| Summary: | 博士 === 國立清華大學 === 輻射生物研究所 === 84 === Arsenic compounds are widely distributed natural toxicants.n
vitro studies indicate that arsenic compounds can
inducehromosome aberrations, sister-chromatid exchanges, and
lung-pecific DNA strand break and DNA-protein crosslinking.
Chronicxposures to arsenic increase the incidence of skin,
lung, bladdernd possibly liver cancer in human beings. The
molecularechanism of arsenic induced cancer is largely unknown,
althoughnvolvement of free radicals has been suggested. Since
the X-rayensitive Chinese hamster ovary cells, xrs-5 are
also o several free-radicals generating agents, including H2
O2, we sed this cell line to test whether the genotoxic
effect of ediated via the generation of reactive oxygen
species (ROS).he results indicate that the xrs-5 cells were
also more sensitive rsenite in terms of cell-killing and
micronuclei (MN) induction omparison to the parental CHO-K1
cells. The level of arsenicptake and release, the levels of
elementary components forrsenic detoxification, such as
glutathione, glutathione S-ransferase (GST), glutathione
reductase (GSHR), superoxideismutase (SOD) were similar in
these two cell lines. Thectivities of catalase and
glutathione peroxidase (GPx), however,ere 6- and 7-fold lower,
respectively in the xrs-5 cells inomparison to the CHO-K1
cells. Moreover, extra-cellular additionf Cat or GPx, could
effectively reduce the frequency of arsenite-nduced MN.
Pretreating CHO-K1 cells with mercaptosuccinate,n inhibitor of
GPx, enhanced the MN induction by arsenite and2O2.
Simultaneous treatment with mercaptosuccinate and
3-minotriazole, an inhibitor of Cat, synergistically
increased nduced MN. Furthermore, sodium selenium, a
stimulator of Gpxctivity, significantly reduced arsenite- and H2
O2-induced MN.
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