Table III.
Genotype | Treatment | Total mice | Tumors per mouse (mean ± SE) | # Tumors of specific diameter per mouse |
||
≤0.5 mm | ∼1 mm | ≥2 mm | ||||
B6 | No Zn | 24 | 7.00 ± 1.21 | 4.08 | 2.04 | 0.88 |
Zn | 29 | 5.00 ± 0.74a | 3.21 | 1 | 0.79 | |
Fhit−/− | No Zn | 34 | 8.00 ± 0.69 | 5.41 | 1.62 | 0.97 |
Zn | 29 | 5.72 ± 1.01a | 3.93 | 1.24 | 0.55 | |
Fhit−/−Nit1−/− | No Zn | 24 | 9.21 ± 1.63 | 4.46 | 3.21 | 1.54 |
Zn | 26 | 5.39 ± 0.82a | 3.23 | 1.31 | 0.85 | |
Fhit−/−Rassf1a−/− | No Zn | 26 | 9.12 ± 1.54 | 5.35 | 2.58 | 1.19 |
Zn | 27 | 5.93 ± 0.59a | 3.48 | 1.52 | 0.93 |
Immediately after the final NMBA dose, mice were supplied with regular or Zn-supplemented water. Mice were killed and esophagus, stomach, liver, kidney, spleen and intestine grossly examined at 16 weeks after final NMBA treatment. All mice developed tumors. Statistical analyses showed significant differences between control and Zn-supplemented groups (P < 0.0001), and the reduction of number of total tumors per mouse due to Zn treatment was similar for all genotypes (P = 0.30). In addition, the numbers of tumors with specific diameter were all distributed similarly between control and Zn-supplemented groups based on chi-square test (P = 0.07).
Significantly lower tumor numbers per mouse than no Zn supplement group, P value ≤ 0.01.