through an increased intracellular calcium level, activation of JNK and p38 MAPK and NADPH oxidase-dependent generation of reactive oxygen species

H2O2-induced secretion of tumor necrosis factor-α evokes apoptosis of cardiac myocytes through reactive oxygen species-dependent activation of p38 MAPK

Hellebrigenin induces apoptosis in colorectal cancer Cells through induction of excessive reactive oxygen species

Carnosic Acid, a Rosemary Phenolic Compound, Induces Apoptosis Through Reactive Oxygen Species-Mediated p38 Activation in Human Neuroblastoma IMR-32 Cells

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Soy soluble polysaccharide induces apoptosis in HCT116 human colon cancer cells via reactive oxygen species generation.