Arsenic trioxide (ATO) is highly effective in
the treatment of patients with acute promyelocytic leukemia (APL). It is a
chemotherapeutic agent that has been shown to induce apoptosis in several tumor
cell lines. However, research into its effects on colon carcinoma cells is
still very limited.
We previously reported that ATO is cytotoxic
and causes DNA damage in HT-29 human colorectal adenocarcinoma cells. In the
present study, we further evaluated its effect on oxidative stress (OS), and
examined its apoptotic mechanisms of action on HT-29 cells. Methods: OS
was assessed by spectrophotometric measurements of MDA levels while cell
cycle analysis was evaluated by flow cytometry to determine whether ATO induces
cell cycle arrest. Its effect on early apoptosis was also evaluated by flow
cytometry using Annexin V-FITC/PI staining.
Fluorescence microscopy was used to detect the
morphological changes, and Western blotting was carried out to determine the
expression of apoptosis-related proteins. Results: The lipid peroxidation assay
revealed a dose-dependent increase in MDA production. DAPI staining showed
morphological changes in the cell’s nucleus due to apoptosis.
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