Catalases and thioredoxin peroxidase protect Saccharomyces cerevisiae against Ca2+‐induced mitochondrial membrane permeabilization and cell death

FEBS Letters

Vercesi, Anibal E.²  Netto, Luis E.S.³  Kowaltowski, Alicia J.²  Rhee, Sue Goo¹ 

[1] Laboratory of Cell Signaling, NHLBI, National Institutes of Health, Bethesda, MD 20892, USA;Departamento de Patologia Clı́nica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, 13083-970 Campinas, SP, Brazil;Departamento de Biologia, Instituto de Biociências, Universidade de São Paulo, Rua do Matão, Travessa 14 #321, 05508-900 São Paulo, SP, Brazil

关键词: Mitochondrion;    Yeast;    Antioxidant;    Mitochondrial permeability transition;    Cell death;    ATZ;    3-amino-1;    2;    4-triazole;    EGTA;    ethylene glycol-bis(β-aminoethyl ether) N;    N;    N′;    N′-tetraacetic acid;    DTT;    dithiothreitol;    FCCP;    carbonyl cyanide m-clorophenyl-hydrazone;    HEPES;    N-(hydroxyethyl)piperazine-N′-(4-butanesulfonic acid);    MPT;    mitochondrial permeability transition;    ROS;    reactive oxygen species;    WTSC;    wild-type Saccharomyces cerevisiae spheroblasts;    ΔTSASC;    Saccharomyces cerevisiae spheroblasts lacking thioredoxin peroxidase;    ATZ–WTSC;    3-amino-1;    2;    4-triazole-treated wild-type Saccharomyces cerevisiae spheroblasts;    ATZ–ΔTSASC;    3-amino-1;    2;    4-triazole-treated Saccharomyces cerevisiae spheroblasts lacking thioredoxin peroxidase;    Pi;    inorganic phosphate;    t-bOOH;    t-butyl hydroperoxide;    PhAsO;    phenylarsine oxide;    TPx;    thioredoxin peroxidase;   

DOI  :  10.1016/S0014-5793(00)01526-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The involvement of reactive oxygen species in Ca²⁺-induced mitochondrial membrane permeabilization and cell viability was studied using yeast cells in which the thioredoxin peroxidase (TPx) gene was disrupted and/or catalase was inhibited by 3-amino-1,2,4-triazole (ATZ) treatment. Wild-type Saccharomyces cerevisiae cells were very resistant to Ca²⁺ and inorganic phosphate or t-butyl hydroperoxide-induced mitochondrial membrane permeabilization, but suffered an immediate decrease in mitochondrial membrane potential when treated with Ca²⁺ and the dithiol binding reagent phenylarsine oxide. In contrast, S. cerevisiae spheroblasts lacking the TPx gene and/or treated with ATZ suffered a decrease in mitochondrial membrane potential, generated higher amounts of hydrogen peroxide and had decreased viability under these conditions. In all cases, the decrease in mitochondrial membrane potential could be inhibited by ethylene glycol-bis(β-aminoethyl ether) N,N,N′,N′-tetraacetic acid, dithiothreitol or ADP, but not by cyclosporin A. We conclude that TPx and catalase act together, maintaining cell viability and protecting S. cerevisiae mitochondria against Ca²⁺-promoted membrane permeabilization, which presents similar characteristics to mammalian permeability transition.

【 授权许可】

Unknown