Lipoic acid ameliorates arsenic trioxide-induced HO-1 expression and oxidative

doi:10.1016/j.cbi.2011.02.001

CNU IR > Pharmacy and Science > Dept. of Food Science & Technology > Periodical Articles > Item 310902800/26742

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/26742

Title:	Lipoic acid ameliorates arsenic trioxide-induced HO-1 expression and oxidative
Authors:	Wang, Lisu Weng, Ching-Yi Wang, Ying-Jan Wu, Ming-Jiuan
Contributors:	食品科技系生物科技系
Keywords:	Arsenic α-Lipoic acid Heme oxygenase-1 Glutathione Scavenger receptors
Date:	2011-04
Issue Date:	2013-06-26 15:34:28 (UTC+8)
Publisher:	Elsevier Elsevier
Abstract:	Inorganic arsenic is a common environmental contaminant; chronic exposure to arsenic can alter the physiology of various key immune cells, particularly macrophages. The aim of this research is to elucidate the key parameters associated with arsenic-induced toxicity and investigate the potential and mechanism of α-lipoic acid (LA), a potent thioreducant, for reducing the toxicity in human promonocytic THP-1 cells. We found that a non-lethal concentration of arsenic trioxide (1 μM) significantly induced the expression of heme oxygenase-1 (HO-1), a response biomarker to arsenic, without stimulating measurable superoxide production. Co-treatment of cells with the HO-1 competitive inhibitor zinc protoporphyrin (Znpp) potentiated arsenic-induced cytotoxicity, indicating that HO-1 confers a cytoprotective effect against arsenic toxicity. In addition, low concentrations of arsenic trioxide (1 and 2.5 μM) markedly inhibited monocyte-to-macrophage differentiation and expression of macrophage markers. Treatment of cells with LA attenuated arsenic trioxide-induced cytotoxicity and HO-1 over-expression and restored the redox state. In addition, LA neutralized arsenic trioxide-inhibition of monocyte maturation into macrophages and reversed the expression and activity of scavenger receptors. In conclusion, the cytotoxicity of arsenic trioxide is associated with an imbalance of the cellular redox state, and LA can protect cells from arsenic-induced malfunctions either through its reducing activity, direct interacting with arsenic or stimulating other unidentified signaling pathways.
Relation:	Chemico-Biological Interactions 190(2-3), pp.129-138
Appears in Collections:	[Dept. of Food Science & Technology] Periodical Articles [Dept. of Biotechnology (including master's program)] Periodical Articles

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