Candida albicans erythroascorbate peroxidase regulates intracellular methylglyoxal and reactive oxygen species independently of D-erythroascorbic acid

Candida albicans erythroascorbate peroxidase regulates intracellular methylglyoxal and reactive oxygen species independently of D-erythroascorbic acid
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DOI:
10.1016/j.febslet.2015.04.050
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发表时间:
2015-07-08
期刊:
影响因子:
3.5
通讯作者:
Kang, Sa-Ouk
Kang, Sa-Ouk
中科院分区:
生物学3区
文献类型:
--
作者:
Kwak, Min-Kyu;Song, Sung-Hyun;Kang, Sa-Ouk

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白色念珠菌D-赤式抗坏血酸过氧化物酶(EAPX 1)可以催化D-赤式抗坏血酸(EASC)氧化成水,通过活性染色观察到EAPX 1在EAPX 1缺陷和EAPX 1过表达细胞中是可诱导的。EAPX 1缺陷细胞具有显著增加的细胞内活性氧和丙酮醛,而与细胞内EASC含量无关。丙酮醛的增加导致EAPX 1缺陷细胞激活过氧化氢酶-渗透酶和细胞色素c过氧化物酶,从而导致细胞生长、活力、线粒体呼吸、表达和毒力的缺陷。这些发现表明,EAPX 1介导细胞分化和毒力,通过调节细胞内甲基乙二醛沿着氧化应激,无论内源性EASC生物合成或替代氧化酶的表达。(C)2015年欧洲生物化学学会联合会。Elsevier B. V.出版,保留所有权利。
Candida albicans D-erythroascorbate peroxidase (EAPX1), which can catalyze the oxidation of D-erythroascorbic acid (EASC) to water, was observed to be inducible in EAPX1-deficient and EAPX1-overexpressing cells via activity staining. EAPX1-deficient cells have remarkably increased intracellular reactive oxygen species and methylglyoxal independent of the intracellular EASC content. The increased methylglyoxal caused EAPX1-deficient cells to activate catalase-permddase and cytochrome c peroxidase, which led to defects in cell growth, viability, mitochondria respiration, filamentation and virulence. These findings indicate that EAPX1 mediates cell differentiation and virulence by regulating intracellular methylglyoxal along with oxidative stresses, regardless of endogenous EASC biosynthesis or alternative oxidase expression. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.