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- Title
Cellular Toxicity of Cadmium Ions and Their Detoxification by Heavy Metal-Specific Plant Peptides, Phytochelatins, Expressed in Mammalian Cells1.
- Authors
Takagi, Masahiro; Satofuka, Hiroyuki; Amano, Satoshi; Mizuno, Haruo; Eguchi, Yutaka; Hirata, Kazumasa; Miyamoto, Kazuhisa; Fukui, Kiichi; Imanaka, Tadayuki
- Abstract
The apoptotic cell death of Jurkat cells due to Cd2+ toxicity was studied by fluorescence microscopic observation and DNA fragmentation assaying. It was suggested that the apoptotic response to Cd2+ was less clear than that to a typical apoptosis inducer, ultraviolet light (254 Dm), Examination of MAP kinase phosphorylation (p38, JNKs, and c-Jun) due to Cd2+ toxicity indicated that the phosphorylation was very slowly activated(4 h after stimulation), while UV light could activate the phosphorylation immediately. Therefore, it was suggested that Cd2+ may not be a typical apoptosis inducer. Antioxidants [glutathione (GSH) and N-acetylcysteine (NAC)] could detoxify Cd2+, indicating that the toxicity is a kind of oxidative stress. The detoxification effect of antioxidants showed cooperation with Bcl-2, suggesting that Cd2+treatment causes diversified toxic signals including oxidative stress. On the addition of a plant-specific peptide, phytochelation [PC7, (γGlu-Cys)7-Gly], to the medium, the detoxification of Cd2+ and cooperation with Bcl-2 were more intense than in the cases of GSH and NAC. Using an appropriate vector, a PC synthase gene was transferred from Arabidopsis thaliana to the Jurkat cell The transfectant exhibited resistance to Cd2+ and production of plant-specific PC(PC2–6)
- Subjects
PHYTOCHELATINS; EFFECT of poisons on plants; CADMIUM; CELL death; PHOSPHORYLATION; APOPTOSIS; OXIDATIVE stress
- Publication
Journal of Biochemistry, 2002, Vol 131, Issue 2, p233
- ISSN
0021-924X
- Publication type
Article
- DOI
10.1093/oxfordjournals.jbchem.a003093