scholarly journals Cytosolic Ca2+ transients during pulsed focused ultrasound generate reactive oxygen species and cause DNA damage in tumor cells

Theranostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 602-613
Author(s):  
Robert B. Rosenblatt ◽  
Joseph A. Frank ◽  
Scott R. Burks
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Tumor Cells ◽  
Focused Ultrasound ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pulsed Focused Ultrasound

scholarly journals The Study of Enhanced High-Intensity Focused Ultrasound Therapy by Sonodynamic N2O Microbubbles

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Xiaowen Zhong ◽  
Mei Zhang ◽  
Zedan Tian ◽  
Qi Wang ◽  
Zhigang Wang
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Cell ◽  
Tumor Cells ◽  
High Intensity ◽  
Focused Ultrasound ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
High Intensity Focused Ultrasound ◽  
Target Area ◽  
Oxygen Species

AbstractHigh-intensity focused ultrasound (HIFU) is a representative non-invasive method of cancer therapy, but its low therapeutic efficacy and risk of damage to surrounding normal tissue hinder its further clinical development and application. Sonodynamic therapy (SDT) kills tumor cells through reactive oxygen molecules produced by sonosensitizers during ultrasound treatment. SDT can enhance HIFU efficacy like microbubbles. In this work, we developed nanoscale N2O microbubbles (N2O-mbs) by an improved mechanical oscillation method. These microbubbles showed good biocompatibility and tumor cell binding. The sonosensitivity of the N2O-mbs was detected both extracellularly and intracellularly through the detection of reactive oxygen species generation. The toxic effects of these sonodynamic microbubbles on tumor cells and the synergistic effect on HIFU treatment were evaluated. Significant apoptosis was caused by reactive oxygen species produced by N2O-mbs under ultrasound irradiation. N2O-mbs combined with HIFU increased tumor cell necrosis and apoptosis in vitro and the coagulative necrotic volume and echo intensity in the bovine liver target area ex vivo. These sonodynamic microbubbles have been also demonstrated to efficiently inhibit tumor growth in vivo. N2O-mbs have a significant impact on the treatment and ablation effect of HIFU due to the advantages of microbubble and extraordinary sonosensitivity. This finding suggests that N2O-mbs may be a novel auxiliary agent for ultrasound that can be used to promote HIFU tumor thermal ablation.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

Identification of the signature genes and network of Reactive Oxygen Species (ROS) related genes and DNA repair genes in Lung Adenocarcinoma (LUAD)

2021 ◽  
Author(s):  
Ye Zhao ◽  
Hai-Ming Feng ◽  
Xiao-Ping Wei ◽  
Wei-Jian Yan ◽  
Bin Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Repair ◽  
Tumor Cell ◽  
Lung Adenocarcinoma ◽  
Tumor Cells ◽  
Patient Survival ◽  
Reactive Oxygen ◽  
Dna Repair Genes ◽  
Oxygen Species ◽  
Repair Genes

Abstract Reactive Oxygen Species (ROS) are present in high amount in patients with tumors, and these ROS can kill and destroy tumor cells. Thus, tumor cells upregulate ROS-related genes to protect themselves and reduce their destruction. Cancer cells already damaged by ROS can be repaired by expressing DNA repair genes consequently promoting their proliferation. In this work, lung adenocarcinoma (LUAD) transcriptome data in the TCGA database was analyzed and samples were clustered into 5 ROS-related categories and 6 DNA repair categories. Survival analysis revealed a significant difference in patient survival between the two classification methods. In addition, the samples corresponding to the two categories overlap, thus, the gene expression profile of the same sample with different categories and survival prognosis was further explored, and the connection between ROS-related genes and DNA repair genes was investigated. The interactive sample recombination classification was used, revealing that the patient's prognosis was worse when the ROS-related genes and DNA repair genes were expressed at the same time. The further research on the potential regulatory network of the two categories of genes and the correlation analysis revealed that ROS-related genes and DNA repair genes have a mutual regulatory relationship. The ROS-related genes NQO1, TXNRD1, and PRDX4 could establish links with other DNA repair genes through the DNA repair gene NEIL3, thereby increasing the growth of tumor cells and balancing the level of ROS, leading to tumor cell death and constant damage to the tumor cell repair system, thus prolonging patient survival. Thus, targeting ROS-related genes and DNA repair genes might be a promising strategy in the treatment of LUAD. Finally, a survival prognostic model of ROS-related genes and DNA repair genes was established (TERT, PRKDC, PTTG1, SMUG1, TXNRD1, CAT, H2AFX and PFKP), the risk score might be used as an independent prognostic factor in LUAD patients.

scholarly journals The differential role of reactive oxygen species in early and late stages of cancer

2017 ◽  
Vol 313 (6) ◽  
pp. R646-R653 ◽  
Author(s):  
Mohamad Assi
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Reactive Oxygen ◽  
Pentose Phosphate ◽  
Oxygen Species ◽  
Redox Biology ◽  
Oxidative Damages ◽  
Late Stages

The large doses of vitamins C and E and β-carotene used to reduce reactive oxygen species (ROS) production and oxidative damages in cancerous tissue have produced disappointing and contradictory results. This therapeutic conundrum was attributed to the double-faced role of ROS, notably, their ability to induce either proliferation or apoptosis of cancer cells. However, for a ROS-inhibitory approach to be effective, it must target ROS when they induce proliferation rather than apoptosis. On the basis of recent advances in redox biology, this review underlined a differential regulation of prooxidant and antioxidant system, respective to the stage of cancer. At early precancerous and neoplastic stages, antioxidant activity decreases and ROS appear to promote cancer initiation via inducing oxidative damage and base pair substitution mutations in prooncogenes and tumor suppressor genes, such as RAS and TP53, respectively. Whereas in late stages of cancer progression, tumor cells escape apoptosis by producing high levels of intracellular antioxidants, like NADPH and GSH, via the pentose phosphate pathway to buffer the excessive production of ROS and related intratumor oxidative injuries. Therefore, antioxidants should be prohibited in patients with advanced stages of cancer and/or undergoing anticancer therapies. Interestingly, the biochemical and biophysical properties of some polyphenols allow them to selectively recognize tumor cells. This characteristic was exploited to design and deliver nanoparticles coated with low doses of polyphenols and containing chemotherapeutic drugs into tumor-bearing animals. First results are encouraging, which may revolutionize the conventional use of antioxidants in cancer.

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