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2.
Fig. 3

Fig. 3. From: Acrolein-derived DNA adduct formation in human colon cancer cells: its role in apoptosis induction by docosahexaenoic acid.

Acr-dG and 8-oxo-dG levels in HT-29 cells treated with different concentrations of PUFAs. Acr-dG adduct levels were measured with the 32P/SPE/HPLC-based postlabeling assay (A) and 8-oxo-dG levels were measured with an HPLC/electrochemical assay (B).

Jishen Pan, et al. Chem Res Toxicol. ;22(5):798-806.
3.
Fig. 7

Fig. 7. From: Acrolein-derived DNA adduct formation in human colon cancer cells: its role in apoptosis induction by docosahexaenoic acid.

Cell cycle arrest analysis of HT-29 cells treated with PUFAs. Cells treated with different concentrations of DHA, AA, or LA were harvested and stained with propidium iodide for flow-cytometry-based FACT analysis.

Jishen Pan, et al. Chem Res Toxicol. ;22(5):798-806.
4.
Fig. 6

Fig. 6. From: Acrolein-derived DNA adduct formation in human colon cancer cells: its role in apoptosis induction by docosahexaenoic acid.

DNA strand breaks in HT-29 cells treated with DHA. Cells were treated with different concentrations of DHA and DNA strand breaks were measured with an electrophoresis-based comet assay. Irradiation of 9Gy was to treated cells as positive control.

Jishen Pan, et al. Chem Res Toxicol. ;22(5):798-806.
5.
Fig. 5

Fig. 5. From: Acrolein-derived DNA adduct formation in human colon cancer cells: its role in apoptosis induction by docosahexaenoic acid.

Comparison of apoptosis and Acr-dG formation of HT-29 cells treated with Acr. Cells were incubated with from 0 to 200µM of Acr for 24h. Then, the Annexin V-FITC / PI assay were used to measure apoptosis (A), and Acr-dG adduct levels were measured (B).

Jishen Pan, et al. Chem Res Toxicol. ;22(5):798-806.
6.
Fig. 2

Fig. 2. From: Acrolein-derived DNA adduct formation in human colon cancer cells: its role in apoptosis induction by docosahexaenoic acid.

Apoptosis induction in HT-29 cells by DHA, AA or LA. In A and B, HT-29 cells were treated with different concentrations of PUFAs for 24h. The apoptotic responses were measured using caspase-3 activities (A) and PARP cleavage (B). In C and D, cells were treated with indicated concentrations of DHA, AA or LA for 0,4,8,12 and 24h and the apoptotic responses were measured by caspase-3 activities (C) and PARP cleavage (D).

Jishen Pan, et al. Chem Res Toxicol. ;22(5):798-806.
7.

Fig. 4. From: Acrolein-derived DNA adduct formation in human colon cancer cells: its role in apoptosis induction by docosahexaenoic acid.

Comparison of apoptotic responses of HT-29 cells treated with DHA delivered with ethanol or BSA. HT-29 cells were treated with different concentrations of DHA delivered with and without BSA for 24h, then caspase-3 activities (A) and PARP cleavage (B) were measured. In another experiment, cells were treated with 200µM DHA in the presence of different concentrations of BSA for 24h, the dose-dependent effect of BSA on caspase-3 activities (C) and PARP cleavage (D) were examined. To investigate the oxidative effects of DHA on protein and DNA in the presence of BSA, the cells were treated with 0 or 250µM of DHA with and without 100µM BSA. The total protein carbonyl formation in media (E) and Acr-dG in DNA were measured (F).

Jishen Pan, et al. Chem Res Toxicol. ;22(5):798-806.

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