scholarly journals Flavonoids from Rosa roxburghii Tratt prevent reactive oxygen species-mediated DNA damage in thymus cells both combined with and without PARP-1 expression after exposure to radiation in vivo

Aging ◽  
2020 ◽  
Vol 12 (16) ◽  
pp. 16368-16389
Author(s):  
Sai-Juan Xu ◽  
Xia Wang ◽  
Tao-Yang Wang ◽  
Zheng-Zhan Lin ◽  
Yong-Jian Hu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rosa Roxburghii Tratt ◽  
Rosa Roxburghii ◽  
Thymus Cells ◽  
Parp 1

Hydroxyl radical is a significant player in oxidative DNA damage in vivo

2021 ◽  
Author(s):  
Barry Halliwell ◽  
Amitava Adhikary ◽  
Michael Dingfelder ◽  
Miral Dizdaroglu
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Hydroxyl Radical ◽  
Chemical Reactions ◽  
Oxidative Dna Damage ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Schematic Representation ◽  
Important Chemical

Schematic representation of the important chemical reactions involved in reactive oxygen species-mediated DNA damage.

scholarly journals SETD1A protects HSCs from activation-induced functional decline in vivo

Blood ◽  
2018 ◽  
Vol 131 (12) ◽  
pp. 1311-1324 ◽  
Author(s):  
Kathrin Arndt ◽  
Andrea Kranz ◽  
Juliane Fohgrub ◽  
Adrien Jolly ◽  
Anita S. Bledau ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Functional Decline ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Reactive Oxygen Species Accumulation ◽  
Dna Damage Signaling ◽  
Key Points

Key Points SETD1A regulates DNA damage signaling and repair in HSCs and hematopoietic precursors in the absence of reactive oxygen species accumulation. SETD1A is important for the survival of mice after inflammation-induced HSC activation in situ.

scholarly journals STING enhances cell death through regulation of reactive oxygen species and DNA damage

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Thomas J. Hayman ◽  
Marta Baro ◽  
Tyler MacNeil ◽  
Chatchai Phoomak ◽  
Thazin Nwe Aung ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Ionizing Radiation ◽  
Tumor Cell ◽  
Cell Survival ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Dna Damaging Agents ◽  
Ros Homeostasis

AbstractResistance to DNA-damaging agents is a significant cause of treatment failure and poor outcomes in oncology. To identify unrecognized regulators of cell survival we performed a whole-genome CRISPR-Cas9 screen using treatment with ionizing radiation as a selective pressure, and identified STING (stimulator of interferon genes) as an intrinsic regulator of tumor cell survival. We show that STING regulates a transcriptional program that controls the generation of reactive oxygen species (ROS), and that STING loss alters ROS homeostasis to reduce DNA damage and to cause therapeutic resistance. In agreement with these data, analysis of tumors from head and neck squamous cell carcinoma patient specimens show that low STING expression is associated with worse outcomes. We also demonstrate that pharmacologic activation of STING enhances the effects of ionizing radiation in vivo, providing a rationale for therapeutic combinations of STING agonists and DNA-damaging agents. These results highlight a role for STING that is beyond its canonical function in cyclic dinucleotide and DNA damage sensing, and identify STING as a regulator of cellular ROS homeostasis and tumor cell susceptibility to reactive oxygen dependent, DNA damaging agents.

UVB-induced DNA damage, generation of reactive oxygen species, and inflammation are effectively attenuated by the flavonoid luteolin in vitro and in vivo

2011 ◽  
Vol 50 (9) ◽  
pp. 1081-1093 ◽  
Author(s):  
Ute Wölfle ◽  
Philipp R. Esser ◽  
Birgit Simon-Haarhaus ◽  
Stefan F. Martin ◽  
Jürgen Lademann ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Targeting autophagy enhances atezolizumab-induced mitochondria-related apoptosis in osteosarcoma

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhuochao Liu ◽  
Hongyi Wang ◽  
Chuanzhen Hu ◽  
Chuanlong Wu ◽  
Jun Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Antitumor Immunity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Specific Monoclonal Antibody ◽  
Osteosarcoma Cells ◽  
Jnk Pathway ◽  
In Vivo Experiments

AbstractIn this study, we identified the multifaceted effects of atezolizumab, a specific monoclonal antibody against PD-L1, in tumor suppression except for restoring antitumor immunity, and investigated the promising ways to improve its efficacy. Atezolizumab could inhibit the proliferation and induce immune-independent apoptosis of osteosarcoma cells. With further exploration, we found that atezolizumab could impair mitochondria of osteosarcoma cells, resulting in increased release of reactive oxygen species and cytochrome-c, eventually leading to mitochondrial-related apoptosis via activating JNK pathway. Nevertheless, the excessive release of reactive oxygen species also activated the protective autophagy of osteosarcoma cells. Therefore, when we combined atezolizumab with autophagy inhibitors, the cytotoxic effect of atezolizumab on osteosarcoma cells was significantly enhanced in vitro. Further in vivo experiments also confirmed that atezolizumab combined with chloroquine achieved the most significant antitumor effect. Taken together, our study indicates that atezolizumab can induce mitochondrial-related apoptosis and protective autophagy independently of the immune system, and targeting autophagy is a promising combinatorial approach to amplify its cytotoxicity.

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