• Journal of Photoscience
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• 제9권2호
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• pp.142-145
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• 2002

A strict anaerobe, Prevotella melaninogenica is highly sensitive to oxidative stress. Oxidative stress such as exposure to oxygen or addition of hydrogen peroxide, increased 8-hydroxydeoxyguanosine (80HdG), a typical of oxidative DNA damage, and decreased the bacterial cell survival rate. We could detect the generation of reactive oxygen species in P. melaninogenica after exposure to oxygen. UVA irradiation also increased 80HdG in the bacterium. On the other hand, such oxidative stress did not increase 80HdG in a facultative anaerobe. These findings suggest that P. melaninogenica is a suitable material to study the biological effects of oxidative stress, to evaluate antioxidants, and to study the effects of oxygen or reactive oxygen species on molecular evolution.

• Journal of Yeungnam Medical Science
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• 제38권2호
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• pp.83-94
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• 2021

The global obesity epidemic and the growing elderly population largely contribute to the increasing incidence of type 2 diabetes. Insulin resistance acts as a critical link between the present obesity pandemic and type 2 diabetes. Naturally occurring reactive oxygen species (ROS) regulate intracellular signaling and are kept in balance by the antioxidant system. However, the imbalance between ROS production and antioxidant capacity causes ROS accumulation and induces oxidative stress. Oxidative stress interrupts insulin-mediated intracellular signaling pathways, as supported by studies involving genetic modification of antioxidant enzymes in experimental rodents. In addition, a close association between oxidative stress and insulin resistance has been reported in numerous human studies. However, the controversial results with the use of antioxidants in type 2 diabetes raise the question of whether oxidative stress plays a critical role in insulin resistance. In this review article, we discuss the relevance of oxidative stress to insulin resistance based on genetically modified animal models and human trials.

• Journal of Applied Biological Chemistry
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• 제43권4호
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• pp.211-217
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• 2000

Oxidative stress is implicated in a number of diseases, in ageing of organisms, and in damage to plants that have been exposed to freezing and thawing or water stress. From the perspective of yeast as a model eukaryotic system, this article reviews the systems that are involved in the cellular responses to exposure to reactive oxygen species (ROS) generated during aerobic growth of the organism. The discussion includes the defense systems involved, the ability of cells to adapt to ROS treatment, cell-division cycle delay and the systems regulating gene expression that are activated by oxidative stress.

• 고신대학교 의과대학 학술지
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• 제33권2호
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• pp.135-140
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• 2018

Endometriosis is an estrogen-dependent chronic inflammatory condition that affects women in their reproductive period and is associated with pelvic pain and infertility. Oxidative stress (OS) occurs when reactive oxygen stress (ROS) and anti-oxidants are in imbalance. OS is a potential factor involved in the pathophysiology of endometriosis. Iron-induced ROS may trigger a chain of events resulting in the development and progression of endometriosis. Endogenous ROS are correlated with increased cellular proliferation and ERK1/2 activation in human endometriotic cells. An oxidative environment leads to stimulation of the ERK and PI3K/AKT/mTOR signaling pathways that facilitate endometriotic lesion progression through adhesion, angiogenesis, and proliferation. OS is also known to be involved in epigenetic mechanisms in endometriosis. We summarize the recent knowledge in our understanding of the role of oxidative stress in the pathogenesis of endometriosis.

• Asian Pacific Journal of Cancer Prevention
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• 제15권12호
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• pp.4745-4751
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• 2014

Oxidative stress is caused by an imbalance in the redox status of the body. In such a state, increase of free radicals in the body can lead to tissue damage. One of the most important species of free radicals is reactive oxygen species (ROS) produced by various metabolic pathways, including aerobic metabolism in the mitochondrial respiratory chain. It plays a critical role in the initiation and progression of various types of cancers. ROS affects different signaling pathways, including growth factors and mitogenic pathways, and controls many cellular processes, including cell proliferation, and thus stimulates the uncontrolled growth of cells which encourages the development of tumors and begins the process of carcinogenesis. Increased oxidative stress caused by reactive species can reduce the body's antioxidant defense against angiogenesis and metastasis in cancer cells. These processes are main factors in the development of cancer. Bimolecular reactions cause free radicals in which create such compounds as malondialdehyde (MDA) and hydroxyguanosine. These substances can be used as indicators of cancer. In this review, free radicals as oxidizing agents, antioxidants as the immune system, and the role of oxidative stress in cancer, particularly breast cancer, have been investigated in the hope that better identification of the factors involved in the occurrence and spread of cancer will improve the identification of treatment goals.

• Asian Pacific Journal of Cancer Prevention
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• 제15권2호
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• pp.561-568
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• 2014

Background: The skin is the largest body organ that regulates excretion of metabolic waste products, temperature, and plays an important role in body protection against environmental physical and chemical, as well as biological factors. These include agents that may act as oxidants or catalysts of reactions producing reactive oxygen species (ROS), reactive nitrogen species (RNS), and other oxidants in skin cells. An increased amount of the oxidants, exceeding the antioxidant defense system capacity is called oxidative stress, leading to chronic inflammation, which, in turn, can cause collagen fragmentation and disorganization of collagen fibers and skin cell functions, and thus contribute to skin diseases including cancer. Moreover, research suggests that oxidative stress participates in all stages of carcinogenesis. We report here a summary of the present state of knowledge on the role of oxidative stress in pathogenesis of dermatologic diseases, defensive systems against ROS/RNS, and discuss how physical activity may modulate skin diseases through effects on oxidative stress. The data show duality of physical activity actions: regular moderate activity protects against ROS/RNS damage, and endurance exercise with a lack of training mediates oxidative stress. These findings indicate that the redox balance should be considered in the development of new antioxidant strategies linked to the prevention and therapy of skin diseases.

• Natural Product Sciences
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• 제13권4호
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• pp.369-372
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• 2007

Oxidative stress induced by reactive oxygen species (ROS) has been suggested to be the cause of various degenerative diseases as well as aging. To evaluate the antioxidant potential of stilbenes, we have investigated the cytoprotective effect of 10 stilbenes derived from plants on the oxidative stress induced by tertiary butyl hydroperoxide (t-BuOOH). Of the stilbenes tested, piceatannol (3) showed the most potent activity, which was further investigated using an animal model. When 3 (30 or 10 mg/kg) was topically administered prior to UVB irradiation, the amount of the thiobarbituric acid reactive substances (TBARS) was significantly reduced compared to that of the control (vehicle). Our findings suggest that piceatannol is capable of protecting cells and tissues from oxidative stress.

• 한국안광학회지
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• 제13권3호
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• pp.103-109
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• 2008

목적: 본 논문에서는 활성산소(reactive oxygen species, ROS)와 활성질소(reactive oxygen species, RNS)생성의 결과 초래되는 산화스트레스(oxidative stress)와 안질환과의 관계, 특히, 백내장발생과의 관련성 연구에 대한 고찰과, 안구의 기능이상에 있어 산화스트레스의 매개체(mediator)로서 과산화지질(lipid peroxide)의 역할에 대해 논의하고자 한다. 방법: 산화스트레스는 단백질 산화, DNA 파괴, 세포사(apoptosis), 지질과산화(lipid peroxidation) 등의 다양한 세포손상을 나타낸다. 이러한 손상은 많은 질병의 발생과 관련되어 있다. 백내장 발생의 주요한 원인중의 하나가 안구조직이 일정하고 지속적으로 산화스트레스의 환경에 노출되는 것으로 알려져 있다. 따라서 산화스트레스의 안구기능이상에 대한 역할을 조사하였다. 결과: 수정체는 자외선에의 만성적인 노출과 세포대사과정에서 필수불가결하게 생성되는 활성산소에 의해 끊임없이 공격을 받는다. 과도하게 생성된 활성산소에 의한 수정체 단백질의 분해(degradation), 산화(oxidation), 가교형성(crosslinking), 응집(aggregation) 등은 백내장발생에 있어 중요한 요인으로 사료된다. 결론: 산화스트레스와 체내의 산화/항산화 불균형이 과도한 활성산소를 생성하게 되고 결국, 안구의 기능이상을 일으킨다고 할 수 있다. 이러한 결과들에도 불구하고, 산화스트레스와 안구이상과의 관계를 더욱 정확하게 설명할 수 있는 분자기전에 대한 정보는 아직 부족한 상태이며, 더욱 많은 연구가 필요하다.

• BMB Reports
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• 제44권8호
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• pp.497-505
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• 2011

Reactive oxygen species (ROS), which include superoxide anions and peroxides, induce oxidative stress, contributing to the initiation and progression of cardiovascular diseases involving atherosclerosis. The endogenous and exogenous factors hypercholesterolemia, hyperglycemia, hypertension, and shear stress induce various enzyme systems such as nicotinamide adenine dinucleotide (phosphate) oxidase, xanthine oxidase, and lipoxygenase in vascular and immune cells, which generate ROS. Besides inducing oxidative stress, ROS mediate signaling pathways involved in monocyte adhesion and infiltration, platelet activation, and smooth muscle cell migration. A number of antioxidant enzymes (e.g., superoxide dismutases, catalase, glutathione peroxidases, and peroxiredoxins) regulate ROS in vascular and immune cells. Atherosclerosis results from a local imbalance between ROS production and these antioxidant enzymes. In this review, we will discuss 1) oxidative stress and atherosclerosis, 2) ROS-dependent atherogenic signaling in endothelial cells, macrophages, and vascular smooth muscle cells, 3) roles of peroxidases in atherosclerosis, and 4) antioxidant drugs and therapeutic perspectives.

• Molecules and Cells
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• 제39권3호
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• pp.186-194
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• 2016

Epidemiological evidence suggests that bone is especially sensitive to oxidative stress, causing bone loss in the elderly. Previous studies indicated that human amnion-derived mesenchymal stem cells (HAMSCs), obtained from human amniotic membranes, exerted osteoprotective effects in vivo. However, the potential of HAMSCs as seed cells against oxidative stress-mediated dysfunction is unknown. In this study, we systemically investigated their antioxidative and osteogenic effects in vitro. Here, we demonstrated that HAMSCs significantly promoted the proliferation and osteoblastic differentiation of $H_2O_2$-induced human bone marrow mesenchymal stem cells (HBMSCs), and down-regulated the reactive oxygen species (ROS) level. Further, our results suggest that activation of the ERK1/2 MAPK signal transduction pathway is essential for both HAMSCs-mediated osteogenic and protective effects against oxidative stress-induced dysfunction in HBMSCs. U0126, a highly selective inhibitor of extracellular ERK1/2 MAPK signaling, significantly suppressed the antioxidative and osteogenic effects in HAMSCs. In conclusion, by modulating HBMSCs, HAMSCs show a strong potential in treating oxidative stress- mediated bone deficiency.