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Start Over Search Limiters Peer Reviewed Topic lipid peroxidation
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1. Antioxidant properties and neuroprotective effects of isocampneoside II on hydrogen peroxide-induced oxidative injury in PC12 cells.

Author

Si CL, Shen T, Jiang YY, Wu L, Yu GJ, Ren XD, Xu GH, and Hu WC

Subjects
Animals, Apoptosis Regulatory Proteins biosynthesis, Apoptosis Regulatory Proteins genetics, Apoptosis Regulatory Proteins metabolism, Cell Survival drug effects, Chelating Agents pharmacology, Gene Expression Regulation drug effects, Hydrogen Peroxide antagonists & inhibitors, Hydrogen Peroxide toxicity, Nerve Tissue Proteins biosynthesis, Nerve Tissue Proteins genetics, Nerve Tissue Proteins metabolism, Neurons enzymology, Neurons metabolism, Oxidants antagonists & inhibitors, Oxidants toxicity, Oxidation-Reduction, Oxidoreductases metabolism, PC12 Cells, Rats, Reactive Oxygen Species antagonists & inhibitors, Reactive Oxygen Species metabolism, Antioxidants pharmacology, Apoptosis drug effects, Caffeic Acids pharmacology, Disaccharides pharmacology, Glycosides pharmacology, Lipid Peroxidation drug effects, Neurons drug effects, Neuroprotective Agents pharmacology, Oxidative Stress drug effects
Abstract

Oxidative stress has been considered as a major cause of cell damage in various neurodegenerative disorders. One of the reasonable strategies for delaying the disease's progression is to prevent reactive oxygen species (ROS) mediated cellular injury by dietary or pharmaceutical augmentation of free radical scavengers. Isocampneoside II (ICD) is an active phenylethanoid glycoside isolated from the medicinal hardwood genus Paulownia. This study was designed to explore free radical scavenging potential of ICD in different in vitro systems and its protective role in hydrogen peroxide (H₂O₂)-induced oxidative stress and apoptotic death in cultured rat pheochromocytoma (PC12) cells. The results showed ICD eliminated approximately 80.75% superoxide radical at the concentration of 0.1mg/ml and inhibited metal chelating by 22.07% at 8 mg/ml. Additionally, ICD showed a strong ability on reducing power and provided protection against oxidative protein damage induced by hydroxyl radicals. Pretreatment of PC12 cells with ICD prior to H₂O₂ exposure elevated cell viability, enhanced activity of superoxide dismutase and catalase, and decreased levels of malondialdehyde and intracellular ROS. Furthermore, ICD inhibited cell apoptosis and Bax/Bcl-2 ratio induced by H₂O₂. These findings suggested ICD may be considered as a potential antioxidant agent and should encourage for further research in neurodegenerative diseases., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Published
2013
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2. Ilex aquifolium: protection against enzymatic and non-enzymatic lipid peroxidation.

Author

Müller K, Ziereis K, and Paper DH

Subjects
12-Hydroxy-5,8,10,14-eicosatetraenoic Acid biosynthesis, Animals, Arachidonate 5-Lipoxygenase blood, Brain Chemistry, Cattle, Chlorogenic Acid pharmacology, Female, Flavonoids isolation & purification, Leukotriene B4 blood, Liposomes, Lipoxygenase Inhibitors, Medicine, Traditional, Mice, Mice, Inbred Strains, Neutrophils enzymology, Neutrophils metabolism, Plant Extracts chemistry, Plants, Medicinal, Quercetin analogs & derivatives, Quercetin pharmacology, Rutin analogs & derivatives, Rutin pharmacology, Skin drug effects, Flavonoids pharmacology, Lipid Peroxidation drug effects, Neutrophils drug effects, Plant Extracts pharmacology, Skin metabolism
Abstract

The ethanolic extract of Ilex aquifolium L. (Aquifoliaceae) concentration-dependently inhibited leukotriene B4 biosynthesis in isolated bovine PMNL with an IC50 value of about 60 micrograms/ml, whereas the effect on epidermal 12(S)-HETE biosynthesis was much less pronounced. The extract also inhibited the non-enzymatic, peroxyl radical-stimulated lipid peroxidation in model membranes and was further a scavenger of the iron-dependent generation of hydroxyl radicals from hydrogen peroxide as determined by protection against deoxyribose degradation. While inhibition of leukotriene biosynthesis was not mediated by its known phenolic constituents such as hyperoside, rutoside, and chlorogenic acid, these compounds were responsible for the inhibitory effects of I. aquifolium against non-enzymatic lipid peroxidation and deoxyribose degradation.

Published
1998
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3. Ilex aquifolium: Protection Against Enzymatic and Non-Enzymatic Lipid Peroxidation

Author

D. H. Paper, Klaus Müller, and Klaus Ziereis

Subjects
Antioxidant, Neutrophils, Leukotriene B4, Rutin, medicine.medical_treatment, Pharmaceutical Science, Hyperoside, Mice, Inbred Strains, Analytical Chemistry, Lipid peroxidation, Mice, chemistry.chemical_compound, Biosynthesis, Chlorogenic acid, Drug Discovery, medicine, Animals, 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid, Lipoxygenase Inhibitors, Hydrogen peroxide, Skin, Brain Chemistry, Flavonoids, Pharmacology, Arachidonate 5-Lipoxygenase, Plants, Medicinal, Plant Extracts, Organic Chemistry, Complementary and alternative medicine, chemistry, Biochemistry, Deoxyribose, Liposomes, Molecular Medicine, Cattle, Female, Quercetin, Lipid Peroxidation, Medicine, Traditional, Chlorogenic Acid
Abstract

The ethanolic extract of Ilex aquifolium L. (Aquifoliaceae) concentration-dependently inhibited leukotriene B4 biosynthesis in isolated bovine PMNL with an IC50 value of about 60 micrograms/ml, whereas the effect on epidermal 12(S)-HETE biosynthesis was much less pronounced. The extract also inhibited the non-enzymatic, peroxyl radical-stimulated lipid peroxidation in model membranes and was further a scavenger of the iron-dependent generation of hydroxyl radicals from hydrogen peroxide as determined by protection against deoxyribose degradation. While inhibition of leukotriene biosynthesis was not mediated by its known phenolic constituents such as hyperoside, rutoside, and chlorogenic acid, these compounds were responsible for the inhibitory effects of I. aquifolium against non-enzymatic lipid peroxidation and deoxyribose degradation.

Published
1998

4. Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

Author

Taha Najar, Manef Abdrabbah, Abdeljelil Ghram, Moncef Ben Mrad, Imen Belhadj Slimen, Hajer Dabbebi, Preparatory Institute for Scientific and Technical Studies [La Marsa] (IPEST), Université de Carthage - University of Carthage, Institut National Agronomique de Tunis (INAT), Ministère de l'Enseignement Supérieur et de Recherche Scientifique [Tunisie], Institut Pasteur de Tunis, Réseau International des Instituts Pasteur (RIIP), and The authors thank Gillian Murphy, Emeritus Professor in the Department of Oncology at the University of Cambridge, for her assistance and help with English editing of this paper.

Subjects
Cancer Research, Antioxidant, MESH: Oxidative Stress, Physiology, Cellular respiration, medicine.medical_treatment, Apoptosis, Oxidative phosphorylation, Mitochondrion, Biology, medicine.disease_cause, reactive oxygen species (ROS), DNA, Mitochondrial, MESH: Lipid Peroxidation, heat stress, Electron Transport, Physiology (medical), medicine, Humans, MESH: Electron Transport, chemistry.chemical_classification, MESH: DNA Damage, Reactive oxygen species, MESH: Humans, MESH: Apoptosis, MESH: DNA, Mitochondrial, Metabolism, MESH: Heat-Shock Response, mitochondria, Oxidative Stress, chemistry, Biochemistry, MESH: Reactive Oxygen Species/metabolism, Lipid Peroxidation, Reactive Oxygen Species, Oxidative stress, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Heat-Shock Response, DNA Damage
Abstract

International audience; In recent years there has been enormous interest in researching oxidative stress. Reactive oxygen species (ROS) are derived from the metabolism of oxygen as by-products of cell respiration, and are continuously produced in all aerobic organisms. Oxidative stress occurs as a consequence of an imbalance between ROS production and the available antioxidant defence against them. Nowadays, a variety of diseases and degenerative processes such as cancer, Alzheimer’s and autoimmune diseases are mediated by oxidative stress. Heat stress was suggested to be an environmental factor responsible for stimulating ROS production because of similarities in responses observed following heat stress compared with that occurring following exposure to oxidative stress. This manuscript describes the main mitochondrial sources of ROS and the antioxidant defences involved to prevent oxidative damage in all the mitochondrial compartments. It also deals with discussions concerning the cytotoxic effect of heat stress, mitochondrial heat-induced alterations, as well as heat shock protein (HSP) expression as a defence mechanism.

Published
2014