RapamycinFungusV1, Main, Exploration, bibRecord, 000E91

Elimination of damaged mitochondria through mitophagy reduces mitochondrial oxidative stress and increases tolerance to trichothecenes.

Identifieur interne : 000E91 ( Main/Exploration ); précédent : 000E90; suivant : 000E92

Elimination of damaged mitochondria through mitophagy reduces mitochondrial oxidative stress and increases tolerance to trichothecenes.

Auteurs : Mohamed Anwar Bin-Umer [États-Unis] ; John E. Mclaughlin [États-Unis] ; Matthew S. Butterly [États-Unis] ; Susan Mccormick [États-Unis] ; Nilgun E. Tumer [États-Unis]

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2014.

RBID : pubmed:25071194

Descripteurs français

KwdFr :
- Animaux (MeSH), Contamination des aliments (MeSH), Espèces réactives de l'oxygène (métabolisme), Gènes fongiques (MeSH), Humains (MeSH), Mitochondries (effets des médicaments et des substances chimiques), Mitochondries (métabolisme), Résistance des champignons aux médicaments (génétique), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Stress oxydatif (MeSH), Sécurité des aliments (MeSH), Techniques de knock-out de gènes (MeSH), Trichothécènes (toxicité).
MESH :
- effets des médicaments et des substances chimiques : Mitochondries, Saccharomyces cerevisiae.
- génétique : Résistance des champignons aux médicaments, Saccharomyces cerevisiae.
- métabolisme : Espèces réactives de l'oxygène, Mitochondries, Saccharomyces cerevisiae.
- pharmacologie : Sirolimus.
- toxicité : Trichothécènes.
- Animaux, Contamination des aliments, Gènes fongiques, Humains, Stress oxydatif, Sécurité des aliments, Techniques de knock-out de gènes.

English descriptors

KwdEn :
- Animals (MeSH), Drug Resistance, Fungal (genetics), Food Contamination (MeSH), Food Safety (MeSH), Gene Knockout Techniques (MeSH), Genes, Fungal (MeSH), Humans (MeSH), Mitochondria (drug effects), Mitochondria (metabolism), Mitophagy (drug effects), Oxidative Stress (MeSH), Reactive Oxygen Species (metabolism), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Sirolimus (pharmacology), Trichothecenes (toxicity).
MESH :
- chemical , metabolism : Reactive Oxygen Species.
- drug effects : Mitochondria, Mitophagy, Saccharomyces cerevisiae.
- genetics : Drug Resistance, Fungal, Saccharomyces cerevisiae.
- metabolism : Mitochondria, Saccharomyces cerevisiae.
- chemical , pharmacology : Sirolimus.
- chemical , toxicity : Trichothecenes.
- Animals, Food Contamination, Food Safety, Gene Knockout Techniques, Genes, Fungal, Humans, Oxidative Stress.

Abstract

Trichothecene mycotoxins are natural contaminants of small grain cereals and are encountered in the environment, posing a worldwide threat to human and animal health. Their mechanism of toxicity is poorly understood, and little is known about cellular protection mechanisms against trichothecenes. We previously identified inhibition of mitochondrial protein synthesis as a novel mechanism for trichothecene-induced cell death. To identify cellular functions involved in trichothecene resistance, we screened the Saccharomyces cerevisiae deletion library for increased sensitivity to nonlethal concentrations of trichothecin (Tcin) and identified 121 strains exhibiting higher sensitivity than the parental strain. The largest group of sensitive strains had significantly higher reactive oxygen species (ROS) levels relative to the parental strain. A dose-dependent increase in ROS levels was observed in the parental strain treated with different trichothecenes, but not in a petite version of the parental strain or in the presence of a mitochondrial membrane uncoupler, indicating that mitochondria are the main site of ROS production due to toxin exposure. Cytotoxicity of trichothecenes was alleviated after treatment of the parental strain and highly sensitive mutants with antioxidants, suggesting that oxidative stress contributes to trichothecene sensitivity. Cotreatment with rapamycin and trichothecenes reduced ROS levels and cytotoxicity in the parental strain relative to the trichothecene treatment alone, but not in mitophagy deficient mutants, suggesting that elimination of trichothecene-damaged mitochondria by mitophagy improves cell survival. These results reveal that increased mitophagy is a cellular protection mechanism against trichothecene-induced mitochondrial oxidative stress and a potential target for trichothecene resistance.

DOI: 10.1073/pnas.1403145111
PubMed: 25071194
PubMed Central: PMC4136610

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000E05
to stream Main, to step Curation: 000E05

Le document en format XML

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<term>Gene Knockout Techniques (MeSH)</term>
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<term>Saccharomyces cerevisiae</term>
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<front><div type="abstract" xml:lang="en">Trichothecene mycotoxins are natural contaminants of small grain cereals and are encountered in the environment, posing a worldwide threat to human and animal health. Their mechanism of toxicity is poorly understood, and little is known about cellular protection mechanisms against trichothecenes. We previously identified inhibition of mitochondrial protein synthesis as a novel mechanism for trichothecene-induced cell death. To identify cellular functions involved in trichothecene resistance, we screened the Saccharomyces cerevisiae deletion library for increased sensitivity to nonlethal concentrations of trichothecin (Tcin) and identified 121 strains exhibiting higher sensitivity than the parental strain. The largest group of sensitive strains had significantly higher reactive oxygen species (ROS) levels relative to the parental strain. A dose-dependent increase in ROS levels was observed in the parental strain treated with different trichothecenes, but not in a petite version of the parental strain or in the presence of a mitochondrial membrane uncoupler, indicating that mitochondria are the main site of ROS production due to toxin exposure. Cytotoxicity of trichothecenes was alleviated after treatment of the parental strain and highly sensitive mutants with antioxidants, suggesting that oxidative stress contributes to trichothecene sensitivity. Cotreatment with rapamycin and trichothecenes reduced ROS levels and cytotoxicity in the parental strain relative to the trichothecene treatment alone, but not in mitophagy deficient mutants, suggesting that elimination of trichothecene-damaged mitochondria by mitophagy improves cell survival. These results reveal that increased mitophagy is a cellular protection mechanism against trichothecene-induced mitochondrial oxidative stress and a potential target for trichothecene resistance. </div>
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<Abstract><AbstractText>Trichothecene mycotoxins are natural contaminants of small grain cereals and are encountered in the environment, posing a worldwide threat to human and animal health. Their mechanism of toxicity is poorly understood, and little is known about cellular protection mechanisms against trichothecenes. We previously identified inhibition of mitochondrial protein synthesis as a novel mechanism for trichothecene-induced cell death. To identify cellular functions involved in trichothecene resistance, we screened the Saccharomyces cerevisiae deletion library for increased sensitivity to nonlethal concentrations of trichothecin (Tcin) and identified 121 strains exhibiting higher sensitivity than the parental strain. The largest group of sensitive strains had significantly higher reactive oxygen species (ROS) levels relative to the parental strain. A dose-dependent increase in ROS levels was observed in the parental strain treated with different trichothecenes, but not in a petite version of the parental strain or in the presence of a mitochondrial membrane uncoupler, indicating that mitochondria are the main site of ROS production due to toxin exposure. Cytotoxicity of trichothecenes was alleviated after treatment of the parental strain and highly sensitive mutants with antioxidants, suggesting that oxidative stress contributes to trichothecene sensitivity. Cotreatment with rapamycin and trichothecenes reduced ROS levels and cytotoxicity in the parental strain relative to the trichothecene treatment alone, but not in mitophagy deficient mutants, suggesting that elimination of trichothecene-damaged mitochondria by mitophagy improves cell survival. These results reveal that increased mitophagy is a cellular protection mechanism against trichothecene-induced mitochondrial oxidative stress and a potential target for trichothecene resistance. </AbstractText>
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	Serveur d'exploration sur la rapamycine et les champignons
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Elimination of damaged mitochondria through mitophagy reduces mitochondrial oxidative stress and increases tolerance to trichothecenes.

Elimination of damaged mitochondria through mitophagy reduces mitochondrial oxidative stress and increases tolerance to trichothecenes.

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