• International Journal of Industrial Entomology and Biomaterials
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• 제22권2호
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• pp.95-100
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• 2011

The effect of diet supplementation of Antheraea pernyi (A. pernyi) silk fibroin on the lipid metabolism and antioxidant defense status in high fat-fed mice was investigated. The animals were given normal control diet (NC group), high fat diet (HF group), or high fat diet supplemented with A. pernyi silk fibroin powder (HFS group) for 7 weeks. After the experimental period, the HF group showed significant increase in body weight, plasma and hepatic total cholesterol levels, and hepatic triglyceride concentration, and decreased activities of hepatic antioxidant enzymes relative to NC group. However, the HFS group exhibited marked reduction in body weight, plasma cholesterol and hepatic triglyceride levels, hepatic lipogenic enzyme activities, and lipid peroxidation rate, and higher high-density lipoprotein (HDL)-cholesterol level, fecal triglyceride content, and antioxidant enzymes activities compared with that of HF group. These findings demonstrate that dietary feeding of A. pernyi silk fibroin could improve the lipid metabolism and antioxidant defense system via regulation of hepatic antioxidant and lipogenic enzymes activities. Hence, this silk fibroin may be beneficial as a functional biomaterial for the development of therapeutic agent against high fat diet-induced hyperlipidemia and its related diseases.

• Archives of Pharmacal Research
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• 제29권7호
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• pp.577-581
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• 2006

Oxidative mechanisms are thought to have a major role in cataract formation and diabetic complications. Antioxidant enzymes play an essential role in the antioxidant system of the cells that work to maintain low steady-state concentrations of the reactive oxygen species. When HLE-B3 cells, a human lens cell line were exposed to 50-100 mM glucose for 3 days, decrease of viability, inactivation of antioxidant enzymes, and modulation of cellular redox status were observed. Significant increase of cellular oxidative damage reflected by lipid peroxidation and DNA damage were also found. The glycation-mediated inactivation of antioxidant enzymes may result in the perturbation of cellular antioxidant defense mechanisms and subsequently lead to a pro-oxidant condition and may contribute to various pathologies associated with the long term complications of diabetes.

• Journal of Forest and Environmental Science
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• 제26권3호
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• pp.171-179
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• 2010

Effect of chromium (Cr) stress on antioxidant enzyme activities and malondialdehyde (MDA) content were investigated in leaves and roots of mangrove (italic (L.) Druce) seedlings. Cr toxicity effects were also assessed on young seedlings. The seedlings were grown in green house condition for three months in nutrient solution with 0, 0.5, 1, 1.5, 2, 2.5, and 3 mg $L^{-1}$ $CrCl_3$. This study showed that Cr led to the change of antioxidant enzymes such as superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT) and activities at different concentrations. The activity of antioxidant enzymes in leaves of K. candel seedlings indicates that enzymes engaged in antioxidant defense in certain level especially in low concentration of Cr treatments. The activities of SOD and POD were activated by Cr in the root level, while CAT activity was inhibited. CAT activity decreased in response to high concentrations of Cr. In the present study indicated that SOD in root was active in scavenging the superoxide produced by Cr. Both in roots and leaves, an increase in malondialdehyde (MDA) content was observed with increase in metal concentration and exposure periods. Our finding indicated that the high concentration of excessive Cr supply may interfere with several metabolic processes of seedlings, causing toxicity to plants as exhibited by chlorosis, necrosis, photosynthetic impairing and finally, plant death.

• Toxicological Research
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• 제17권
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• pp.299-304
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• 2001

Xenobiotics and their reactive intermediates bind to cellular macromolecules and/or generate oxidative stress. which provoke deleterious effects on the cell function. Induction of xenobiotic-biotrans-forming enzymes and antioxidant molecules is an important defense mechanism against such insults. A group of genes involved in the defense mechanism. e.g. genes encoding glutathione S-transferases. NAD(P)H: quinone oxidoreductase, UDP-glucuronosyltransferase (UDP-GT) and ${\gamma}$-glutamylcysteine synthetase (GGCS). have a common regulatory sequence, Antioxidant or Electrophile Responsive Element (ARE/EpRE). Recently. Nrf2. discovered as a homologue of erythroid transcription factor p45 NF-E2, was shown to bind ARE/EpRE and induce the expression of these defense genes. Mice that lack Nrf2 show low basal levels of expression and/or impaired induction of these genes. which makes the animals highly sensitive to xenobiotic toxicity. Indeed. we show here that nrf2-deficient mice had a higher mortality than did the wild-type mice when exposed to acetaminophen (APAP). Detailed analyses of APAP hepatotoxicity in the nrf2 knockout mice indicate that a large amount of reactive APAP metabolites was generated in the livers due to the impaired basal expression of two detoxifying enzyme genes, UDP-GT (Ugt1a6) and GGCS. while the cytochrome P450 content was unchanged. Thus. the studies using the nrf2 knockout mice clearly demonstrate significance of the expression of Nrf2-regulated enzymes in protection against xenobiotic toxicity.

• The Plant Pathology Journal
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• 제17권2호
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• pp.88-93
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• 2001

Oxidative stress is one of the major limiting factor in plant productivity. Reactive oxygens species (ROS) generated during metabolic processes damage cellular functions and consequently lead to disease, senescence and cell death. Plants have evolved an efficient defense system by which the ROS is scavenged by antioxidant enzymes such as superoxide dismutase (SOD) and ascorbate peroxidase (APX). Attempts to reduce oxidative damages under the stress conditions have included the manipulation of 갠 scavenging enzymes by gene transfer technology. Increased SOD activities of transgenic plants lead to increased resistance against oxidative stresses derived from methyl viologen (MV), and from photooxidative damage caused by high light and low temperature. Transgenic tobacco plants overexpressing APX showed reduced damage following either MV treatment of photooxidative treatment. Overexpression of glutathion reductase (GR) leads to increase in pool of ascorbate and GSH, known as small antioxidant molecules. These results indicate through overexpression of enzymes involved in ROS-scavenging could maintain or improve the plant productivities under environment stress condition. In this study, the rational approaches to develop stress-tolerant plants by gene manipulation of antioxidant enzymes will be introduced to provide solutions for the global food and environmental problems in the $21^\textrm{st}$ century.

• 한국어병학회지
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• 제27권2호
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• pp.115-125
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• 2014

본 연구에서는 수온변화에 따른 비소 (As) 노출의 영향을 틸라피아 Oreochromis niloticus의 간과 아가미에서 항산화 방어기작 (antioxidant defense system)을 통해 알아보고자 한다. 틸라피아를 수온이 각각, 20, 25 및 $30^{\circ}C$ 일때, 비소 농도 0, 200 및 $400{\mu}g/L$에서 10일간 노출시킨 후, glutathione (GSH) levels, glutathione reductase (GR), glutathione peroxidase (GPx) and glutathione S-treansferase (GST) 효소 활성을 측정하였다. 비소 노출 이후, 틸라피아의 간과 아가미에서 이들 항산화 효소는 수온 변화에 따라 유의하게 변화하였다. 특히, 다른 온도구간에 비하여 수온이 $30^{\circ}C$ 일 때, 비소에 노출된 틸라피아의 간에서 이들 효소의 변동폭은 가장 유의하게 증가하였다. 즉, 본 연구는 틸라피아의 간과 아가미에서 GSH 및 항산화 효소인 GR, GPx 및 GST에 미치는 비소의 영향은 수온 상승이 동반되었을 때, 어류의 산화 스트레스에 대한 방어 기작의 감소를 촉진시켰음을 보여준다.

• Biomolecules & Therapeutics
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• 제24권1호
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• pp.33-39
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• 2016

Oxidative stress activates several intracellular signaling cascades that may have deleterious effects on neuronal cell survival. Thus, controlling oxidative stress has been suggested as an important strategy for prevention and/or treatment of neurodegenerative diseases. In this study, we found that ginsenoside Rh1 inhibited hydrogen peroxide-induced reactive oxygen species generation and subsequent cell death in rat primary astrocytes. Rh1 increased the expression of phase II antioxidant enzymes, such as heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1, superoxide dismutase-2, and catalase, that are under the control of Nrf2/ARE signaling pathways. Further mechanistic studies showed that Rh1 increased the nuclear translocation and DNA binding of Nrf2 and c-Jun to the antioxidant response element (ARE), and increased the ARE-mediated transcription activities in rat primary astrocytes. Analysis of signaling pathways revealed that MAP kinases are important in HO-1 expression, and act by modulating ARE-mediated transcriptional activity. Therefore, the upregulation of antioxidant enzymes by Rh1 may provide preventive therapeutic potential for various neurodegenerative diseases that are associated with oxidative stress.

• The Korean Journal of Physiology and Pharmacology
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• 제23권6호
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• pp.519-528
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• 2019

Mitochondrial dysfunction is closely associated with reactive oxygen species (ROS) generation and oxidative stress in cells. On the other hand, modulation of the cellular antioxidant defense system by changes in the mitochondrial DNA (mtDNA) content is largely unknown. To determine the relationship between the cellular mtDNA content and defense system against oxidative stress, this study examined a set of myoblasts containing a depleted or reverted mtDNA content. A change in the cellular mtDNA content modulated the expression of antioxidant enzymes in myoblasts. In particular, the expression and activity of glutathione peroxidase (GPx) and catalase were inversely correlated with the mtDNA content in myoblasts. The depletion of mtDNA decreased both the reduced glutathione (GSH) and oxidized glutathione (GSSG) slightly, whereas the cellular redox status, as assessed by the GSH/GSSG ratio, was similar to that of the control. Interestingly, the steady-state level of the intracellular ROS, which depends on the reciprocal actions between ROS generation and detoxification, was reduced significantly and the lethality induced by $H_2O_2$ was alleviated by mtDNA depletion in myoblasts. Therefore, these results suggest that the ROS homeostasis and antioxidant enzymes are modulated by the cellular mtDNA content and that the increased expression and activity of GPx and catalase through the depletion of mtDNA are closely associated with an alleviation of the oxidative stress in myoblasts.

• 한국양식학회:학술대회논문집
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• 한국양식학회 2003년도 추계학술발표대회 논문요약집
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• pp.39-39
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• 2003

Antioxidant enzyme genes play a key role in cell defense against the lethal effects of oxidative stresses in animals and have an essential function which has allowed the evolution of aerobic respiration starting from an ancient form of oxygen-insensitive life. Piscine antioxidant enzymes are also involved in the rapid response to various toxic chemicals as well as many biological stresses, indicating that they could be used as biomarkers for health and aquatic environment. With the purpose for developing fine molecular probing tool to assess the stresses in marine fish, we identified three major antioxidant enzyme genes (superoxide dismutase, catalase and glutathione-S-transferase) from Korean rock bream using expressed sequence tag analysis and/or high density filter screening. Here we report the molecular information on these gene transcripts including complete sequence data and expression profiles.

• Environmental Analysis Health and Toxicology
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• 제24권4호
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• pp.303-309
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• 2009

Hepatic antioxidant defense systems were examined in rats treated with tetrabromobisphenol-A (TBBPA), a brominated flame retardant, at the doses of 0, 250, 500 and 1,000 mg/kg for four weeks. Hepatic ratio of glutathione disulfide to glutathione (GSH) and levels of malondialdehyde, oxidative stress markers were not changed in rats treated with TBBPA. Hepatic expression of antioxidant enzymes including GSH peroxdiase-1 (GPX-1)/GSH reductase (GR), alpha-, mu- and pi-class glutathione-S-transferase (GST) and gamma-glutamylcysteine ligase catalytic subunit was determined using immunoblot analysis. Alpha-class GSTs, GPX-1 and GR levels were significantly decreased in rats treated with TBBPA at the dose of 500 or 1,000 mg/kg. These results show that TBBPA results in down-regulation of hepatic expression of antioxidant enzymes related with GSH, suggesting the liver in TBBPA-treated rats may be more sensitive to oxidants.