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Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy.

Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy. Research Abstract Details 

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  • Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy. Abstract Text:

    katey m lemarKatey M Lemar,miguel a aonMiguel A Aon,sonia cortassaSonia Cortassa,brian o'rourkeBrian O'Rourke,carsten t Carsten T ,david lloydDavid Lloyd,

    Using two-photon scanning laser microscopy, we investigated the effect of an Allium sativum (garlic) constituent, diallyl disulphide (DADS), on key physiological functions of the opportunistic pathogen Candida albicans. A short 30 min exposure to 0.5 mM DADS followed by removal induced 70% cell death (50% necrotic, 20% apoptotic) within 2 h, increasing to 75% after 4 h. The early intracellular events associated with DADS-induced cell death were monitored with two-photon fluorescence microscopy to track mitochondrial membrane potential (Deltapsi(m)), reactive oxygen species (ROS) and NADH or reduced glutathione (GSH) under aerobic conditions. DADS treatment decreased intracellular GSH and elevated intracellular ROS levels. Additionally, DADS induced a marked decrease of Deltapsi(m) and lowered respiration in cell suspensions and isolated mitochondria. In vitro kinetic experiments in cell-free extracts suggest that glutathione-S-transferase (GST) is one of the intracellular targets of DADS. Additional targets were also identified, including inhibition of a site or sites between complexes II-IV in the electron transport chain, as well as the mitochondrial ATP-synthase. The results indicate that DADS is an effective antifungal agent able to trigger cell death in Candida, most probably by eliciting oxidative stress as a consequence of thiol depletion and impaired mitochondrial function.

    Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy. Publishing Authors By Initials

    km lemarKM Lemar,ma aonMA Aon,s cortassaS Cortassa,b o'rourkeB O'Rourke,ct CT ,d lloydD Lloyd,

    For similar biochemical phenomena, metabolism, and nutrition: metabolism: oxidative stress research abstracts see: biochemical phenomena, metabolism, and nutrition: metabolism: oxidative stress research

    PUBMED ID PMID:

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    Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Yeast (Chichester, England)

    VOLUME: 24

    Page Numbers: 695-706

    Journal Abbreviation: Yeast

    ISSN: 0749-503X

    DAY: 3

    MONTH: Aug

    YEAR: 2007

    Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8607637

    Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy. Keywords Mesh Terms:

    KEYWORDS: Oxidative Stress

    MESH TERMS: drug effects

    Chemical & Substance for Abstract: Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy. Information

    Substance Name: Glutathione

    Registry Number: 70-18-8

    Grant and Affiliation Information for Diallyl disulphide depletes glutathione in Candida albicans: oxidative stress-mediated cell death studied by two-photon microscopy.

    AFFILIATION: Microbiology (BIOSI 1), Main Building, Cardiff University, PO Box 915, Cardiff CF10 3TL, UK.

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NHLBI

    GRANT: R01-HL54598

    ACRONYM: HL

    MEDLINETA: Yeast

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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