The down-regulation of galectin-1 expression is a specific biomarker of arsenic toxicity

Yu Ying Chang, Ming Chang Chiang, Tai Chih Kuo, Li Ling Chi, Yung Hsi Kao, Rong Nan Huang

研究成果: 雜誌貢獻文章同行評審

3 引文 斯高帕斯(Scopus)

摘要

Galectin-1 (GAL1) is known as a β-galactoside-binding protein that also can bind with arsenic to regulate cell functions. Using RNA interference technique, we investigated the possible mechanism involved in GAL1 modulation of arsenite-inhibited cell survival in 3T3 fibroblast and KB oral cancer cells. GAL1 gene knockdown significantly attenuated sodium arsenite (NaAsO2) and arsenic trioxide (As2O3) inhibition of cell survival. However, GAL1 gene knockdown did not alter the inhibition of cell survival by antimony chloride, cadmium chloride or nickel sulfate. These results suggested the GAL1 selectively affects particular types of heavy metal elements. Flow cytometric analysis indicated GAL1 gene knockdown also suppressed As(III)-stimulated levels of sub-G1 and G2/M growth arrest in both cells. Moreover, atomic absorption spectrophotometric results showed that GAL1 gene knockdown reduced the total arsenic accumulation of both cells after the NaAsO2 and As2O3 treatment. These results suggested that GAL1 gene knockdown mediates the apoptotic effects of arsenic in 3T3 and KB cells via regulation of the cellular arsenic levels. We propose that down-regulation of GAL1 expression may be a useful and specific biomarker in assessing the toxicity of arsenic exposure.

原文英語
頁(從 - 到)38-46
頁數9
期刊Toxicology Letters
205
發行號1
DOIs
出版狀態已發佈 - 八月 10 2011

ASJC Scopus subject areas

  • Toxicology

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