Low concentration platinum nanoparticles effectively scavenge reactive oxygen species in rat skeletal L6 cells

Hidekazu Nakanishi, Takeki Hamasaki, Tomoya Kinjo, Hanxu Yan, Noboru Nakamichi, Shigeru Kabayama, Kiichiro Teruya, Sanetaka Shirahata

研究成果: ジャーナルへの寄稿学術誌査読

8 被引用数 (Scopus)

抄録

Prolonged exposure to excessive reactive oxygen species (ROS) increases risk factorsfor many diseases. Therefore, elimination of ROS as well as prevention of its production becomes critically important. In the present study, we evaluated the levels of cytotoxicity and ROS scavenging activity induced by synthetic platinum nanoparticles (PtNPs). Average size of synthesized PtNPs was 2.2 nm. Synthetic PtNPs were found to scavenge both induced and endogenous H2O2 significantly in L6 rat skeletal muscle cells at a very low concentration (10-2 mg/l). To investigate the mechanism of action, the hierarchical oxidative stress model was used as an experimental model. To evaluate this possibility, we assessedglutathione concentration and gene levels of several antioxidant enzymes in PtNPs-treated(10-3-10 mg/l) L6 cells. Reduced glutathione (GSH) was increased in the range of 10-3-1 mg/l, but not in the 10 mg/l PtNP-treated cells. The GSH/GSSG ratio increased significantly at 1 mg/l and decreased in the 10 mg/l PtNPtreated cells. Most of the gene transcripts for oxidative stress inducible heme oxygenase-1 (HO-1), glutathione reductase (GR), copper-zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx), and catalase were increased significantly by PtNPs at 10-1-10 mg/l.Such upregulatory effects induced by synthetic PtNPs at high concentrations (1-10 mg/l) in L6 cells can be explained by the hierarchical oxidative stress model. However, the cellular responses induced by low levels (10-3-10-2 mg/l) of PtNPs could not be fully explained by this model.

本文言語英語
ページ(範囲)76-85
ページ数10
ジャーナルNano Biomedicine and Engineering
5
2
DOI
出版ステータス出版済み - 2013

!!!All Science Journal Classification (ASJC) codes

  • 生体医工学

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