scholarly journals Exogenous Hydrogen Peroxide Contributes to Heme Oxygenase-1 Delaying Programmed Cell Death in Isolated Aleurone Layers of Rice Subjected to Drought Stress in a cGMP-Dependent Manner

2018 ◽  
Vol 9 ◽  
Author(s):  
Guanghui Wang ◽  
Yu Xiao ◽  
Xiaojiang Deng ◽  
Heting Zhang ◽  
Tingge Li ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Drought Stress ◽  
Programmed Cell Death ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Dependent Manner

scholarly journals Flutamide Induces Hepatic Cell Death and Mitochondrial Dysfunction via Inhibition of Nrf2-Mediated Heme Oxygenase-1

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Li Zhang ◽  
Jiabin Guo ◽  
Qiang Zhang ◽  
Wei Zhou ◽  
Jin Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Liver Injury ◽  
Mitochondrial Dysfunction ◽  
Heme Oxygenase ◽  
Hepatic Cell ◽  
Atp Depletion ◽  
Heme Oxygenase 1 ◽  
Hydrogen Peroxide Accumulation

Flutamide is a widely used nonsteroidal antiandrogen for prostate cancer therapy, but its clinical application is restricted by the concurrent liver injury. Increasing evidence suggests that flutamide-induced liver injury is associated with oxidative stress, though the precise mechanism is poorly understood. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master transcription factor regulating endogenous antioxidants including heme oxygenase-1 (HO-1). This study was designed to delineate the role of Nrf2/HO-1 in flutamide-induced hepatic cell injury. Our results showed that flutamide concentration dependently induced cytotoxicity, hydrogen peroxide accumulation, and mitochondrial dysfunction as indicated by mitochondrial membrane potential loss and ATP depletion. The protein expression of Nrf2 and HO-1 was induced by flutamide at 12.5 μM but was downregulated by higher concentrations of flutamide. Silencing either Nrf2 or HO-1 was found to aggravate flutamide-induced hydrogen peroxide accumulation and mitochondrial dysfunction as well as inhibition of the Nrf2 pathway. Moreover, preinduction of HO-1 by Copp significantly attenuated flutamide-induced oxidative stress and mitochondrial dysfunction, while inhibition of HO-1 by Snpp aggravated these deleterious effects. These findings suggest that flutamide-induced hepatic cell death and mitochondrial dysfunction is assoicated with inhibition of Nrf2-mediated HO-1. Pharmacologic intervention of Nrf2/HO-1 may provide a promising therapeutic approach in flutamide-induced liver injury.

scholarly journals Involvement of Nrf2-Mediated Upregulation of Heme Oxygenase-1 in Mollugin-Induced Growth Inhibition and Apoptosis in Human Oral Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Young-Man Lee ◽  
Q-Schick Auh ◽  
Deok-Won Lee ◽  
Jun-Yeol Kim ◽  
Ha-Jin Jung ◽  
...  
Keyword(s):  
Cell Death ◽  
Oral Cancer ◽  
Growth Inhibition ◽  
Heme Oxygenase ◽  
Flow Cytometric Analysis ◽  
Annexin V ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Antitumor Effects

Although previous studies have shown that mollugin, a bioactive phytochemical isolated from Rubia cordifolia L. (Rubiaceae), exhibits antitumor effects, its biological activity in oral cancer has not been reported. We thus investigated the effects and putative mechanism of apoptosis induced by mollugin in human oral squamous cell carcinoma cells (OSCCs). Results show that mollugin induces cell death in a dose-dependent manner in primary and metastatic OSCCs. Mollugin-induced cell death involved apoptosis, characterized by the appearance of nuclear shrinkage, flow cytometric analysis of sub-G1 phase arrest, and annexin V-FITC and propidium iodide staining. Western blot analysis and RT-PCR revealed that mollugin suppressed activation of NF-κB and NF-κB-dependent gene products involved in antiapoptosis (Bcl-2 and Bcl-xl), invasion (MMP-9 and ICAM-1), and angiogenesis (FGF-2 and VEGF). Furthermore, mollugin induced the activation of p38, ERK, and JNK and the expression of heme oxygenase-1 (HO-1) and nuclear factor E2–related factor 2 (Nrf2). Mollugin-induced growth inhibition and apoptosis of HO-1 were reversed by an HO-1 inhibitor and Nrf2 siRNA. Collectively, this is the first report to demonstrate the effectiveness of mollugin as a candidate for a chemotherapeutic agent in OSCCs via the upregulation of the HO-1 and Nrf2 pathways and the downregulation of NF-κB.

1,2,3,4,6-Penta-O-galloyl-beta-d-glucose protects rat neuronal cells (Neuro 2A) from hydrogen peroxide-mediated cell death via the induction of heme oxygenase-1

2002 ◽  
Vol 328 (2) ◽  
pp. 185-189 ◽  
Author(s):  
Byung-Min Choi ◽  
Hyung-Jin Kim ◽  
Gi-Su Oh ◽  
Hyun-Ock Pae ◽  
Hyuncheol Oh ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Heme Oxygenase ◽  
Neuronal Cells ◽  
Heme Oxygenase 1

scholarly journals Attenuated heme oxygenase-1 responses predispose the elderly to pulmonary nontuberculous mycobacterial infections

2016 ◽  
Vol 311 (5) ◽  
pp. L928-L940 ◽  
Author(s):  
Ranu Surolia ◽  
Suman Karki ◽  
Zheng Wang ◽  
Tejaswini Kulkarni ◽  
Fu Jun Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Heme Oxygenase ◽  
The Elderly ◽  
Granuloma Formation ◽  
Heme Oxygenase 1 ◽  
Blood Monocytes ◽  
Mycobacterial Infections ◽  
Cellular Necrosis ◽  
Old Mice

Pulmonary infections with nontuberculous mycobacteria (P-NTM), such as by Mycobacterium avium complex ( M. avium), are increasingly found in the elderly, but the underlying mechanisms are unclear. Recent studies suggest that adaptive immunity is necessary, but not sufficient, for host defense against mycobacteria. Heme oxygenase-1 (HO-1) has been recognized as a critical modulator of granuloma formation and programmed cell death in mycobacterial infections. Old mice (18–21 mo) infected with M. avium had attenuated HO-1 response with diffuse inflammation, high burden of mycobacteria, poor granuloma formation, and decreased survival (45%), while young mice (4–6 mo) showed tight, well-defined granuloma, increased HO-1 expression, and increased survival (95%). To further test the role of HO-1 in increased susceptibility to P-NTM infections in the elderly, we used old and young HO-1+/+and HO-1−/−mice. The transcriptional modulation of the JAK/STAT signaling pathway in HO-1−/−mice due to M. avium infection demonstrated similarities to infected wild-type old mice with upregulation of SOCS3 and inhibition of Bcl2. Higher expression of SOCS3 with downregulation of Bcl2 resulted in higher macrophage death via cellular necrosis. Finally, peripheral blood monocytes (PBMCs) from elderly patients with P-NTM also demonstrated attenuated HO-1 responses after M. avium stimulation and increased cell death due to cellular necrosis (9.69% ± 2.02) compared with apoptosis (4.75% ± 0.98). The augmented risk for P-NTM in the elderly is due, in part, to attenuated HO-1 responses, subsequent upregulation of SOCS3, and inhibition of Bcl2, leading to programmed cell death of macrophages, and sustained infection.

scholarly journals Hydrogen peroxide induces programmed cell death features in cultured tobacco BY‐2 cells, in a dose‐dependent manner

2001 ◽  
Vol 52 (361) ◽  
pp. 1721-1730 ◽  
Author(s):  
Valérie Houot ◽  
Philippe Etienne ◽  
Anne‐Sophie Petitot ◽  
Stéphane Barbier ◽  
Jean‐Pierre Blein ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Dependent Manner ◽  
Dose Dependent
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