Neurotoxic Mode of Action of Artemisinin

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Published inAntimicrobial Agents and Chemotherapy Vol. 46; no. 3; pp. 821 - 827
Main Authors SCHMUCK, Gabriele, ROEHRDANZ, Elke, HAYNES, Richard K, KAHL, Regine
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.03.2002
Subjects
Adenosine Triphosphate - metabolism
Animals
Antimalarials
Antimalarials - toxicity
artemisinin
Artemisinins
Artemsisia Annua
Biological and medical sciences
Cell Survival
Cells, Cultured
Cytoskeleton - drug effects
Cytoskeleton - metabolism
Drug toxicity and drugs side effects treatment
Energy Metabolism - drug effects
Enzyme-Linked Immunosorbent Assay
Lipid Peroxidation - drug effects
Mechanisms of Action: Physiological Effects
Medical sciences
Membrane Potentials
Mitochondria - drug effects
Mitochondria - physiology
Neurofilament Proteins - metabolism
Neurons - drug effects
Neurons - metabolism
Neurotoxicity Syndromes
Neurotoxicity Syndromes - pathology
Neurotoxins
Neurotoxins - toxicity
Oxidative Stress - drug effects
Pharmacology. Drug treatments
Rats
Reactive Oxygen Species - metabolism
RNA - biosynthesis
RNA - genetics
Sesquiterpenes
Sesquiterpenes - toxicity
Toxicity: nervous system and muscle
Glutathione peroxidase
Antimalarial
Oxidative stress
Enzyme
Toxicity
Artemisinin
Lipids
Superoxide dismutase
Gene expression
Cerebral disorder
Neuron
Peroxidases
Parasiticid
Central nervous system disease
Cytoskeleton
Oxidoreductases
Mechanism of action
Peroxidation
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Abstract Classifications Services AAC Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue AAC About AAC Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy AAC RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0066-4804 Online ISSN: 1098-6596 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to AAC .asm.org, visit: AAC       
AbstractList We recently described a screening system designed to detect neurotoxicity of artemisinin derivatives based on primary neuronal brain stem cell cultures (G. Schmuck and R. K. Haynes, Neurotoxicity Res. 2:37-49, 2000). Here, we probe possible mechanisms of this brain stem-specific neurodegeneration, in which artemisinin-sensitive neuronal brain stem cell cultures are compared with nonsensitive cultures (cortical neurons, astrocytes). Effects on the cytoskeleton of brain stem cell cultures, but not that of cortical cell cultures, were visible after 7 days. However, after a recovery period of 7 days, this effect also became visible in cortical cells and more severe in brain stem cell cultures. Neurodegeneration appears to be induced by effects on intracellular targets such as the cytoskeleton, modulation of the energy status by mitochondrial or metabolic defects, oxidative stress or excitotoxic events. Artemisinin reduces intracellular ATP levels and the potential of the inner mitochondrial membrane below the cytotoxic concentration range in all three cell cultures, with these effects being most dominant in the brain stem cultures. Surprisingly, there were substantial effects on cortical neurons after 7 days and on astrocytes after 1 day. Artemisinin additionally induces oxidative stress, as observed as an increase of reactive oxygen species and of lipid peroxidation in both neuronal cell types. Interestingly, an induction of expression of AOE was only seen in astrocytes. Here, manganese superoxide dismutase (MnSOD) expression was increased more than 3-fold and catalase expression was increased more than 1.5-fold. In brain stem neurons, MnSOD expression was dose dependently decreased. Copper-zinc superoxide dismutase and glutathione peroxidase, two other antioxidant enzymes that were investigated, did not show any changes in their mRNA expression in all three cell types after exposure to artemisinin.
ABSTRACT We recently described a screening system designed to detect neurotoxicity of artemisinin derivatives based on primary neuronal brain stem cell cultures (G. Schmuck and R. K. Haynes, Neurotoxicity Res. 2:37-49, 2000). Here, we probe possible mechanisms of this brain stem-specific neurodegeneration, in which artemisinin-sensitive neuronal brain stem cell cultures are compared with nonsensitive cultures (cortical neurons, astrocytes). Effects on the cytoskeleton of brain stem cell cultures, but not that of cortical cell cultures, were visible after 7 days. However, after a recovery period of 7 days, this effect also became visible in cortical cells and more severe in brain stem cell cultures. Neurodegeneration appears to be induced by effects on intracellular targets such as the cytoskeleton, modulation of the energy status by mitochondrial or metabolic defects, oxidative stress or excitotoxic events. Artemisinin reduces intracellular ATP levels and the potential of the inner mitochondrial membrane below the cytotoxic concentration range in all three cell cultures, with these effects being most dominant in the brain stem cultures. Surprisingly, there were substantial effects on cortical neurons after 7 days and on astrocytes after 1 day. Artemisinin additionally induces oxidative stress, as observed as an increase of reactive oxygen species and of lipid peroxidation in both neuronal cell types. Interestingly, an induction of expression of AOE was only seen in astrocytes. Here, manganese superoxide dismutase (MnSOD) expression was increased more than 3-fold and catalase expression was increased more than 1.5-fold. In brain stem neurons, MnSOD expression was dose dependently decreased. Copper-zinc superoxide dismutase and glutathione peroxidase, two other antioxidant enzymes that were investigated, did not show any changes in their mRNA expression in all three cell types after exposure to artemisinin.
Classifications Services AAC Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue AAC About AAC Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy AAC RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0066-4804 Online ISSN: 1098-6596 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to AAC .asm.org, visit: AAC       
Author Regine Kahl
Elke Roehrdanz
Richard K. Haynes
Gabriele Schmuck
AuthorAffiliation Pharma Research Center, Bayer AG, D-42096, Wuppertal, 1 Department of Toxicology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany, 3 Department of Chemistry, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong 2
AuthorAffiliation_xml – name: Pharma Research Center, Bayer AG, D-42096, Wuppertal, 1 Department of Toxicology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany, 3 Department of Chemistry, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong 2
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  surname: SCHMUCK
  fullname: SCHMUCK, Gabriele
  organization: Pharma Research Center, Bayer AG, 42096, Wuppertal, South Africa
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  givenname: Elke
  surname: ROEHRDANZ
  fullname: ROEHRDANZ, Elke
  organization: Pharma Research Center, Bayer AG, 42096, Wuppertal, South Africa
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  givenname: Richard K
  surname: HAYNES
  fullname: HAYNES, Richard K
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  surname: KAHL
  fullname: KAHL, Regine
  organization: Department of Toxicology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany
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Issue 3
Keywords Glutathione peroxidase
Antimalarial
Oxidative stress
Enzyme
Toxicity
Artemisinin
Lipids
Superoxide dismutase
Gene expression
Cerebral disorder
Neuron
Peroxidases
Parasiticid
Central nervous system disease
Cytoskeleton
Oxidoreductases
Mechanism of action
Peroxidation
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Present address: Bundesinstitut für Arzneimittel und Medizinprodukte (BfArM), 53113 Bonn, Germany.
Corresponding author. Mailing address: BAYER AG, Pharma Research Centre, Aprather Weg, D-42096 Wuppertal, Germany. Phone: 0049 202 368830. Fax: 0049 202 364137. E-mail: GABRIELE.SCHMUCK.GS@bayer-ag.de.
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We recently described a screening system designed to detect neurotoxicity of artemisinin derivatives based on primary neuronal brain stem cell cultures (G....
ABSTRACT We recently described a screening system designed to detect neurotoxicity of artemisinin derivatives based on primary neuronal brain stem cell...
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SubjectTerms Adenosine Triphosphate - metabolism
Animals
Antimalarials
Antimalarials - toxicity
artemisinin
Artemisinins
Artemsisia Annua
Biological and medical sciences
Cell Survival
Cells, Cultured
Cytoskeleton - drug effects
Cytoskeleton - metabolism
Drug toxicity and drugs side effects treatment
Energy Metabolism - drug effects
Enzyme-Linked Immunosorbent Assay
Lipid Peroxidation - drug effects
Mechanisms of Action: Physiological Effects
Medical sciences
Membrane Potentials
Mitochondria - drug effects
Mitochondria - physiology
Neurofilament Proteins - metabolism
Neurons - drug effects
Neurons - metabolism
Neurotoxicity Syndromes
Neurotoxicity Syndromes - pathology
Neurotoxins
Neurotoxins - toxicity
Oxidative Stress - drug effects
Pharmacology. Drug treatments
Rats
Reactive Oxygen Species - metabolism
RNA - biosynthesis
RNA - genetics
Sesquiterpenes
Sesquiterpenes - toxicity
Toxicity: nervous system and muscle
Title Neurotoxic Mode of Action of Artemisinin
URI http://aac.asm.org/content/46/3/821.abstract
https://www.ncbi.nlm.nih.gov/pubmed/11850267
https://journals.asm.org/doi/10.1128/AAC.46.3.821-827.2002
https://search.proquest.com/docview/18265817
https://pubmed.ncbi.nlm.nih.gov/PMC127487
Volume 46
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