Table 3. Tumour development and acquisition of metastatic ability of QR-32 tumour cells were inhibited by oral administration of oxykin, but not by a single component of oxykine formulation or by a different administration route.
| Incidence of tumorigenicity | Incidence of metastasis | ||
|---|---|---|---|
| Treatmenta | Route of administration | No. of mice with tumour take/no. of mice treated (%) | No. of mice with lung metastasis/no. of mice treated (%) |
| Saline | Per oral | 9/10 (90)b | 20/20 (100)c |
| Gliadin | Per oral | 8/9 (89) | 18/20 (90) |
| Melon SOD | Per oral | 9/10 (90) | 18/20 (90) |
| Oxykine | Per oral | 4/10 (40)b | 5/19 (26)c |
| Saline | Intraperitoneal | 10/10 (100) | 18/20 (90) |
| Gliadin | Intraperitoneal | 8/10 (80) | 19/20 (95) |
| Melon SOD | Intraperitoneal | 10/10 (100) | 21/22 (95) |
| Oxykine | Intraperitoneal | 8/10 (80) | 20/22 (91) |
a
1 × 105 QR-32 tumour cells were coimplanted with gelatine sponge in normal mice to which oxykine, gliadin or melon SOD had been administered orally or intraperitoneally (10 mg kg−1) once daily throughout the experiment.
b
P<0.05 vs saline.
c
1 × 106 cells of each cell line established from the arising tumours were injected into mice. After 25 days, the mice were killed and metastatic nodules at the surface of lung were counted macroscopically. Incidences of lung metastasis were evaluated as follows: P<0.001 vs lung-colonising incidence of saline-treated group.