• BMB Reports
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• 제51권11호
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• pp.557-562
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• 2018

Reactive oxygen species (ROS) are major sources of cellular oxidative stress. Specifically, cancer cells harbor genetic alterations that promote a continuous and elevated production of ROS. While such oxidative stress conditions could be harmful to normal cells, they facilitate cancer cell growth in multiple ways by causing DNA damage and genomic instability, and ultimately by reprogramming cancer cell metabolism. This review provides up to date findings regarding the roles of ROS generation induced by diverse biological molecules and chemicals in representative women's cancer. Specifically, we describe the cellular signaling pathways that regulate direct or indirect interactions between ROS homeostasis and metabolism within female genital cancer cells.

• The Korean Journal of Ecology
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• 제17권1호
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• pp.91-100
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• 1994

비록 스트레스의 종류는 다를지라도, 환경 스트레스들은 공통적으로 식물채 내의 활성 산소의 양을 증가시킨다. 활성산소에 의하여 스트레스-에틸렌의 생성량은 증가하고 결국 식물체의 노화는 촉진된다. 반면에, 활성산소 분해 효소들과 antioxidiant들에 의하여 활성산소에 의한 스트레스-에틸렌 생성이 제한될 경우 한정된 양의 에틸렌에 의하여 스트레스에 대한 저항이 유도될 가능성이 있다.

• 한국환경과학회지
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• 제15권5호
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• pp.479-484
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• 2006

Removal of elemental mercury $(Hg^0)$ with the reactive species produced from dielectric barrier discharge (DBD) was studied. We investigated the effect of operating parameters such as the applied voltage, residence time, initial concentration and co-existence of other pollutants. The removal of $(Hg^0)$ was significantly promoted by an increase in the applied voltage of the DBD reactor system. It is important to note that at the same input power, the removal efficiency of $(Hg^0)$ was much higher than that of NO gas. These results imply that if the DBD system is used as a NOx treatment facility, it is capable of removing $(Hg^0)$ simultaneously with NOx.

• 대한의생명과학회지
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• 제11권3호
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• pp.253-258
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• 2005

Reactive oxygen species (ROS) and sex hormones affect the proliferation of cells and are believed to play important roles in tumorigenesis. However, little is known regarding how these two factors interact to affect cell proliferation. In this study, hepal-6 cells were treated with ROS and sex hormones (testosterone and steroidal) either separately or in combination. The sex hormones had no significant influence the cell proliferation up to a concentration of $1{\mu}M$. However, cell proliferation was inhibited when the cells were treated simultaneously with $H_2O_2$, which alone was found to promote cell proliferation at the concentrations of $15{\mu}M$. In conclusion, this study indicates that instead of promoting the cell proliferation, ROS interact with sex hormones to inhibit the Hepa 1-6 cell proliferation.

• 약학회지
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• 제45권1호
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• pp.101-107
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• 2001

Green tea catechins (GTC) and its major component, (-)-epigallocatechin gallate (EGCG) were studied for their protective effects against reactive oxygen species (ROS)-induced oxidative stress. GTC and EGCG skewed the strong antioxidative effects on the lipid peroxidation of ethyl linolate with Fenton's reagent and free radical scavenging effect to DPPH radical generation. They also protected $H_2O$$_2$- or KO$_2$-induced cytotoxicity in CHL cells or mouse splenocytes. These results indicate that GTC and EGCG are capable of protecting the lipid peroxidation, flee radical generation and cytotoxicity induced by ROS. The mechanism of inhibition in ROS-induced cytotoxicity may be due to their antiofidative and free radical scavenging properties. Therefore, GTC and EGCG may be useful chemopreventive agents by protecting the free radical generation which are involved in cancer and aging.

• Archives of Pharmacal Research
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• 제28권10호
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• pp.1183-1189
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• 2005

Although plant-derived phenolic acids have been reported to have anti-cancer activity, the exact mechanism is not completely understood. In this study, we investigated the role for reactive oxygen species (ROS) as a mediator of the apoptosis induced by caffeic acid (CA) and ferulic acid (FA), common phenolic acids in plants in HepG2 human hepatoma cells. CA and FA reduced cell viability, and induced apoptotic cell death in a dose-dependent manner. In addition, they evoked a dose-related elevation of intracellular ROS. Treatment with various inhibitors of NADPH oxidase (diphenylene iodonium, apocynin, neopterine) significantly blunted both the generation of ROS and the induction of apoptosis induced CA and FA. These results suggest that ROS generated through activation of NADPH oxidase may play an essential role in the apoptosis induced by CA and FA in HepG2 cells. These results further suggest that CA and FA may be valuable for the therapeutic management of human hepatomas.

• Journal of Ginseng Research
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• 제33권4호
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• pp.355-360
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• 2009

Phenanthrene ($C_{14}H_{10}$) is a polycyclic aromatic hydrocarbon with three aromatic rings, and it can be produced by incomplete combustion of fossil fuels. Comet assay was used to examine the oxidative DNA damage of lymphocytes by phenanthrene and to measure the suppressive effects of ginseng extract on the DNA damage in this investigation. The in vitro oxidative DNA damage by phenanthrene increased in a dose-dependent manner in the lymphocyte. However, the DNA damage was significantly inhibited by ascorbate. Moreover, pretreatment, cotreatment and posttreatment with ginseng extract enhanced lymphocyte resistance to the phenanthrene-induced DNA damage. Phenanthrene enhanced the generation of intracellular reactive oxygen species, and the elevated reactive oxygen species level was reduced by treatment with ginseng extract.

• Journal of Microbiology and Biotechnology
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• 제24권11호
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• pp.1455-1463
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• 2014

In the past, reactive oxygen species (ROS) have been considered a harmful byproduct of aerobic metabolism. However, accumulating evidence implicates redox homeostasis, which maintains appropriate ROS levels, in cell proliferation and differentiation in plants and animals. Similarly, ROS generation and signaling are instrumental in fungal development and host-fungus interaction. In fungi, NADPH oxidase, a homolog of human $gp91^{phox}$, generates superoxide and is the main source of ROS. The mechanism of activation and signaling by NADPH oxidases in fungi appears to be largely comparable to those in plants and animals. Recent studies have shown that the fungal NADPH oxidase homologs NoxA (Nox1), NoxB (Nox2), and NoxC (Nox3) have distinct functions. In particular, these studies have consistently demonstrated the impact of NoxA on the development of fungal multicellular structures. Both NoxA and NoxB (but not NoxC) are involved in host-fungus interactions, with the function of NoxA being more critical than that of NoxB.

• Journal of Medicine and Life Science
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• 제20권1호
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• pp.1-7
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• 2023

Transient receptor potential ankyrin 1 (TRPA1) receptors are major polymodal nociceptors that generate primary pain responses in the peripheral nerve endings of the dorsal root ganglion neurons. Recently, we reported that the activation of TRPA1 receptors by reactive oxygen species (ROS) signaling, which is triggered by Ca²⁺ influx through T-type Ca²⁺ channels, contributes to prolonged pain responses induced by jellyfish toxin. In this review, we focus on the characteristics of the TRPA1 receptor involved in intracellular signaling as a secondary pain modulator. Unlike other transient receptor potential receptors, TRPA1 receptors can induce membrane depolarization by ROS without exogenous stimuli in peripheral and central sensory neurons. Therefore, it is important to identify the functional characteristics of TRPA1 receptors to understand pain modulation under several pathogenic conditions such as neuropathic pain syndromes and autoimmune diseases, which are mediated by oxidative signaling to cause chronic pain in the sensory system.

• Journal of Microbiology and Biotechnology
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• 제33권8호
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• pp.992-997
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• 2023

Ferroptosis is a new kind of programmed cell death of which occurrence in microorganisms is not clearly verified. The elevated level of reactive oxygen species (ROS) influences cellular metabolisms through highly reactive hydroxyl radical formation under the iron-dependent Fenton reaction. Iron contributes to ROS production and acts as a cofactor for lipoxygenase to catalyze poly unsaturated fatty acid (PUFA) oxidation, exerting oxidative damage in cells. While ferroptosis is known to take place only in mammalian cells, recent studies discovered the possible ferroptosis-like death in few specific microorganisms. Capacity of integrating PUFA into intracellular membrane phospholipid has been considered as a key factor in bacterial or fungal ferroptosis-like death. Vibrio species in bacteria and Saccharomyces cerevisiae in fungi exhibited certain characteristics. Therefore, this review focus on introducing the occurrence of ferroptosis-like death in microorganisms and investigating the mode of action underlying the cells based on contribution of lipid peroxidation and iron-dependent reaction.