Combination of Ionising Irradiation and Hyperthermia Activates Programmed Apoptotic and Necrotic Cell Death Pathways in Human Colorectal Carcinoma Cells

2010 ◽  
Vol 186 (11) ◽  
pp. 587-599 ◽  
Author(s):  
Frederick Mantel ◽  
Benjamin Frey ◽  
Stefan Haslinger ◽  
Petra Schildkopf ◽  
Renate Sieber ◽  
...  
2018 ◽  
Vol 46 (sup3) ◽  
pp. S247-S253 ◽  
Author(s):  
Firdos Alam Khan ◽  
Sultan Akhtar ◽  
Dana Almohazey ◽  
Munthar Alomari ◽  
Sarah Ameen Almofty ◽  
...  

2012 ◽  
Vol 40 (4) ◽  
pp. 1267-1276 ◽  
Author(s):  
ANA CRISTINA DE ALBUQUERQUE-XAVIER ◽  
LILIAN GONÇALVES R. BASTOS ◽  
JULIO CESAR MADUREIRA DE FREITAS ◽  
FERNANDA LEVE ◽  
WALDEMIR FERNÁNDEZ DE SOUZA ◽  
...  

2008 ◽  
Vol 179 (4S) ◽  
pp. 370-370 ◽  
Author(s):  
William A See ◽  
Guangjian Zhang ◽  
Fanghong Chen ◽  
Margaret Kressin ◽  
Peter Langenstroer

2011 ◽  
Vol 30 (2) ◽  
pp. 197-206 ◽  
Author(s):  
Victor Paromov ◽  
Marianne Brannon ◽  
Sudha Kumari ◽  
Mallikarjun Samala ◽  
Min Qui ◽  
...  

2-Chloroethyl ethyl sulfide (CEES) or half-mustard gas, a sulfur mustard (HD) analog, is a genotoxic agent that causes oxidative stress and induces both apoptotic and necrotic cell death. Sodium pyruvate induced a necrosis-to-apoptosis shift in HaCaT cells exposed to CEES levels ≤ 1.5 mmol/L and lowered markers of DNA damage, oxidative stress, and inflammation. This study provides a rationale for the future development of multicomponent therapies for HD toxicity in the skin. We hypothesize that a combination of pyruvates with scavengers/antioxidants encapsulated in liposomes for optimal local delivery should be therapeutically beneficial against HD-induced skin injury. However, the latter suggestion should be verified in animal models exposed to HD.


2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Gopitkumar Shah ◽  
Fanghong Chen ◽  
GuangJian Zhang ◽  
William See

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Teru Kamogashira ◽  
Chisato Fujimoto ◽  
Tatsuya Yamasoba

Reactive oxygen species (ROS) production is involved in several apoptotic and necrotic cell death pathways in auditory tissues. These pathways are the major causes of most types of sensorineural hearing loss, including age-related hearing loss, hereditary hearing loss, ototoxic drug-induced hearing loss, and noise-induced hearing loss. ROS production can be triggered by dysfunctional mitochondrial oxidative phosphorylation and increases or decreases in ROS-related enzymes. Although apoptotic cell death pathways are mostly activated by ROS production, there are other pathways involved in hearing loss that do not depend on ROS production. Further studies of other pathways, such as endoplasmic reticulum stress and necrotic cell death, are required.


Planta Medica ◽  
2009 ◽  
Vol 75 (09) ◽  
Author(s):  
CM Strüh ◽  
S Jäger ◽  
CM Schempp ◽  
T Jakob ◽  
A Scheffler ◽  
...  

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