三氧化二砷激發氧化自由基之分子機轉
Date Issued
2005
Date
2005
Author(s)
周文堅
DOI
932320B002129
Abstract
Arsenic trioxide (ATO) can induce superoxide production by up-regulation of NADPH
oxidase, an enzyme complex in phagocytes for bactericidal effects via “respiratory burst ”.
However, the mechanisms of NADPH oxidase activation remain to be defined. In this
report, we showed that arsenic trioxide can induce superoxide in various kinds of leukemia
cells via activation of NADPH oxidase. Reciprocally, large amount of superoxide produced
by cell differentiation can further augment the activation of NADPH oxidase. Thus, there
seems to be a positive feedback loop of NADPH oxidase and superoxide production.
Furthermore, we show that ATO did not induce leukemia cell differentiation, thus excluding
the possibility of cellular differentiation as a mechanism of NADPH oxidase activation and
superoxide formation. We also generate a cell line, XCGD-gp91, which replenishes
NADPH oxidase function in XCGD cells. Upon differentiation, this cell line exhibits huge
amount of superoxide production while the parental cells still do not have detectable
superoxide. We believe this pair of cell lines can be an excellent tool for research of
biological effects of superoxide. Finally, we encounter a problem in matching the induction of in vivo NADPH oxidase and in vitro luciferase reporter activity. Several possibilities
exist, but we have solutions to solve this problem. We have solved the technical problems in
the past year, and we are ready to collect the data by use of these techniques. We believe
there will soon be exciting data coming up by your further support next year.
Subjects
arsenic trioxide
NADPH oxidase
Publisher
臺北市：國立臺灣大學醫學院內科
Type
report
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