• Proceedings of the Korean Society of Plant Biotechnology Conference
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• 2002.04a
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• pp.49-58
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• 2002

Oxidative stress derived from reactive oxygen species (ROS) is one of the major damaging factors in plants exposed to environmental stress. In order to develop the platform technology to solve the global food and environmental problems in the 21s1 century, we focus on the understanding of the antioxidative mechanism in plant cells, the development of oxidative stress-inducible antioxidant genes, and the development of transgenic plants with enhanced tolerance to stress. In this report, we describe our recent results on industrial transgenic plants by the gene manipulation of antioxidant enzymes. Transgenic tobacco plants expressing both superoxide dismutase (SOD) and ascorbate peroxidase (APX) in chloroplasts were developed and were evaluated their protection effects against stresses, suggesting that simultaneous overexpression of both SOD and APX in chloroplasts has synergistic effects to overcome the oxidative stress under unfavorable environments. Transgenic tobacco plants expressing a human dehydroascorbate reductase gene in chloroplasts were showed the protection against the oxidative stress in plants. Transgenic cucumber plants expressing high level of SOD in fruits were successfully generated to use the functional cosmetic purpose as a plant bioreactor. In addition, we developed a strong oxidative stress-inducible peroxidase promoter, SWPA2 from sweetpotato (Ipomoea batatas). We anticipate that SWPA2 promoter will be biotechnologically useful for the development of transgenic plants with enhanced tolerance to environmental stress and particularly transgenic cell lines engineered to produce key pharmaceutical proteins.

• Journal of The Korean Society of Grassland and Forage Science
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• v.42 no.2
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• pp.114-119
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• 2022

The objective of this study was to determine phosphorus effects on drought stress-induced oxidative stress in Kentucky bluegrass. Drought stress was induced by reducing of water to plants in pots. Two types of phosphorus were applied as potassium phosphate (P) or potassium phosphonate (PA). Application of phosphorus was efficient to ameliorate the adverse effects of drought. Osmotic potential, total chlorophyll and carotenoid content were significantly decreased by drought stress, but was relieved by P or PA application. Superoxide (O₂^•-) concentration was significantly increased more than 14-fold under drought-stressed plants, was accompanied with increase of hydrogen peroxide (H₂O₂) and lipid peroxidation (MDA). However, malondialdehyde (MDA) was much less in P or PA applied plants under drought stress condition. Activities of catalase (CAT), ascorbate peroxidase (APX) and guaiacol-peroxidase (GPX) were largely increased by drought stress and its increase rate was much higher in P or PA applied plants except APX. These results indicate that drought stress-induced oxidative stress is alleviated by P or PA application due to the increase of activities of antioxidant enzymes.

• 대한생식의학회:학술대회논문집
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• 2000.06a
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• pp.9-9
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• 2000

• Journal of Plant Biotechnology
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• v.50
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• pp.76-81
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• 2023

As cultured plant cells can grow in high oxidative stress conditions, they form an excellent system to study antioxidant mechanisms and the mass production of antioxidants. Oxidative stress is a major cause of damage in plants exposed to various types of environmental stress, including heavy metals, such as cadmium (Cd). Heavy metal accumulation can interfere with many cell functions and plant growth. To evaluate the contribution of oxidative stress to Cd-induced toxicity, cultured sweetpotato (Ipomoea batatas) cells were treated with increasing concentrations of Cd (0, 10, 25, and 50 μM) and cultured further. Cell growth was significantly inhibited by 25 and 50 μM of Cd, and the total protein content increased with 50 μM of Cd. Additionally, the activity of peroxidase (POD) and ascorbate peroxidase (APX), antioxidant enzymes that remove hydrogen peroxide (a reactive oxygen species), increased in the cells after treatment with 50 μM of Cd. The expression analysis of POD, APX, and peroxiredoxin (PRX) isolated from sweetpotato cultured cells in a previous study revealed the differential expression of POD in response to Cd. In this study, the expression levels of several acidic POD (swpa2, swpa3, and swpa4) and basal POD (swpb1, swpb2, and swpb3) genes were increased in Cd-treated cultured cells. These results indicate that Cd-mediated oxidative stress is closely linked to improved POD-mediated antioxidant defense capacity in sweetpotato suspension-cultured cells.

• BMB Reports
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• v.44 no.8
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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.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4405-4409
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• 2014

Reactive oxygen species (ROS), highly reactive molecules, are produced by living organisms as a result of normal cellular metabolism and environmental factors, and can damage nucleic acids and proteins, thereby altering their functions. The human body has several mechanisms to counteract oxidative stress by producing antioxidants. A shift in the balance between oxidants and antioxidants in favor of oxidants is termed as "oxidative stress". Paradoxically, there is a large body of research demonstrating the general effect of oxidative stress on signaling pathways, less is known about the initial and direct regulation of signaling molecules by ROS, or what we term the "oxidative interface." This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival (MAP kinases and PI3 kinase), ROS homeostasis, and antioxidant gene regulation (Ref-1 and Nrf-2). This review also deals with classification as well as mechanisms of formation of free radicals, examining their beneficial and deleterious effects on cellular activities and focusing on the potential role of antioxidants in preventing and repairing damage caused by oxidative stress. A discussion of the role of phytochemical antioxidants in oxidative stress, disease and the epigenome is included.

• Asian-Australasian Journal of Animal Sciences
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• v.33 no.5
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• pp.722-731
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• 2020

Objective: Two experiments were conducted using 28 healthy multiparous sows to evaluate the oxidative stress status and reproductive performance of sows during gestation and lactation under different thermal environments. Methods: Fourteen multiparous sows were used in Exp. 1 under a high thermal environment, and the other 14 multiparous sows were used in Exp. 2 under a moderate thermal environment. In both experiments, reproductive performances of sows were recorded. Plasma samples were collected on d 35, 60, 90, and 109 of gestation, and d 1 and 18 of lactation for malondialdehyde, protein carbonyls, 8-hydroxy-deoxyguanosine, immunoglobulin g (IgG), and IgM analysis. Results: For sows in Exp. 1, plasma malondialdehyde concentration on d 109 of gestation tended to be greater (p<0.05) than it on d 18 of lactation. Plasma concentration of protein carbonyl on d 109 of gestation was the greatest (p<0.05) compared with all the other days. Plasma concentrations of 8-hydroxy-deoxyguanosine on d 109 of gestation was greater (p<0.05) than d 18 of lactation in Exp. 1. For sows in Exp. 2, there was no difference of malondialdehyde and protein carbonyl concentration during gestation and lactation. In both Exp. 1 and 2, litter size and litter weight were found to be negatively correlated with oxidative stress indicators. Conclusion: Sows under a high thermal environment had increased oxidative stress during late gestation indicating that increased oxidative damage to lipid, protein, and DNA could be one of the contributing factors for reduced reproductive performance of sows in this environment. This study indicates the importance of providing a moderate thermal environment to gestating and lactating sows to minimize the increase of oxidative stress during late gestation which can impair reproductive outcomes.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.13
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• pp.5343-5348
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• 2015

Promoter hypermethylation of the runt-related transcription factor 3 (RUNX3) gene is associated with increased risk of hepatocellular carcinoma (HCC). Oxidative stress plays a vital role in both carcinogenesis and progression of HCC. However, whether oxidative stress and RUNX3 hypermethylation in HCC have a cause-and-effect relationship is not known. In this study, plasma protein carbonyl and total antioxidant capacity (TAC) in patients with hepatitis B virus (HBV)-associated HCC (n=60) and age-matched healthy subjects (n=80) was determined. RUNX3 methylation in peripheral blood mononuclear cells (PBMC) of subjects was measured by methylation-specific PCR. Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Plasma protein carbonyl content was significantly higher, whereas plasma TAC was significantly lower, in HCC patients than healthy controls. Based on logistic regression, increased plasma protein carbonyl and decreased plasma TAC were independently associated with increased risk for HCC. PBMC RUNX3 methylation in the patient group was significantly greater than in the healthy group. RUNX3 methylation in hydrogen peroxide ($H_2O_2$)-treated HepG2 cells was significantly higher than in untreated control cells. In conclusion, increase in oxidative stress in Thai patients with HBV-associated HCC was demonstrated. This oxidative increment was independently associated with an increased risk for HCC development. RUNX3 in PBMC was found to be hypermethylated in the HCC patients. In vitro, RUNX3 hypermethylation was experimentally induced by $H_2O_2$. Our findings suggest that oxidative stress is a cause of RUNX3 promoter hypermethylation in HCC cells.

• Korean Journal of Agricultural Science
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• v.46 no.3
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• pp.427-437
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• 2019

Oxidative stress and overproduction of free radicals have been reported to be a major pathological hallmark of neurodegenerative diseases. Samultang has been known as a beneficial agent to treat liver disease and cardiovascular diseases. However, the anti-oxidant activities and neuro-protective effects of Samultang against oxidative stress still have not been evaluated yet. The aim of the present study was to investigate the anti-oxidant and protective effects of Samultang and its four herbal plants, Paeonia lactiflora (PL), Ligusticum striatum (LS), Rehmannia glutinosa (RG), and Angelica gigas (AG), in vitro system and in SH-SY5Y neuronal cells. The extracts of Samultang strongly increased the radical scavenging activities of 1,1-diphenyl-2-picrylhydrazyl (DPPH), hydroxyl radical (${\cdot}OH$), and nitric oxide (NO) in a concentration-dependent manner. Furthermore, we investigated the protective effects of Samultang on cellular damage against oxidative stress induced by hydrogen peroxide ($H_2O_2$) in SH-SY5Y cells. Treatment with Samultang alleviated the oxidative stress from $H_2O_2$ by increasing the cell viability and decreasing the intracellular reactive oxygen species levels. Based on these results, we further investigated the radical scavenging effects of PL, LS, RG, and AG. In our results, PL had the highest DPPH, ${\cdot}OH$, and NO radical scavenging activities. Thus, PL has a crucial role in Samultang, which has anti-oxidative and neuro-protective effects. The present research suggests that Samultang and PL have protective roles against oxidative stress from $H_2O_2$-induced neuronal cell death.

• Bulletin of the Korean Chemical Society
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• v.22 no.5
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• pp.514-518
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• 2001

We have explored the importance of two ATP binding domains of Hsp104 protein in protection of yeast cells from cadmium exposure. In the previous study we have discovered that the presence of two ATP binding sites was essential in providing heat sh ock protection as well as rescuing cells from oxidative stress. In this paper we first report wild type cell with functional hsp104 gene is more resistant to cadmium stress than hsp104-deleted mutant cell, judging from decrease in survival rates as a result of cadmium exposure. In order to demonstrate functional role of two ATP binding sites in cadmium defense, we have transformed both wild type (SP1) and hyperactivated ras mutant (IR2.5) strains with several plasmids differing in the presence of ATP binding sites. When an extra copy of functional hsp104 gene with both ATP binding sites was overexpressed with GPD-promoter, cells showed increased survival rate against cadmium stress than mutants with ATP binding sites changed. The degree of protection in the presence of two ATP binding sites was similarly observed in ira2-deleted hyperactivated ras mutant, which was more sensitive to oxidative stress than wild type cell. We have concluded that the greater sensitivity to cadmium stress in the absence of two ATP binding sites is attributed to the higher concentration of reactive oxygen species (ROS) produced by cadmium exposure based on the fluorescence tests. These findings, taken all together, imply that the mechanism by which cadmium put forth toxic effects may be closely associated with the oxidative stress, which is regulated independently of the Ras-cAMP pathway. Our study provides a better understanding of cadmium defense itself and cross-talks between oxidative stress and metal stress, which can be applied to control human diseases due to similar toxic environments.