Apigenin drives the production of reactive oxygen species and initiates a mitochondrial mediated cell death pathway in prostate epithelial cells

The Prostate ◽  
2005 ◽  
Vol 63 (2) ◽  
pp. 131-142 ◽  
Author(s):  
Colm Morrissey ◽  
Amanda O'Neill ◽  
Barbara Spengler ◽  
Volker Christoffel ◽  
John M. Fitzpatrick ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Epithelial Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Death Pathway ◽  
Prostate Epithelial Cells

scholarly journals Reactive oxygen species as transducers of sphinganine-mediated cell death pathway

2011 ◽  
Vol 6 (10) ◽  
pp. 1616-1619 ◽  
Author(s):  
Mariana Saucedo-García ◽  
Ariadna González-Solís ◽  
Priscila Rodríguez-Mejía ◽  
Teresa de Jesús Olivera-Flores ◽  
Sonia Vázquez-Santana ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Death Pathway

scholarly journals Reactive oxygen species induced by Streptococcus pyogenes invasion trigger apoptotic cell death in infected epithelial cells

2010 ◽  
Vol 12 (6) ◽  
pp. 814-830 ◽  
Author(s):  
Chihiro Aikawa ◽  
Takashi Nozawa ◽  
Fumito Maruyama ◽  
Kohei Tsumoto ◽  
Shigeyuki Hamada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Epithelial Cells ◽  
Streptococcus Pyogenes ◽  
Apoptotic Cell ◽  
Reactive Oxygen ◽  
Apoptotic Cell Death ◽  
Oxygen Species

scholarly journals N-Acetylglucosamine-Induced Cell Death in Candida albicans and Its Implications for Adaptive Mechanisms of Nutrient Sensing in Yeasts

mBio ◽  
2015 ◽  
Vol 6 (5) ◽  
Author(s):  
Han Du ◽  
Guobo Guan ◽  
Xiaoling Li ◽  
Megha Gulati ◽  
Li Tao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Candida Albicans ◽  
Fungal Pathogen ◽  
Reactive Oxygen ◽  
Nutrient Sensing ◽  
Oxygen Species ◽  
Gi Tract ◽  
Content Type ◽  
Cell Death Pathway

ABSTRACT Single-celled organisms have different strategies to sense and utilize nutrients in their ever-changing environments. The opportunistic fungal pathogen Candida albicans is a common member of the human microbiota, especially that of the gastrointestinal (GI) tract. An important question concerns how C. albicans gained a competitive advantage over other microbes to become a successful commensal and opportunistic pathogen. Here, we report that C. albicans uses N-acetylglucosamine (GlcNAc), an abundant carbon source present in the GI tract, as a signal for nutrient availability. When placed in water, C. albicans cells normally enter the G0 phase and remain viable for weeks. However, they quickly lose viability when cultured in water containing only GlcNAc. We term this phenomenon GlcNAc-induced cell death (GICD). GlcNAc triggers the upregulation of ribosomal biogenesis genes, alterations of mitochondrial metabolism, and the accumulation of reactive oxygen species (ROS), followed by rapid cell death via both apoptotic and necrotic mechanisms. Multiple pathways, including the conserved cyclic AMP (cAMP) signaling and GlcNAc catabolic pathways, are involved in GICD. GlcNAc acts as a signaling molecule to regulate multiple cellular programs in a coordinated manner and therefore maximizes the efficiency of nutrient use. This adaptive behavior allows C. albicans’ more efficient colonization of the gut. IMPORTANCE The ability to rapidly and appropriately respond to nutrients in the environment is crucial to free-living microorganisms. To maximize the use of available nutrients, microorganisms often use a limiting nutritional component as a signal to coordinate multiple biological processes. The human fungal pathogen Candida albicans uses N-acetylglucosamine (GlcNAc) as a signal for the availability of external nutrient resources. GlcNAc induces rapid cell death in C. albicans due to the constitutive activation of oxidative metabolism and accumulation of reactive oxygen species (ROS), and multiple pathways are involved in its regulation. This study sheds light on the mechanisms of niche specialization of pathogenic fungi and raises the possibility that this cell death pathway could be an unexplored therapeutic target.

Amplification of the γ-irradiation-induced cell death pathway by reactive oxygen species in human U937 cells

2008 ◽  
Vol 20 (5) ◽  
pp. 916-924 ◽  
Author(s):  
Eun Mi Kim ◽  
Hyun Sook Yang ◽  
Sung Wook Kang ◽  
Jin-Nyoung Ho ◽  
Seung Bum Lee ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
U937 Cells ◽  
Oxygen Species ◽  
Γ Irradiation ◽  
Cell Death Pathway

scholarly journals Reactive oxygen species activate a Ca2+-dependent cell death pathway in the unicellular organism Trypanosoma brucei brucei

1999 ◽  
Vol 340 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Evelyn L. RIDGLEY ◽  
Zhao-hui XIONG ◽  
Larry RUBEN
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Trypanosoma Brucei ◽  
Reactive Oxygen ◽  
Cell Permeability ◽  
Death Process ◽  
Oxygen Species ◽  
Trypanosoma Brucei Brucei ◽  
Acetoxymethyl Ester ◽  
Cell Death Pathway

Here we examine a cell death process induced by reactive oxygen species (ROS) in the haemoflagellate Trypanosoma brucei brucei. Ca2+ distribution in cellular compartments was measured with stable transformants expressing aequorin targeted to the cytosol, nucleus or mitochondrion. Within 1.5 h of ROS production, mitochondrial Ca2+ transport was impaired and the Ca2+ barrier between the nuclear envelope and cytosol was disrupted. Consequently the mitochondrion did not accumulate Ca2+ efficiently in response to an extracellular stimulus, and excess Ca2+ accumulated in the nucleus. The terminal transferase deoxytidyl uridine end labelling assay revealed that, 5 h after treatment with ROS, extensive fragmentation of nuclear DNA occurred in over 90% of the cells. Permeability changes in the plasma membrane did not occur until an additional 2 h had elapsed. The intracellular Ca2+ buffer, EGTA acetoxymethyl ester, prevented DNA fragmentation and prolonged the onset of changes in cell permeability. Despite some similarities to apoptosis, nuclease activation was not a consequence of caspase 3, caspase 1, calpain, serine protease, cysteine protease or proteasome activity. Moreover, trypanosomes expressing mouse Bcl-2 were not protected from ROS even though protection from mitochondrial dysfunction and ROS have been reported for mammalian cells. Overall, these results demonstrate that Ca2+ pathways can induce pathology in trypanosomes, although the specific proteins involved might be distinct from those in metazoans.

scholarly journals Reactive Oxygen Species Are Required for Hyperoxia-induced Bax Activation and Cell Death in Alveolar Epithelial Cells

2003 ◽  
Vol 279 (8) ◽  
pp. 6753-6760 ◽  
Author(s):  
Leonard J. Buccellato ◽  
May Tso ◽  
Ozkan I. Akinci ◽  
Navdeep S. Chandel ◽  
G. R. Scott Budinger
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Epithelial Cells ◽  
Reactive Oxygen ◽  
Alveolar Epithelial Cells ◽  
Oxygen Species ◽  
Alveolar Epithelial
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