Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 130, Issue -, Pages 133-145Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2016.04.010
Keywords
Chlamydomonas reinhardtii; Heavy metals; Oxidative stress; Plastoquinone; alpha-Tocopherol
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Funding
- National Science Center Poland [2013/11/D/NZ1/00303]
- Society-Environment-Technology project
- European Union
- Ministry of Science and Higher Education
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Acclimation to heavy metal-induced stress is a complex phenomenon. Among the mechanisms of heavy metal toxicity, an important one is the ability to induce oxidative stress, so that the antioxidant response is crucial for providing tolerance to heavy metal ions. The effect of chronic stress induced by ions of five heavy metals, Ag, Cu, Cr (redox-active metals) Cd, Hg (nonredox-active metals) on the green microalga Chlamydomonas reinhardtii was examined at two levels - the biochemical (content of photosynthetic pigments and prenyllipid antioxidants, lipid peroxidation) and the physiological (growth rate, photosynthesis and respiration rates, induction of nonphotochemical quenching of chlorophyll fluorescence). The expression of the genes which encode the enzymes participating in the detoxification of reactive oxygen species (APX1, CAT1, FSD1, MSD1) was measured. The other gene measured was one required for plastoquinone and alpha-tocopherol biosynthesis (VTE3). The application of heavy metal ions partly inhibited growth and biosynthesis of chlorophyll. The growth inhibition was accompanied by enhanced lipid peroxidation. An increase in the content of prenyllipid antioxidants was observed in cultures exposed to Cr2O72-, Cd2+ (alpha- and gamma-tocopherol and plastoquinone) and Cu2+ (only tocopherols). The induction of nonphotochemical quenching was enhanced in cultures exposed to Cu2+, Cr2O72- and Cd2+, as compared to the control. Chronic heavy metal-induced stress led to changes in gene expression dependent on the type and concentration of heavy metal ions. The up-regulation of antioxidant enzymes was usually accompanied by the up-regulation of the VTE3 gene. (C) 2016 Elsevier Inc. All rights reserved.
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