Is vitamin E a useful agent to protect against oxy radical-promoted lung tumorigenesis in ddY mice?

We have previously reported that oxy radicals can contribute to the enhancing effect of glycerol on 4-nitroquinoline 1-oxide (4NQO)-induced lung tumorigenesis in ddY mice. In this study, we established that feeding high doses of vitamin E to male ddY mice treated with 4NQO plus glycerol could reduce glycerol-enhanced lung tumorigenesis, due to the inhibition of glycerol-induced oxidative stress on the pulmonary nuclei. At 4 weeks after 4NQO injection (10 mg/kg, s.c.), the levels of nuclear thiobarbituric acid reactive substances and oxidative damage to DNA in the lungs of mice treated with 4NQO plus glycerol (5% solution as drinking water) were significantly higher than those in mice treated with 4NQO. The glycerol-induced increase was completely inhibited when a high vitamin E diet was provided for 4 weeks after 4NQO injection. As previously reported, at 23 weeks after 4NQO administration (at the end of this experiment), the 4 week treatment with glycerol enhanced 4NQO-induced lung tumorigenesis in ddY mice. In contrast, the supply of high doses of vitamin E at 4 and 23 weeks after 4NQO injection suppressed glycerol's ability to enhance lung tumorigenesis. These results suggest that vitamin E is useful in protecting against oxy radical-enhanced lung tumorigenesis in mice.