| Summary: | 碩士 === 國立臺灣大學 === 毒理學研究所 === 86 === The thesis of this study is on the factors of different types of chemicals
on the rat C6 Glioma cells -->focusing on these chemicals and the type of
impact they have on the following relationship between cells:
oxidation-reduction, copper content, transcription factor and apoptosis.
Doxorubicin is commonly used for cancer treatment in the medical practice.
It can induce superoxide. Treating C6 cells with Doxorubicin can also induce
apoptosis. Combining with N-acetyl-cysteine the cytotoxicity shows no sign of
decreasing. However, when in combination with H2O2, the H2O2 level within a
cell increases and the cytotoxicity of Doxorubicin remain the same. Hence the
conclusion is that apoptosis induced by Doxorubicin is not effected by
superoxide. Further, a detected p53 increment i ated a correlation between the
p53 and C6 cells apoptosis and DNA damage.
Curcumin has been known of having the anti-oxidation and anti-apoptosis
quality. A study result from this research shows that through apoptosis,
Curcumin can induce C6 cells deterioration. An observed fact from the study
show that Curcumin emits fluorescent light when excited. This emission
interfere the analysis of Flow Cytometry, and therefore a more in-depth study
is required for the mechanism behind Curcumin's induction of C6 apoptosis.
PDTC and DETC are also able to induce the apoptosis of C6 cells. In
particular, when comparing with astrocytes and other cell lines, C6 glioma is
more sensitive to PDTC and DETC. When treated with BCDS, it can prevent
toxicity. By the same token, BCDS can also defend itself from the combined
toxicity of dithiocarbamates and copper. This can prove that toxicity induced
by PDTC and DETC is in fact resulted from the entry of chelated copper into
the cells. Also note that Doxorubicin is able to chelat pper. A result from
atomic-absorption spectrophotometer shows that without adding copper, PDTC can
increase the copper content within the cells and yet, Doxorubicin dose not
have the same ablity. On the other hand, when copper is added, PDTC and
Doxorubicin can both increase the copper content within the cells. In
comparison with cytoxicity, it is observed that copper does not reinforce the
toxicity of Doxorubicin but can reinforce the toxicity of PDTC. In addition,
copper does not increase the p53 cont ent induced by Doxorubicin, and yet it
indeed increase the p53 content induced by PDTC. Judging from the various
results, copper in fact plays an important role in apoptosis, and its end
result of Doxorubicin and PDTC chelation can be different as well.
To sum up, C6 is more sensitive to the toxicity of PDTC and DETC,
comparing with other cells. Doxorubicin can activate p53 through the damage it
has on DNA and this process can eventually cause apoptosis. PDTC and DETC can
chelate copper into cells. PDTC in union with copper can increase the p53
level and copper can induce apoptosis.
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