• Title/Summary/Keyword: Oxidative damage

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Application of Toxicogenomic Analysis to the Monitoring of Environmental Toxicity Using Recombinant Bioluminescent Bacteria and Cultured Mammalian Cells

  • Choi, Sue Hyung;Gu, Man Bock;Yasuyuki, Sakai
    • Proceedings of the Korean Society for Applied Microbiology Conference
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    • 2003.06a
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    • pp.129-131
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    • 2003
  • Recombinant bioluminescent bacteria and cultured human cells were applied for toxicogenomic analysis of environmentally hazardous chemicals. Recombinant bioluminescent biosensing cells were used to detect and classify the toxicity caused by various chemicals. Classification of toxicity was realized based upon the chemicals' mode of action using DNA-, oxidative-, protein, and membrane-damage sensitive strains. As well, a simple double-layered cell culture system using Caco-2 cells and Hep G2 cells, which mimic the metabolic processes occurring in humans, such as adsorption through the small intestine and biotransformationin both the small intestine and the liver, was developed to investigate the toxicity of hazardous materials to humans. For a more in-depth analysis, a DNA microarray was used to study the transcriptional responses of Caco-2 and Hep G2 cells to benzo〔a〕pyrene.

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Ferroptosis-Like Death in Microorganisms: A Novel Programmed Cell Death Following Lipid Peroxidation

  • Min Seok Kwun;Dong Gun Lee
    • Journal of Microbiology and Biotechnology
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    • v.33 no.8
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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.

Protective Effect of Dietary Buchu (Chinese chives) Against Oxidative Damage from Aging and Ultraviolet Irradiation in ICR Mice Skin

  • Lee, Min-Ja;Ryu, Bog-Mi;Kim, Mi-Hyang;Lee, Yu-Soon;Moon, Gap-Soon
    • Preventive Nutrition and Food Science
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    • v.7 no.3
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    • pp.238-244
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    • 2002
  • Protective effect of skin by antioxidative dietary buchu (Chinese chives, Allium tuberosum Router), was evaluated in ICR mice fed diets containing 2% or 5% buchu for 12 months. Lipid peroxidation and protein oxidation in skin, with or without ultraviolet B (UVB) irradiation, activities of antioxidative enzymes, total glutathione concentrations, and non-soluble collagen contents were measured. Dietary buchu decreased significantly in TBARS and protein carbonyl levels in skin compared to the control group, and were lower in those fed 5% than 2% buchu diet group. ICR mice exhibited an age-dependent decrease in antioxidative enzyme activities and total glutathione concentrations on the control diet, but in the groups fed buchu diet the enzyme activities and glu-tathione concentrations remained at youthful levels for most of the study. SOD, glutathione peroxidase, and catalase activities as well as total glutathione concentrations increased with time in the skins of the mice fed buchu diets. Lipid peroxidation and protein oxidation provoked by UVB irradiation on ICR mice skin homogenates were also significantly inhibited by dietary buchu. The buchu diets also decreased the formation of non-soluble collagen in mice skin, compared to the control group. These results suggest that antioxidative components and sulfur-compounds in buchu may confer protective effect against oxidative stress resulting from aging and exposure to ultraviolet irradiation.

Longevity Genes: Insights from Calorie Restriction and Genetic Longevity Models

  • Shimokawa, Isao;Chiba, Takuya;Yamaza, Haruyoshi;Komatsu, Toshimitsu
    • Molecules and Cells
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    • v.26 no.5
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    • pp.427-435
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    • 2008
  • In this review, we discuss the genes and the related signal pathways that regulate aging and longevity by reviewing recent findings of genetic longevity models in rodents in reference to findings with lower organisms. We also paid special attention to the genes and signals mediating the effects of calorie restriction (CR), a powerful intervention that slows the aging process and extends the lifespan in a range of organisms. An evolutionary view emphasizes the roles of nutrient-sensing and neuroendocrine adaptation to food shortage as the mechanisms underlying the effects of CR. Genetic and non-genetic interventions without CR suggest a role for single or combined hormonal signals that partly mediate the effect of CR. Longevity genes fall into two categories, genes relevant to nutrient-sensing systems and those associated with mitochondrial function or redox regulation. In mammals, disrupted or reduced growth hormone (GH)-insulin-like growth factor (IGF)-1 signaling robustly favors longevity. CR also suppresses the GH-IGF-1 axis, indicating the importance of this signal pathway. Surprisingly, there are very few longevity models to evaluate the enhanced anti-oxidative mechanism, while there is substantial evidence supporting the oxidative stress and damage theory of aging. Either increased or reduced mitochondrial function may extend the lifespan. The role of redox regulation and mitochondrial function in CR remains to be elucidated.

Increased antioxidative effects of Seolitae Chungkukjang added with green tea powders (녹차 첨가 서리태 청국장의 항산화 증진 효과)

  • Cho, Eun-Ju;Park, Hyun-Young;Kim, Hyun-Young
    • Korean Journal of Agricultural Science
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    • v.39 no.1
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    • pp.75-79
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    • 2012
  • To increase antioxidative activity and minimize off-flavor of Chungkukjang, Seoliate as main ingredient and green tea as minor ingredient were selected. The protective efffect of green tea for Chungkukjang was evaluated under in vitro. Seolitae Chungkukjang added with green tea (SCG) was prepared on the basis of the protective effect of green tea from oxidative stress. Green tea showed the strong protective effect against nitric oxide (NO) and superoxide anion ($O_2{^-}$) radicals. The SCG perparation method was as follows. Seolitae was cleaned and washed, soaked in 1.5-fold water ($15^{\circ}C$) of Seolitae weight for 48 hr. Seolitae was steamed about 40 min by autoclave and then cooled about $40^{\circ}C$. Bacillus subtilis was inoculated and 5.0-fold green tea of weight was added, and then it was fermented for 60 hr at $40^{\circ}C$. According to the preparation method, Seolitae Chungkukjang (SC) and Seolitae Chungkukjang added with green tea 5.0% (SCG5.0) were prepared. Among the Chungkukjang groups SCG5.0 exerted more effective scavenging activity of NO than SC. In addition, SC added with green tea 5.0% showed high $O_2{^-}$ scavenging effect. These results suggest the antioxidative potential against free radical-induced oxidative damage of SCG.

Comparison of the Antioxidant Effects of Diallyl Sulfide, Capsaicin, Gingerol and Sulforaphane in $H_2O_2$-Stressed HepG2 Cells (산화스트레스가 유도된 인체 간암세포 (HepG2)에서 Sulforaphane과 Diallyl Sulfide, Capsaicin, Gingerol의 항산화효과 비교연구)

  • Lee, So-Youn;Wi, Hae-Ri;Lee, Myoung-Sook
    • Journal of Nutrition and Health
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    • v.44 no.6
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    • pp.488-497
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    • 2011
  • Oxygen is necessary to sustain life, yet cellular oxygen metabolism creates destructive elements called free radicals. Free radicals are chemically unbalanced and carrying free electrons that can damage molecules, potentially damaging the cell itself. For this reason, many antioxidant products, including supplements and functional foods, are being developed. In particular, natural products are rich sources of pharmacologically active compounds. The purpose of this study was to investigate the antioxidant effects of target biomaterials in Korean traditional spices such as diallyl sulfide (DAS), capsaicin (CAP), and gingerol (GGR), and to investigate the response of the antioxidant defense system to oxidative stress by hydrogen peroxide ($H_2O_2$) compared to sulforaphane (SFN) in HepG2 cells. After the analysis of the cell viability using Cell Counting kit-8 (CCK-8) assay, we determined that the optimum levels were $200{\mu}M$ DAS, $25{\mu}M$ CAP, $50{\mu}M$ GGR, and $12.5{\mu}M$ SFN. Antioxidant enzymes were measured and protein expression was detected by Western blotting. All treatments showed a significant decrease in antioxidant enzyme activity such as superoxide dismutase, catalse, and glutathione peroxidase in HepG2 cells. Additionally, DAS, CAP, GGR and SFN increased the antioxidant system-related transcription factor Nrf2 which was found to be regulated by the activation of MAPK-JNK in this study. In conclusion, these results indicate the protective effects of DAS CAP, GGR, and SFN against $H_2O_2$-induced oxidative stress.

Korean Red Ginseng enhances cardiac hemodynamics on doxorubicin-induced toxicity in rats

  • Jang, Young-Jin;Lee, Dongbin;Hossain, Mohammad Amjad;Aravinthan, Adithan;Kang, Chang-Won;Kim, Nam Soo;Kim, Jong-Hoon
    • Journal of Ginseng Research
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    • v.44 no.3
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    • pp.483-489
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    • 2020
  • Background: Korean Red Ginseng (KRG) has been known to possess many ginsenosides. These ginsenosides are used for curing cardiovascular problems. The present study show the protective potential of KRG against doxorubicin (DOX)-induced myocardial dysfunction, by assessing electrocardiographic, hemodynamic, and biochemical parameters and histopathological findings. Methods: Animals were fed a standard chow and adjusted to their environment for 3 days before the experiments. Next, the rats were equally divided into five groups (n = 9, each group). The animals were administered with KRG (250 and 500 mg/kg) for 10 days and injected with DOX (20 mg/kg, subcutaneously, twice at a 24-h interval) on the 8th and 9th day. Electrocardiography and echocardiography were performed to study hemodynamics. Plasma levels of superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were measured. In addition, the dose of troponin I and activity of myeloperoxidase in serum and cardiac tissue were analyzed, and the histopathological findings were evaluated using light microscopy. Results: Administration of KRG at a dose of 250 and 500 mg/kg recovered electrocardiographic changes, ejection fraction, fractional shortening, left ventricular systolic pressure, the maximal rate of change in left ventricle contraction (-dP/dtmax), and left ventricle relaxation (-dP/dtmax). In addition, KRG treatment significantly normalized the oxidative stress markers in plasma, dose dependently. In addition, the values of troponin I and myeloperoxidase were ameliorated by KRG treatment, dose dependently. And, KRG treatment showed better histopathological findings when compared with the DOX control group. Conclusion: These mean that KRG mitigates myocardial damage by modulating the hemodynamics, histopathological abnormality, and oxidative stress related to DOX-induced cardiomyopathy in rats. The results of the present study show protective effects of KRG on cardiac toxicity.

Neuroprotective Effects of Some Plant Extracts against Oxygen-Glucose Deprivation (OGD)-Induced Oxidative Cell Death on Neuronal Cell (산소-포도당 결핍(OGD) 유도성 신경세포 사멸에 대한 뇌 보호 효과를 가지는 수종 생약추출물의 검색)

  • Lee, Hak-Ju;Koo, Uk;Lee, Hyun-Jung;Lee, Dong-Ho;Mar, Woong-Chon
    • Korean Journal of Medicinal Crop Science
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    • v.17 no.5
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    • pp.341-345
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    • 2009
  • Cerebral ischemia results from a transient or permanent reduction in cerebral blood flow that decreases oxygen and glucose supply. When the cellular oxygen supply is reduced to critical level, damage to cells and induction of cell death are occurred by excitotoxicity, oxidative stress and inflammation. Ischemia remains one of the leading causes of death, but there is no effective treatment that might protect neurons gainst ischemia by interrupting the cascade of cell death. In this study, human neuroblastoma SH-SY5Y cells are exposed to oxygen and glucose deprivation (OGD) followed by reoxgenation. OGD can mimic the acute restriction of metabolite and oxygen supply caused by ischemia and is widely used as a model of ischemic conditions. SH-SY5Y cells are treated samples at the commencement of OGD to achieve different final concentrations, and cell viabilities were quantified using the measurement of flow cytometry analysis. Of those tested, the extracts of Polygala tenuifolia (roots), Dictamnus dasycarpus (barks), Polygala tenuifolia (roots), Eucommia ulmoides (branches), Eucommia ulmoides (barks), Poria cocos (whole), Sophora flavescens (roots) showed neuroprotective effects, with $EC_{50}$ values of $4.5{\pm}0.6$, $7.9{\pm}1.5$, $10.5{\pm}0.7$, $18.4{\pm}1.9$, $19.6{\pm}0.3$, $21.6{\pm}1.9$, and $30.7{\pm}3.9{\mu}g/m{\ell}$, respectively.

Effects of Panax ginseng on Stress (스트레스에 대한 고려 인삼의 효능)

  • Lee, Mi-Jeong;Kim, Eun-Hye;Rhee, Dong-Kwon
    • Journal of Ginseng Research
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    • v.32 no.1
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    • pp.8-14
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    • 2008
  • Stress activates hypothalamic-pituitary-adrenal (HPA) axis and subsequently increases the systemic levels of glucocorticoids. It also inhibits the release of gonadotropin-releasing hormone (GnRH) from hypothalamus. Korean ginseng (Panax ginseng CA Meyer) has been proven as an anti-stress agent. However, most of the anti-stress effects of ginseng on stresses such as immobilization, electronic foot shock, and cold swim, which subsequently cause oxidative damage in brain, were obtained by using ginseng extract or ginseng total saponin. Moreover, anti-stress and anti-oxidative effects of ginseng were demonstrated by determination of enzyme or hormone levels but not mRNA as well as transcriptome. Further studies on transcriptome, proteomics, and systems biology as well as signal transduction would be required to elucidate molecular action mechanisms of ginseng on stresses.

The Degree of Lipid Oxidation of Rat Liver Fed Peroxidized Lipid and Its Effects on Anti-Oxidative System (과산화지질의 투여가 흰쥐 간의 산화와 항산화계에 미치는 영향)

  • 권명자;전영수;송영옥
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.23 no.6
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    • pp.899-907
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    • 1994
  • Accumulation of peroxidized lipid, fed or injected in the body of rats was investigated and the effect of peroxidized lipid on the antioxidative system was studied also. Three groups each having six of Sprague-dawley rats were raised for 8 weeks. the peroxide value(POV) of diet fed to the control and the peroxidized group was 5.47 and 22.14meq/kg , respectively. Injected group was given the control diet and peroxidized linoleic acid(POV 31.81meq/kg) was injected into the peritoneal area three times a week. The POV, MDA, and protein carbonyl values of the peroxidized and the injected group (experimental groups) were significantly higher (p<0.05) than those of the control group. Cu, Zn-SOD and M-SOD activity of the experimentla groups increased 1.6 times that of control group at 4 th week. and decreased by 60% of their activityafter 8 weeks of feeding (p<0.05) . Catalase activity, glutathione and Vt, E contents of the experimental groups were significantly lower (p<0.05) than those of the control group during 8 weeks. The accumulation of peroxidcized lipid in liver were ovserved both in the fed or the injected group. The increased of enzyme activity of the experimental group during 4 weeks suggests ianadaptation of antioxidative system to get rid of the peroxidized lipid. Decrease of enzyme activity and glutathione observed as the peroxidized lipid lipid accumulation proceeded further, however, seems to indicate the oxdiative damage of enzyme and protein . Determination of the protein carbonyl content may be used as a method for measuring the oxidative damaging effect of peroxidized lipid.

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