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Mechanism of the toxicity induced by natural humic acid on human vascular endothelial cells

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/53585

Title: Mechanism of the toxicity induced by natural humic acid on human vascular endothelial cells
Authors: Kihara, Yusuke Browse this author
Yustiawati Browse this author
Tanaka, Masato Browse this author
Gumiri, Sulmin Browse this author
Ardianor Browse this author
Hosokawa, Toshiyuki Browse this author →KAKEN DB
Tanaka, Shunitz Browse this author →KAKEN DB
Saito, Takeshi Browse this author →KAKEN DB
Kurasaki, Masaaki Browse this author →KAKEN DB
Keywords: humic acid
tropical peatland
apoptosis
endothelial cell
oxidative stress
Issue Date: 8-Oct-2012
Publisher: Wiley
Journal Title: Environmental Toxicology
Start Page: n/a
End Page: n/a
Publisher DOI: 10.1002/tox.21819
PMID: 23042718
Abstract: Humic acid (HA), a group of high-molecular weight organic compounds characterized by an ability to bind heavy metals, is normally found in natural water. Although the impairment of vascular endothelial cells in the presence of humic substances has been reported to be involved in some diseases, the mechanisms responsible for this involvement remain unclear. In this study, we examined the cytotoxicity of HA obtained from peatland in Central Kalimantan, Indonesia, to human vascular endothelial cells, as well as the mechanisms behind these effects. It was found that 50 mg/L HA showed cytotoxicity, which we considered to be mediated by apoptosis through the mitochondrial pathway because of an increase in the expression of caspases 6 and 9 in response to HA administration. In addition, this cytotoxicity was enhanced when cells in this experimental system were exposed to oxidative stress, while it was decreased by the addition of vitamin C. Thus, we conclude that the apoptosis induced by HA depends upon oxidative stress. Furthermore, an iron chelator, DFO, showed a tendency to decrease HA-induced cytotoxicity, suggesting that iron may potentially mediate HA-induced oxidative stress. In conclusion, long-term consumption of HA-rich water obtained from our study area may cause damage to endothelial cells and subsequent chronic health problems. © 2012 Wiley Periodicals, Inc. Environ Toxicol, 2012.
Description: Early View (Online Version of Record published before inclusion in an issue)
Type: article (author version)
URI: http://hdl.handle.net/2115/53585
Appears in Collections:環境科学院・地球環境科学研究院 (Graduate School of Environmental Science / Faculty of Environmental Earth Science) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 藏崎 正明

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