Prenyllipid antioxidants participate in response to acute stress induced by heavy metals in green microalga Chlamydomonas reinhardtii

被引:29
|
作者
Nowicka, Beatrycze [1 ]
Plucinski, Bartosz [1 ]
Kuczynska, Paulina [1 ]
Kruk, Jerzy [1 ]
机构
[1] Jagiellonian Univ, Fac Biochem Biophys & Biotechnol, Dept Plant Physiol & Biochem, Gronostajowa 7, PL-30387 Krakow, Poland
关键词
Chlamydomonas reinhardtii; Heavy metals; Oxidative stress; Plastoquinone; alpha-Tocopherol; INDUCED OXIDATIVE STRESS; ALPHA-TOCOPHEROL; GENE-EXPRESSION; PHOTOSYSTEM-II; REDOX STATE; BIOLOGICAL PRENYLLIPIDS; ARABIDOPSIS-THALIANA; PLASTOQUINONE POOL; CADMIUM; PLANTS;
D O I
10.1016/j.envexpbot.2015.11.008
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The induction of oxidative stress is an important mechanism of heavy metal toxicity. That is why, isoprenoid antioxidants, such as chromanols and prenylquinones, are thought to participate in the response to heavy metal-induced stress. In the present study, we performed a comparative analysis of the prenyllipid and pigment content and lipid peroxides in Chlamydomonas reinhardtii during 7.5 h of acute stress induced by Cu, Cr, Cd, Hg and Ag ions. We also measured the expression of genes encoding enzymes participating in the detoxification of reactive oxygen species (APX1, CAT1, FSD1, MSD1) and a gene required for a.-tocopherol and plastoquinone biosynthesis (VTE3). In an AgNO3-treated culture, pigments and prenyllipids were degraded at the same rate. The significant peroxidation of lipids was also observed. For other metals, a different pattern of changes in pigment and prenyllipid content was observed. The significant degradation of pigments was observed during the response to Cu2+. The decrease in prenyllipid content occurred in Cu and Cr-stressed algae. Massive oxidation of plastoquinol was observed in the presence of Cu2+, Ag+ and Cr2O72-. The most pronounced increase in the expression of the investigated genes was found in the presence of Cu2+ and Hg2+ ions. The genes whose expression was the most up-regulated were APX1, MSD1, VTE3. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:98 / 107
页数:10
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