• Title/Summary/Keyword: Oxidative species

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Enhanced oxidative stability of meat by including tannin-rich leaves of woody plants in goat diet

  • Garcia, Elisa Mariana;Lopez, Agustin;Zimerman, Maria;Hernandez, Olegario;Arroquy, Jose Ignacio;Nazareno, Monica Azucena
    • Asian-Australasian Journal of Animal Sciences
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    • v.32 no.9
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    • pp.1439-1447
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    • 2019
  • Objective: The aim of this study was to evaluate the effect of dietary incorporation of tanninrich woody species on meat oxidative stability, carcass traits and meat quality in goats. Methods: Two tannin-rich species were tested using a three-treatments feeding trial, where treatments consisted of: Larrea divaricata and Acacia aroma both at 12.5% in dry matter basis of the diet and a control diet (alfalfa hay). All feeding diets were iso-protein and iso-energy. Carcass conformation, carcass compactness, carcass fatness and subcutaneous fat deposition were evaluated. Intake, liveweigh, Longissimus thoracis et lumborum muscles of goats were analyzed in order to evaluate quality parameters such as pH value, instrumental color evaluation, water holding capacity, total phenolic content, antioxidant activity, meat oxidative stability and fatty acid profiles in meat. Results: Feed intake, liveweight gain, carcass, and meat traits did not differ among treatments. Changes in meat lipid profile among treatments were observed for oleic and elaidic acid contents. Meat total phenolic content and antioxidant activity did not differ among treatments; although, meat oxidative status after storage at room temperature, as well as under refrigerated and frozen conditions were different between control and both supplemented groups. Conclusion: The inclusion of Acacia aroma and Larrea divaricata leaves in goat diet enhanced meat oxidative stability. Modulation of the ruminal biohydrogenation of fatty acids produced by condensed tannins of these plant species need to be further investigated.

Screening of Antioxidative Effect of Combined Medicinal Plants on Oxidative Stress (산화적 스트레스에 대한 복합 한약재의 항 산화활성 검색)

  • Kang Kyoung-Ah;Zhang Rui;Kang Dae-Gill;Kim Jin-Sook;Hyun Jin-Won
    • Environmental Mutagens and Carcinogens
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    • v.26 no.1
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    • pp.7-11
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    • 2006
  • 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 diabetes, inflammation, aging, cancer, arteriosclerosis, and hypertension. We screened the anti-oxidative effect on V79-4 hamster lung fibroblast cells induced by hydrogen peroxide with eleven extracts of combined medicinal plants. Dancheonhwankakambang and Samikangyabtang were found to show the scavenging activities of DPPH radical and intracellular reactive oxygen species, which is measured by dichlorodihydrofluorescin diacetate method (DCHF-DA).

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Phenanthrene-induced Oxidative DNA Damage of Lymphocytes and the Suppression by Ginseng Extract (페난트렌에 의한 임파구 DNA의 산화적 손상과 인삼추출물에 의한 억제)

  • Yoo, Ah-Reum;Lee, Mi-Young
    • Journal of Ginseng Research
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    • v.33 no.4
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    • pp.355-360
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    • 2009
  • Phenanthrene ($C_{14}H_{10}$) is a polycyclic aromatic hydrocarbon with three aromatic rings, and it can be produced by incomplete combustion of fossil fuels. Comet assay was used to examine the oxidative DNA damage of lymphocytes by phenanthrene and to measure the suppressive effects of ginseng extract on the DNA damage in this investigation. The in vitro oxidative DNA damage by phenanthrene increased in a dose-dependent manner in the lymphocyte. However, the DNA damage was significantly inhibited by ascorbate. Moreover, pretreatment, cotreatment and posttreatment with ginseng extract enhanced lymphocyte resistance to the phenanthrene-induced DNA damage. Phenanthrene enhanced the generation of intracellular reactive oxygen species, and the elevated reactive oxygen species level was reduced by treatment with ginseng extract.

The role of peroxidases in the pathogenesis of atherosclerosis

  • Park, Jong-Gil;Oh, Goo-Taeg
    • 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.

Acrolein, A Reactive Product of Lipid Peroxidation, Induces Oxidative Modification of Cytochrome c

  • Kang, Jung Hoon
    • 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.

Effect of Kimchi Ingredients to Reactive Oxygen Species in Skin Cell Cytotoxicity (김치 주.부재료의 활성산소에 대한 피부 세포독성 완화효과)

  • 문갑순;류승희;전영수;문정원;이영순
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.26 no.6
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    • pp.998-1005
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    • 1997
  • Kimchi showed protective effect from oxidative damage generated by hydrogen peroxide and paraquat. To investigate the major components of kimchi which reduce the cytotoxicity against reactive oxygen species, keratinocyte(A431, epidermoid carcinoma, human) and fibroblast(CCD-986SK, normal control, human) were cultured under oxidative stress condition provoked by paraquat, a superoxide anion generator, and hydrogen peroxide in the absence or presence of kimchi ingredients. Most keratinocyte and fibroblast cells were killed by hydrogen peroxide and paraquat over 1mM concentration, but kimchi ingredients showed protective effects from oxidative damage generated by hydrogen peroxide and onion, among those, garlic showed the most remarkable preventive effect. Most of kimchi ingredients showed protective effect against paraquat, especially leek notably increased cell survival. For fibroblast cells, ginger had the preventive effect against paraquat, especially leek notably increased cell survival. For fibroblast cells, ginger had the preventive effect from cell killing by high dose of hydrogen peroxide, but most ingredients were not effective against paraquat.

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Human Amnion-Derived Mesenchymal Stem Cells Protect Human Bone Marrow Mesenchymal Stem Cells against Oxidative Stress-Mediated Dysfunction via ERK1/2 MAPK Signaling

  • Wang, Yuli;Ma, Junchi;Du, Yifei;Miao, Jing;Chen, Ning
    • 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.

Modulation of Presynaptic GABA Release by Oxidative Stress in Mechanically-isolated Rat Cerebral Cortical Neurons

  • Hahm, Eu-Teum;Seo, Jung-Woo;Hur, Jin-Young;Cho, Young-Wuk
    • The Korean Journal of Physiology and Pharmacology
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    • v.14 no.3
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    • pp.127-132
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    • 2010
  • Reactive oxygen species (ROS), which include hydrogen peroxide ($H_2O_2$), the superoxide anion (${O_2}^-{\cdot}$), and the hydroxyl radical ($OH{\cdot}$), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated with conditions such as ischemia-reperfusion, Parkinson's disease, and aging. To investigate the effect of ROS on inhibitory GABAergic synaptic transmission, we examined the electrophysiological mechanisms of the modulatory effect of $H_2O_2$ on GABAergic miniature inhibitory postsynaptic current (mIPSCs) in mechanically isolated rat cerebral cortical neurons retaining intact synaptic boutons. The membrane potential was voltage-clamped at -60 mV and mIPSCs were recorded and analyzed. Superfusion of 1-mM $H_2O_2$ gradually potentiated mIPSCs. This potentiating effect of $H_2O_2$ was blocked by the pretreatment with either 10,000-unit/mL catalase or $300-{\mu}M$ N-acetyl-cysteine. The potentiating effect of $H_2O_2$ was occluded by an adenylate cyclase activator, forskolin, and was blocked by a protein kinase A inhibitor, N -(2-[p-bromocinnamylamino] ethyl)-5-isoquinolinesulfonamide hydrochloride. This study indicates that oxidative stress may potentiate presynaptic GABA release through the mechanism of cAMP-dependent protein kinase A (PKA)-dependent pathways, which may result in the inhibition of the cerebral cortex neuronal activity.

Oxidative Characteristics of Triglyceride Molecular Species in the Presence of Prooxidants (산화촉진제 공존하에서의 트리글리세리드 분자종의 산화특성)

  • Yoon, Hyeung-Sik;Kim, Seon-Bong;Park, Yeung-Ho
    • Korean Journal of Food Science and Technology
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    • v.22 no.1
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    • pp.7-12
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    • 1990
  • The effect of $Fe^{2+}$ and myoglobin on the oxidative stability of triglyceride molecular species was investigated at $25^{\circ}C$. The molecular species of soybean oil triglycerides were analyzed by capillary column gas chromatography and electron impact ionization mass spectrometry utilizing selected ion monitoring. When $Fe^{2+}$ and myoglobin were added to soybean oil triglycerides, the oxidative stability of each molecular species of triglycerides appeared to decrease in proportion to the increase in the number of double bonds present in the acyl residues, and it was affected by degree of unsaturation of fatty acid when the total degree of unsaturation of triglyceride was the same. But the length of the saturated acyl chain had no influence on the stabilization of unsaturated fatty acid present in the same glyceride when prooxidants were added.

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BETA-AMYLOID INDUCES OXIDATIVE AND/OR NITRATIVE PC12 CELL DEATH: POSSIBLE INVOLVEMENT OF INFLAMMATORY CASCADES

  • Jang, Jung-Hee;Surh, Young-Joon
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2002.05a
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    • pp.94-94
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    • 2002
  • Oxidative stress induced by reactive oxygen and/or nitrogen species has been considered as a major cause of cellular injuries in a variety of neurodegenerative disorders including Alzheimer's disease (AD). Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of AD, and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD.(omitted)

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