scholarly journals An Antifungal Mechanism of Protolichesterinic Acid from the Lichen Usnea albopunctata Lies in the Accumulation of Intracellular ROS and Mitochondria-Mediated Cell Death Due to Apoptosis in Candida tropicalis

2017 ◽  
Vol 8 ◽  
Author(s):  
S. N. Kumar ◽  
C. Mohandas
Keyword(s):  
Cell Death ◽  
Candida Tropicalis ◽  
Antifungal Mechanism ◽  
Intracellular Ros

scholarly journals Transcriptional network constituted of CBP, Ku70, NOX2, and BAX prevents the cell death of necrosis, paraptosis, and apoptosis in human melanoma

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Liang Ding ◽  
Yalei Wen ◽  
Xin Zhang ◽  
Fang Zhao ◽  
Kenao Lv ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Human Melanoma ◽  
Transcriptional Network ◽  
Multiple Roles ◽  
Creb Binding Protein ◽  
Cycle Arrest ◽  
Intracellular Ros ◽  
High Level

AbstractCREB-binding protein (CBP) is an acetyltransferase known to play multiple roles in the transcriptions of genes involving oxidative metabolism, cell cycle, DNA damage checkpoints, and cell death. In this study, CBP was found to positively regulate the expression of Ku70, and both CBP and Ku70 were found to negatively regulate the expression of NOX2, therefore, mitigating the intracellular ROS in human melanoma. Knocking down CBP or Ku70 induced necrotic and paraptotic cell death as indicated by high-level intracellular ROS, cytoplasmic vacuolization, and cell cycle arrest in the S phase. In addition, chromosomal condensations were also observed in the cells proceeding necrotic and paraptotic cell death, which was found to be related to the BAX-associated intrinsic pathway of apoptotic cell death, when Ku70 was decreased either by CBP depletion or by Ku70 depletion directly. Our results, therefore, supported the idea that CBP, Ku70, BAX, and NOX2 have formed a transcriptional network in the prevention of cell death of necrosis, paraptosis, and apoptosis in human melanoma.

scholarly journals PRDX1 is essential for the viability and maintenance of reactive oxygen species in chicken DT40

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Takahito Moriwaki ◽  
Akari Yoshimura ◽  
Yuki Tamari ◽  
Hiroyuki Sasanuma ◽  
Shunichi Takeda ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Fine Tuning ◽  
Oxygen Species ◽  
Ros Homeostasis ◽  
Intracellular Ros ◽  
Chromosomal Breaks ◽  
Dt40 Cells

Abstract Background Peroxiredoxin 1 (PRDX1) is a member of a ubiquitous family of thiol peroxidases that catalyze the reduction of peroxides, including hydrogen peroxide. It functions as an antioxidant enzyme, similar to catalase and glutathione peroxidase. PRDX1 was recently shown act as a sensor of reactive oxygen species (ROS) and play a role in ROS-dependent intracellular signaling pathways. To investigate its physiological functions, PRDX1 was conditionally disrupted in chicken DT40 cells in the present study. Results The depletion of PRDX1 resulted in cell death with increased levels of intracellular ROS. PRDX1-depleted cells did not show the accumulation of chromosomal breaks or sister chromatid exchange (SCE). These results suggest that cell death in PRDX1-depleted cells was not due to DNA damage. 2-Mercaptoethanol protected against cell death in PRDX1-depleted cells and also suppressed elevations in ROS. Conclusions PRDX1 is essential in chicken DT40 cells and plays an important role in maintaining intracellular ROS homeostasis (or in the fine-tuning of cellular ROS levels). Cells deficient in PRDX1 may be used as an endogenously deregulated ROS model to elucidate the physiological roles of ROS in maintaining proper cell growth.

scholarly journals Antifungal mechanism of [RuIII(NH3)4catechol]+ complex on fluconazole-resistant Candida tropicalis

2017 ◽  
Vol 364 (9) ◽  
Author(s):  
Rafael Araújo Gomes-Junior ◽  
Roberto Santana da Silva ◽  
Renata Galvão de Lima ◽  
Marcos A. Vannier-Santos
Keyword(s):  
Candida Tropicalis ◽  
Antifungal Mechanism ◽  
Fluconazole Resistant

scholarly journals Oxidative Stress in Cell Death and Cardiovascular Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Tao Xu ◽  
Wei Ding ◽  
Xiaoyu Ji ◽  
Xiang Ao ◽  
Ying Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiovascular Diseases ◽  
Death Process ◽  
Ros Production ◽  
Disease Treatment ◽  
Physiological Conditions ◽  
Intracellular Ros ◽  
Cell Death Process ◽  
Molecular Components ◽  
Multiple Signaling

ROS functions as a second messenger and modulates multiple signaling pathways under the physiological conditions. However, excessive intracellular ROS causes damage to the molecular components of the cell, which promotes the pathogenesis of various human diseases. Cardiovascular diseases are serious threats to human health with extremely high rates of morbidity and mortality. Dysregulation of cell death promotes the pathogenesis of cardiovascular diseases and is the clinical target during the disease treatment. Numerous studies show that ROS production is closely linked to the cell death process and promotes the occurrence and development of the cardiovascular diseases. In this review, we summarize the regulation of intracellular ROS, the roles of ROS played in the development of cardiovascular diseases, and the programmed cell death induced by intracellular ROS. We also focus on anti-ROS system and the potential application of anti-ROS strategy in the treatment of cardiovascular diseases.

Zn2+ -induced cell death is mediated by the induction of intracellular ROS in ARPE-19 cells

2004 ◽  
Vol 28 (3) ◽  
pp. 195-201 ◽  
Author(s):  
Jeongmin Song ◽  
Sung Chul Lee ◽  
Sung Soo Kim ◽  
Hyung J. Koh ◽  
Oh Woong Kwon ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracellular Ros

scholarly journals Ionizing Radiation Upregulates Glutamine Metabolism and Induces Cell Death via Accumulation of Reactive Oxygen Species

2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Pengfei Yang ◽  
Xiangxia Luo ◽  
Jin Li ◽  
Tianyi Zhang ◽  
Xiaoling Gao ◽  
...  
Keyword(s):  
Cell Death ◽  
Ionizing Radiation ◽  
Tumor Cells ◽  
Metabolic Flux ◽  
Glutamine Metabolism ◽  
X Rays ◽  
Ros Accumulation ◽  
Intracellular Ros ◽  
Radiation Induced ◽  
Excessive Accumulation

Glutamine metabolism provides energy to tumor cells and also produces reactive oxygen species (ROS). Excessive accumulation of ROS can damage mitochondria and eventually lead to cell death. xCT (SLC7A11) is responsible for the synthesis of glutathione in order to neutralize ROS. In addition, mitophagy can remove damaged mitochondria to keep the cell alive. Ionizing radiation kills tumor cells by causing the accumulation of ROS, which subsequently induces nuclear DNA damage. With this in mind, we explored the mechanism of intracellular ROS accumulation induced by ionizing radiation and hypothesized new methods to enhance the effect of radiotherapy. We used MCF-7 breast cancer cells and HCT116 colorectal cancer cells in our study. The above-mentioned cells were irradiated with different doses of X-rays or carbon ions. Clone formation assays were used to detect cell proliferation, enzyme-linked immunosorbent assay (ELISA) detected ATP, and glutathione (GSH) production, while the expression of proteins was detected by Western blot and quantitative real-time PCR analysis. The production of ROS was detected by flow cytometry, and immunofluorescence was used to track mitophagy-related processes. Finally, BALB/C tumor-bearing nude mice were irradiated with X-rays in order to further explore the protein expression found in tumors with the use of immunohistochemistry. Ionizing radiation increased the protein expressions of ASCT2, GLS, and GLUD in order to upregulate the glutamine metabolic flux in tumor cells. This caused an increase in ATP secretion. Meanwhile, ionizing radiation inhibited the expression of the xCT (SLC7A11) protein and reduced the generation of glutathione, leading to excessive accumulation of intracellular ROS. The mitophagy inhibitor, or knockdown Parkin gene, is able to enhance the ionizing radiation-induced ROS production and increase nucleus DNA damage. This combined treatment can significantly improve the killing effect of radiation on tumor cells. We concluded that ionizing radiation could upregulate the glutamine metabolic flux and enhance ROS accumulation in mitochondria. Ionizing radiation also decreased the SLC7A11 expression, resulting in reduced GSH generation. Therefore, inhibition of mitophagy can increase ionizing radiation-induced cell death.

scholarly journals Translational Medicine in Pulmonary-Renal Crosstalk: Therapeutic Targeting of p-Cresyl Sulfate Triggered Nonspecific ROS and Chemoattractants in Dyspneic Patients with Uremic Lung Injury

2018 ◽  
Vol 7 (9) ◽  
pp. 266 ◽  
Author(s):  
Jia-Feng Chang ◽  
Shih-Shin Liang ◽  
Pounraj Thanasekaran ◽  
Hsueh-Wei Chang ◽  
Li-Li Wen ◽  
...  
Keyword(s):  
Cell Death ◽  
Lung Injury ◽  
Nadph Oxidase ◽  
Serum Creatinine ◽  
Molecular Mechanisms ◽  
Cell Model ◽  
Uremic Toxins ◽  
Alveolar Cell ◽  
Intracellular Ros ◽  
Alveolar Capillary

Molecular mechanisms and pathological features of p-Cresyl sulfate (PCS)-induced uremic lung injury (ULI) in chronic kidney disease (CKD) remain unclear. We analyzed pleural effusions (PE) from CKD and non-CKD patients for uremic toxins, reactive oxygen species (ROS), and chemotactic cytokines. Correlations between PE biomarkers and serum creatinine were also studied. Cell viability and inflammatory signaling pathways were investigated in PCS-treated human alveolar cell model. To mimic human diseases, CKD-ULI mouse model was developed with quantitative comparison of immunostaining and morphometric approach. PE from CKD patients enhance expressions of uremic toxins, hydroxyl radicals, and IL-5/IL-6/IL-8/IL-10/IL-13/ENA-78/GRO α/MDC/thrombopoietin/VEGF. PE concentrations of ENA-78/VEGF/IL-8/MDC/PCS/indoxyl sulphate correlate with serum creatinine concentrations. In vitro, PCS promotes alveolar cell death, cPLA2/COX-2/aquaporin-4 expression, and NADPH oxidase/mitochondria activation-related ROS. Intracellular ROS is abrogated by non-specific ROS scavenger N-acetyl cysteine (NAC), inhibitors of NADPH oxidase and mitochondria-targeted superoxide scavenger. However, only NAC protects against PCS-induced cell death. In vivo, expressions of cPLA2/COX2/8-OHdG, resident alveolar macrophages, recruited leukocytes, alveolar space, interstitial edema and capillary leakage increase in lung tissues of CKD-ULI mice, and NAC pretreatment ameliorates alveolar–capillary injury. PCS causes alveolar–capillary injury through triggering intracellular ROS, downstream prostaglandin pathways, cell death, and activating leukocytes to release multiplex chemoattractants and extracellular ROS. Thus PCS and nonspecific ROS serve as potential therapeutic targets.

(+)-Medioresinol leads to intracellular ROS accumulation and mitochondria-mediated apoptotic cell death in Candida albicans

Biochimie ◽  
2012 ◽  
Vol 94 (8) ◽  
pp. 1784-1793 ◽  
Author(s):  
Ji Hong Hwang ◽  
In-sok Hwang ◽  
Qing-He Liu ◽  
Eun-Rhan Woo ◽  
Dong Gun Lee
Keyword(s):  
Cell Death ◽  
Candida Albicans ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Ros Accumulation ◽  
Intracellular Ros
Sign in / Sign up

Export Citation Format

Share Document