• Kosin Medical Journal
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• v.33 no.2
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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.

• Molecules and Cells
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• v.39 no.3
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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.

• Food Science of Animal Resources
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• v.23 no.2
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• pp.186-192
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• 2003

The health benefits of friendly bacteria first came to the attention of the general public in 1908, when Dr. Elie Metchnikoff, a Russian biologist, wrote The Prolongation of Life. The longevity may be, in part, due to the antioxidative ability of lactic acid bacteria. However, the antioxidative effect of lactic acid bacteria has been reported only recently. Many kinds of reactive oxygen species can be formed in the human body and in food system, oxidative stress plays a significant pathological role in human disease. Antioxidants are effective for the reduction of oxidation induced by oxygen radicals by scavenging reactive oxygen species. Various synthetic and natural antioxidants have been reported, but there are doubts about the safety and long term effects on health. Antioxidants from natural sources are likely to be found more desirable. An elevated scavenging ability of reactive oxygen species would be a good property for commercially applied lactic acid bacteria. Antioxidant supplement or food containing antioxidants would be greatly applied for the reduction of oxidative damage for human body, and lactic acid bacteria are potentiated candidates for the production of functional foods or natural antioxidant supplements.

• Korean journal of food and cookery science
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• v.28 no.6
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• pp.821-828
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• 2012

In an attempt to identify the neuroprotective effect of Cudrania tricuspidata (CT) leaves against ROS (reactive oxygen species)-induced oxidative stress in neuronal cells, the extracts from CT leaves were investigated using PC12 cells and N18-RE-105 cells. The methanolic and ethanolic extracts from CT were denoted as CTM (Cudrania tricuspidata Leaves methanolic extracts) and CTE (Cudrania tricuspidata Leaves ethanolic extracts), respectively. The neuroprotective effects of the extracts were measured by DCF-DA assay, MTT reduction assay, and LDH release assay. The PC12 cells exposed to $H_2O_2$-induced oxidative stress and the N18-RE-105 cells exposed to glutamate-induced oxidative stress were treated with various concentrations of CTM and CTE. The results, CTM treatments resulted in the induction of a dose-dependent protective effect in PC12 cells and N18-RE-105 cells. Interestingly, CTE also showed neuroprotective effect in PC12 cells and N18-RE-105 cells. Therefore, these results suggest that CTM and CTE could be a new potential candidate as neuroprotective agents against ROS-induced oxidative stress in neuronal cells.

• BMB Reports
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• v.46 no.11
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• pp.555-560
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• 2013

Acrolein is the most reactive aldehydic product of lipid peroxidation and is found to be elevated in the brain when oxidative stress is high. The effects of acrolein on the structure and function of human Cu,Zn-superoxide dismutase (SOD) were examined. When Cu,Zn-SOD was incubated with acrolein, the covalent crosslinking of the protein was increased, and the loss of enzymatic activity was increased in a dose-dependent manner. Reactive oxygen species (ROS) scavengers and copper chelators inhibited the acrolein-mediated Cu,Zn-SOD modification and the formation of carbonyl compound. The present study shows that ROS may play a critical role in acrolein-induced Cu,Zn-SOD modification and inactivation. When Cu,Zn-SOD that has been exposed to acrolein was subsequently analyzed by amino acid analysis, serine, histidine, arginine, threonine and lysine residues were particularly sensitive. It is suggested that the modification and inactivation of Cu,Zn-SOD by acrolein could be produced by more oxidative cell environments.

• Bulletin of the Korean Chemical Society
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• v.34 no.11
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• pp.3295-3300
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• 2013

Acrolein (ACR) is a well-known carbonyl toxin produced by lipid peroxidation of polyunsaturated fatty acids, which is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). In Alzheimer's brain, ACR was found to be elevated in hippocampus and temporal cortex where oxidative stress is high. In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with ACR. When cytochrome c was incubated with ACR, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in ACR-treated cytochrome c. Reactive oxygen species scavengers and iron specific chelator inhibited the ACR-mediated cytochrome c modification and carbonyl compound formation. Our data demonstrate that oxidative damage of cytochrome c by ACR might induce disruption of cyotochrome c structure and iron mishandling as a contributing factor to the pathology of AD.

• Clinical and Experimental Reproductive Medicine
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• v.41 no.3
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• pp.125-131
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• 2014

Objective: Under estrogen deficiency, blastocysts cannot initiate implantation and enter dormancy. Dormant blastocysts live longer in utero than normal blastocysts, and autophagy has been suggested as a mechanism underlying the sustained survival of dormant blastocysts during delayed implantation. Autophagy is a cellular degradation pathway and a central component of the integrated stress response. Reactive oxygen species (ROS) are produced within cells during normal metabolism, but their levels increase dramatically under stressful conditions. We investigated whether heightened autophagy in dormant blastocysts is associated with the increased oxidative stress under the unfavorable condition of delayed implantation. Methods: To visualize ROS production, day 8 (short-term dormancy) and day 20 (long-term dormancy) dormant blastocysts were loaded with $1-{\mu}M$ 5-(and-6)-chloromethyl-2', 7'-dichlorodihydrofluorescein diacetate, acetyl ester (CM-$H_2DCFDA$). To block autophagic activation, 3-methyladenine (3-MA) and wortmannin were used in vivo and in vitro, respectively. Results: We observed that ROS production was not significantly affected by the status of dormancy; in other words, both dormant and activated blastocysts showed high levels of ROS. However, ROS production was higher in the dormant blastocysts of the long-term dormancy group than in those of the short-term group. The addition of wortmannin to dormant blastocysts in vitro and 3-MA injection in vivo significantly increased ROS production in the short-term dormant blastocysts. In the long-term dormant blastocysts, ROS levels were not significantly affected by the treatment of the autophagy inhibitor. Conclusion: During delayed implantation, heightened autophagy in dormant blastocysts may be operative as a potential mechanism to reduce oxidative stress. Further, ROS may be one of the potential causes of compromised developmental competence of long-term dormant blastocysts after implantation.

• Biomedical Science Letters
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• v.11 no.3
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• pp.319-326
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• 2005

It is well known that oxidative stress of reactive oxygen species (ROS) may be a causative factor in the pathenogenesis of bone disorder on osteoblast or osteoclast. The purpose of this study was to evaluate the cytotoxicity of oxidative stress, protective effect of glutamate receptor antagoinst against ROS-induced osteotoxicity, secretion of tumor necrosis factor $(TNF)-\alpha$ and the expression of c-fos gene in the cultured rat osteoblasts and osteoclasts. Cell viability by MTS assay or !NT assay, activity of glutathione peroxidase (GPx), lipid peroxidation (LPO) activity, protein synthesis by sulforhodamine B (SRB) assay, alkaline phosphatase (ALP) activity, lactate dehydrogenase (LDH) activity, MTS assay for NMDA (N-methyl-D-aspartate) receptor antagonist or AMPA/kainate receptor antagonist, measurement for $TNF-\alpha$, and c-fos gene expression were performed after these cells were treated with or without various cocentrations of xanthine oxidase (XO), hypoxanthine (HX), D-2-amino-5-phosphonovaleric acid (APV), 7-chlorokynurenic acid (CKA), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 6,7-dinitroquinoxaline-2,3-dione (DNQX), respectively. In this study, XO/HX showed decreased cell viability and glutathione peroxidase (GPx) activity, but it showed increased LPO activity, $TNF-\alpha$ secretion and c-fos expression. APV and CKA incresed protein sythesis and ALP activity. While, CNQX or DNQX did not show any protective effect in LDH activity or cell viability. From these results, XO/HX showed cytotoxic effect in cultured rat osteoblast or osteoclast, and also NMDA receptor antagonist such as APV or CKA was effective in blocking XO/HX-induced osteotoxicity in these cultures.

• Korean Journal of Pharmacognosy
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• v.36 no.1 s.140
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• pp.34-37
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• 2005

Reactive oxygen species (ROS) are known to cause oxidative modification of DNA, proteins, lipids and small cellular molecules and are associated with tissue damage and are the contributing factors for inflammation, aging, cancer, arteriosclerosis, hypertension and diabetes. We screened the anti-oxidants in V79-4 hamster lung fibroblast cells induced by hydrogen peroxide with eighteen pure compounds isolated from natural products. Allantoin, brassicasterol, and hypaconitine were found to strongly scavenge intracellular reactive oxygen species, which is measured by dichlorodihydrofluorescin diacetate method (DCHF-DA), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical.

• Korean Journal of Pharmacognosy
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• v.36 no.3 s.142
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• pp.159-163
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• 2005

We screened the anti-oxidative effect on V79-4 hamster lung fibroblast cells induced by hydrogen peroxide with fifteen herbal extracts. Uncariae rhynchophylla JACKS and Rheum coreanum NAKAI were found to show DPPH radical scavenge activity (25 and 29% compared to control). Rheum coreanum NAKAI and Siegesbeckia orientalis L. were shown to scavenge intracellular reactive oxygen species (57 and 55% compared to control) which is measured by dichlorodihydrofluorescin diacetate method (DCHF-DA). Rheum coreanum NAKAI which showed the most strong intracellular reactive oxygen species scavenging activity had low DPPH radical scavenging activity compared to Uncariae rhynchophylla JACKS.