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1. Senkyunolide H protects against MPP + -induced apoptosis via the ROS-mediated mitogen-activated protein kinase pathway in PC12 cells.

Author

Luo Y, Li X, Liu T, Cao Y, Zhang J, Yaseen A, Sun F, Zheng W, Jiang Y, Si CL, and Hu W

Subjects
1-Methyl-4-phenylpyridinium, Animals, Apoptosis drug effects, Membrane Potential, Mitochondrial drug effects, PC12 Cells, Rats, Signal Transduction drug effects, Benzofurans pharmacology, Mitogen-Activated Protein Kinases metabolism, Neuroprotective Agents pharmacology, Reactive Oxygen Species metabolism
Abstract

Senkyunolide H (SNH) is a phthalide isolated from the rhizome of Ligusticum chuanxiong Hort. that has been reported to have several pharmacological activities, including anti-atherosclerotic, antiproliferative, and cytoprotective effects. In this study, we investigated the neuroprotective effects and potential mechanisms of SNH against 1-methyl-4-phenylpyridinium (MPP + )-induced oxidative stress. We demonstrated that SNH pretreatment significantly attenuated MPP + -induced neurotoxicity and apoptosis in PC12 cells. In addition, SNH attenuated the effect of MPP + on the expression of the pro-apoptotic factors Bax and caspase-3. Meanwhile, SNH prevented oxidative stress by reducing reactive oxygen species generation, mitochondrial membrane potential loss, cytochrome C release, and malondialdehyde levels while increasing antioxidant enzyme activity (e.g., superoxide dismutase, catalase, and glutathione peroxidase). In addition, SNH inhibited nuclear accumulation of nuclear factor-κB and c-Jun N-terminal kinase and phosphorylation p38 mitogen-activated protein kinases (MAPKs). Overall, this investigation provides novel evidence that SNH exerts neuroprotective effects via the ROS-mediated MAPK pathway and represents a potential preventive or therapeutic agent for neuronal disorders., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Published
2019
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2. 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

3. β-lactam antibiotics promote bacterial mutagenesis via an RpoS-mediated reduction in replication fidelity

Author

Jörg Vogel, Ivan Matic, S. Crussard, Jesús Blázquez, Luisa Laureti, Zeynep Baharoglu, Didier Mazel, F. Darfeuille, Alexandro Rodríguez-Rojas, Arnaud Gutierrez, Heni Abida, Robustesse et évolvabilité de la vie (U1001), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Departamento de Biotecnología Microbiana, Centro Nacional de Biotecnología [Madrid] (CNB-CSIC), Consejo Superior de Investigaciones Científicas [Madrid] (CSIC)-Consejo Superior de Investigaciones Científicas [Madrid] (CSIC), Plasticité du Génome Bactérien - Bacterial Genome Plasticity (PGB), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Régulations Naturelles et Artificielles (ARNA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bordeaux Ségalen [Bordeaux 2], Julius-Maximilians-Universität Würzburg (JMU), This work was supported by the FP7-HEALTH-F3-2010-241476 and ANR-09-BLAN-0251 grants. A.G. was supported by a fellowship from the French Ministry of Science and Education. D.M. was supported by the Institut Pasteur, Centre National de la Recherche Scientifique (CNRS-UMR 3525), the French National Research Agency (ANR-08-MIE-016), LABEX IBEID and the European Union Seventh Framework Programme EvoTAR. Z.B. was supported by a postdoctoral fellowship from the DIM Malinf. J.B. was supported by grants PI10/00105 (FIS) and REIPI (RD06/0008), both from Ministerio de Ciencia e Innovacion, Instituto de Salud Carlos III., We thank Dan Andersson’s lab (Uppsala University, Sweden) for providing the anti-DinB antibody, Marie Francoise Norel (Pasteur Institute, Paris) for providing the anti-RpoS antibody and Paul Modrich’s lab for providing the anti-MutS antibody., I.M., A.G., D.M., J.B., F.D. and J.V. designed the research and wrote the paper. A.G., L.L., H.A. and S.C. performed experiments with E. coli. Z.B. performed experiments and analysed data with V. cholerae. A.R.R. performed experiments and analysed data with P. aeruginosa. F.D. and J.V. performed in vitro experiments with SdsR and analysed data., ANR-09-BLAN-0251,bactadapt(2009), ANR-08-MIEN-0016,IIRE,Integrase d'integron recombinaison et expression(2008), European Project: 241476,EC:FP7:HEALTH,FP7-HEALTH-2009-single-stage,PAR(2010), European Project: 282004,EC:FP7:HEALTH,FP7-HEALTH-2011-single-stage,EVOTAR(2011), HOFFMANN, Isabelle, Blanc - - bactadapt2009 - ANR-09-BLAN-0251 - Blanc - VALID, Maladies Infectieuses et environnement - Integrase d'integron recombinaison et expression - - IIRE2008 - ANR-08-MIEN-0016 - MIE - VALID, Predicting antibiotic resistance - PAR - - EC:FP7:HEALTH2010-04-01 - 2013-03-31 - 241476 - VALID, Evolution and Transfer of Antibiotic Resistance - EVOTAR - - EC:FP7:HEALTH2011-10-01 - 2015-09-30 - 282004 - VALID, Centro Nacional de Biotecnologia, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), and Julius-Maximilians-Universität Würzburg [Wurtzbourg, Allemagne] (JMU)

Subjects
DNA Replication, medicine.drug_class, [SDV]Life Sciences [q-bio], Antibiotics, General Physics and Astronomy, Sigma Factor, MESH: DNA Replication, Biology, beta-Lactams, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, Microbiology, 03 medical and health sciences, Antibiotic resistance, Bacterial Proteins, MESH: beta-Lactams, MESH: Anti-Bacterial Agents, Escherichia coli, medicine, Vibrio cholerae, MESH: Bacterial Proteins, 030304 developmental biology, MESH: Mutagenesis, 0303 health sciences, Multidisciplinary, Bacteria, 030306 microbiology, Pseudomonas aeruginosa, MESH: Escherichia coli, Mutagenesis, MESH: Reactive Oxygen Species, MESH: Sigma Factor, General Chemistry, biochemical phenomena, metabolism, and nutrition, Anti-Bacterial Agents, 3. Good health, [SDV] Life Sciences [q-bio], MESH: Bacteria, Regulon, MESH: Pseudomonas aeruginosa, bacteria, Reactive Oxygen Species, rpoS, MESH: Vibrio cholerae
Abstract

Antimicrobials: mismatch excels when ampicillin runs low. [Nat Rev Microbiol. 2013]; International audience; Regardless of their targets and modes of action, subinhibitory concentrations of antibiotics can have an impact on cell physiology and trigger a large variety of cellular responses in different bacterial species. Subinhibitory concentrations of β-lactam antibiotics cause reactive oxygen species production and induce PolIV-dependent mutagenesis in Escherichia coli. Here we show that subinhibitory concentrations of β-lactam antibiotics induce the RpoS regulon. RpoS regulon induction is required for PolIV-dependent mutagenesis because it diminishes the control of DNA-replication fidelity by depleting MutS in E. coli, Vibrio cholerae and Pseudomonas aeruginosa. We also show that in E. coli, the reduction in mismatch-repair activity is mediated by SdsR, the RpoS-controlled small RNA. In summary, we show that mutagenesis induced by subinhibitory concentrations of antibiotics is a genetically controlled process. Because this mutagenesis can generate mutations conferring antibiotic resistance, it should be taken into consideration for the development of more efficient antimicrobial therapeutic strategies.

Published
2013