Role of reactive oxygen species in the anticancer activity of botanicals: Comparing sensitivity profiles

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.

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The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

Current Cardiology Reviews ◽

10.2174/1573403x16666201014142446 ◽

2020 ◽

Vol 16 ◽

Author(s):

Andrey Krylatov ◽

Leonid Maslov ◽

Sergey Y. Tsibulnikov ◽

Nikita Voronkov ◽

Alla Boshchenko ◽

...

Keyword(s):

Nitric Oxide ◽

Reactive Oxygen Species ◽

Hydrogen Sulfide ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

Ischemia And Reperfusion ◽

Oxygen Species ◽

Ischemia And Reperfusion Injury ◽

Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

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Role of Natural Antioxidants on Neuroprotection and Neuroinflammation

Antioxidants ◽

10.3390/antiox10040608 ◽

2021 ◽

Vol 10 (4) ◽

pp. 608

Author(s):

Domenico Nuzzo

Keyword(s):

Reactive Oxygen Species ◽

Energy Metabolism ◽

Respiratory Chain ◽

Reactive Oxygen ◽

Natural Antioxidants ◽

Oxygen Species

All cells continuously generate reactive oxygen species (ROS) through the respiratory chain during the energy metabolism process [...]

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Marine Antimicrobial Peptide TP4 Exerts Anticancer Effects on Human Synovial Sarcoma Cells via Calcium Overload, Reactive Oxygen Species Production and Mitochondrial Hyperpolarization

Marine Drugs ◽

10.3390/md19020093 ◽

2021 ◽

Vol 19 (2) ◽

pp. 93

Author(s):

Bor-Chyuan Su ◽

Giun-Yi Hung ◽

Yun-Chieh Tu ◽

Wei-Chen Yeh ◽

Meng-Chieh Lin ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Cell Death ◽

Antimicrobial Peptide ◽

Anticancer Activity ◽

Synovial Sarcoma ◽

Uncoupling Protein ◽

Reactive Oxygen ◽

Calcium Overload ◽

Oxygen Species ◽

Sarcoma Cells

Synovial sarcoma is a rare but aggressive soft-tissue sarcoma associated with translocation t(X;18). Metastasis occurs in approximately 50% of all patients, and curative outcomes are difficult to achieve in this group. Since the efficacies of current therapeutic approaches for metastatic synovial sarcoma remain limited, new therapeutic agents are urgently needed. Tilapia piscidin 4 (TP4), a marine antimicrobial peptide, is known to exhibit multiple biological functions, including anti-bacterial, wound-healing, immunomodulatory, and anticancer activities. In the present study, we assessed the anticancer activity of TP4 in human synovial sarcoma cells and determined the underlying mechanisms. We first demonstrated that TP4 can induce necrotic cell death in human synovial sarcoma AsKa-SS and SW982 cells lines. In addition, we saw that TP4 initiates reactive oxygen species (ROS) production and downregulates antioxidant proteins, such as uncoupling protein-2, superoxide dismutase (SOD)-1, and SOD-2. Moreover, TP4-induced mitochondrial hyperpolarization is followed by elevation of mitochondrial ROS. Calcium overload is also triggered by TP4, and cell death can be attenuated by a necrosis inhibitor, ROS scavenger or calcium chelator. In our experiments, TP4 displayed strong anticancer activity in human synovial sarcoma cells by disrupting oxidative status, promoting mitochondrial hyperpolarization and causing calcium overload.

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