scholarly journals Real-time in vivo mitochondrial redox assessment confirms enhanced mitochondrial reactive oxygen species in diabetic nephropathy

2017 ◽  
Vol 92 (5) ◽  
pp. 1282-1287 ◽  
Author(s):  
Daniel L. Galvan ◽  
Shawn S. Badal ◽  
Jianyin Long ◽  
Benny H. Chang ◽  
Paul T. Schumacker ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Diabetic Nephropathy ◽  
Real Time ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

scholarly journals Elesclomol-induced increase of mitochondrial reactive oxygen species impairs glioblastoma stem-like cell survival and tumor growth

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Mariachiara Buccarelli ◽  
Quintino Giorgio D’Alessandris ◽  
Paola Matarrese ◽  
Cristiana Mollinari ◽  
Michele Signore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Strong Increase ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

Abstract Background Glioblastoma (GBM) is the most common and aggressive primary malignant brain tumor in adults, characterized by a poor prognosis mainly due to recurrence and therapeutic resistance. It has been widely demonstrated that glioblastoma stem-like cells (GSCs), a subpopulation of tumor cells endowed with stem-like properties is responsible for tumor maintenance and progression. Moreover, it has been demonstrated that GSCs contribute to GBM-associated neovascularization processes, through different mechanisms including the transdifferentiation into GSC-derived endothelial cells (GdECs). Methods In order to identify druggable cancer-related pathways in GBM, we assessed the effect of a selection of 349 compounds on both GSCs and GdECs and we selected elesclomol (STA-4783) as the most effective agent in inducing cell death on both GSC and GdEC lines tested. Results Elesclomol has been already described to be a potent oxidative stress inducer. In depth investigation of the molecular mechanisms underlying GSC and GdEC response to elesclomol, confirmed that this compound induces a strong increase in mitochondrial reactive oxygen species (ROS) in both GSCs and GdECs ultimately leading to a non-apoptotic copper-dependent cell death. Moreover, combined in vitro treatment with elesclomol and the alkylating agent temozolomide (TMZ) enhanced the cytotoxicity compared to TMZ alone. Finally, we used our experimental model of mouse brain xenografts to test the combination of elesclomol and TMZ and confirmed their efficacy in vivo. Conclusions Our results support further evaluation of therapeutics targeting oxidative stress such as elesclomol with the aim of satisfying the high unmet medical need in the management of GBM.

scholarly journals Attenuating Effect of Chlorella Extract on NLRP3 Inflammasome Activation by Mitochondrial Reactive Oxygen Species

2021 ◽  
Vol 8 ◽  
Author(s):  
Yuya Nakashima ◽  
Kazuhito Gotoh ◽  
Soichi Mizuguchi ◽  
Daiki Setoyama ◽  
Yurie Takata ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nlrp3 Inflammasome ◽  
Reactive Oxygen ◽  
Food Supplement ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Nlrp3 Inflammasome Activation

The NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome has been linked to the pathogenesis of a wide variety of human diseases. Although many drugs and inhibitors have been developed to treat NLRP3-associated diseases, only limited clinical data support their efficacy and safety. Chlorella, a unicellular green alga that is widely and safely used as a food supplement, contains various antioxidants. In this study, we obtained a fat-soluble extract from Chlorella (CE) and demonstrated that it reduced NLRP3 inflammasome activation by inhibiting mitochondrial reactive oxygen species and caspase-1 activation. In addition, CE supplementation attenuated lipopolysaccharide-induced interleukin 1β transcription through activation of hypoxia-inducible factor 1α in vitro and in vivo. As Chlorella is a safe and useful food supplement, it may be a practical pharmacological approach for treating NLRP3-driven diseases.

scholarly journals Real-time in vivo detection of biomaterial-induced reactive oxygen species

Biomaterials ◽  
2011 ◽  
Vol 32 (7) ◽  
pp. 1796-1801 ◽  
Author(s):  
Wendy F. Liu ◽  
Minglin Ma ◽  
Kaitlin M. Bratlie ◽  
Tram T. Dang ◽  
Robert Langer ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Real Time ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
In Vivo Detection

scholarly journals Mitochondrial Reactive Oxygen Species Are Essential for the Development of Psoriatic Inflammation

2021 ◽  
Vol 12 ◽  
Author(s):  
Soichi Mizuguchi ◽  
Kazuhito Gotoh ◽  
Yuya Nakashima ◽  
Daiki Setoyama ◽  
Yurie Takata ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Protein ◽  
Reactive Oxygen ◽  
Skin Inflammation ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Immune Mediated ◽  
Important Regulator

Psoriasis is a common immune-mediated, chronic, inflammatory skin disease that affects approximately 2–3% of the population worldwide. Although there is increasing evidence regarding the essential roles of the interleukin (IL)-23/IL-17 axis and dendritic cell (DC)-T cell crosstalk in the development of skin inflammation, the contributions of mitochondrial function to psoriasis are unclear. In a mouse model of imiquimod (IMQ)-induced psoriasiform skin inflammation, we found that hematopoietic cell-specific genetic deletion of p32/C1qbp, a regulator of mitochondrial protein synthesis and metabolism, protects mice from IMQ-induced psoriatic inflammation. Additionally, we demonstrate that p32/C1qbp is an important regulator of IMQ-induced DC activation, both in vivo and in vitro. We also found that p32/C1qbp-deficient DCs exhibited impaired production of IL-1β, IL-23, and mitochondrial reactive oxygen species (mtROS) after IMQ stimulation. Because the inhibition of mtROS suppressed IMQ-induced DC activation and psoriatic inflammation, we presume that p32/C1qbp and mtROS can serve as therapeutic targets in psoriasis.

Sign in / Sign up

Export Citation Format

Share Document