Fig. 8.

Pharmacological ascorbate slows growth of MIA PaCa-2 tumors in comparison to PANC-1 tumorsin vivo.(A) MIA PaCa-2 (k_cell =1.1×10⁻¹² s⁻¹ cell⁻¹ L; 101,000 active catalase monomers per cell) cells and (B) PANC-1 (k_cell =5.1×10⁻¹² s⁻¹ cell⁻¹ L; 459,000 active catalase monomers per cell) cells were injected into mice and formed tumors. Mice were treated with IP ascorbate (4 g/kg) twice daily for two weeks. Tumors were measured on day 3, 7, 10, and 14 following first treatment with ascorbate. P-AscH⁻ slowed the growth rate of PANC-1 xenograft tumors to 42% of the controls; with MIA PaCa-2 tumor xenografts P-AscH⁻ slowed growth to just 9% of controls. The ratio of k_cell(PANC-1)/k_cell(MIA PaCa-2) =4.6; the ratio for the relative growth rates compared to controls is essentially identical, 42%/9% =4.7, a remarkable quantitative comparison. (C) MIA PaCa-2 tumor catalase immunofluorescence, and (D) PANC-1 tumor catalase immunofluorescence. Tumor samples were fixed with 4% paraformaldehyde at 4 °C, and blocked with 5% goat serum for 30 min at 20 °C. The samples were incubated with catalase antibody (1:50) for 20 h at 4 °C. An Alexa Fluor 488 nm goat anti-Rabbit (1:200) was used as secondary antibody. DAPI was used to stain the cell nuclei. The samples were examined using a Zeiss confocal microscope. Scale bar, 20 µm. Tissue samples for PANC-1-derived tumors show considerably more immunofluorescence due to the presence of catalase enzyme than tissue samples from MIA PaCa-2 tumors. (Normalized fluorescent intensity of PANC-1 vs. MIA PaCA-2 is 100±27 vs. 2.0±0.5.).