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Effect of lycopene supplementation on lung carcinogenesis induced by tobacco carcinogen 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) in ferrets

A protective role of lycopene (LYC) against smoke‐induced squamous metaplasia has been previously reported in a ferret model. In this study, we examined the induction of lung cancer in ferrets initiated with the NNK and investigated the effects of supplementing LYC on lung carcinogenesis. Ferrets (6 groups, n=8–10/group) were injected with NNK (50 mg/kg BW, i.p. once a month for 4 consecutive months) or saline as control with or without two doses of LYC supplementation (2.2 or 6.6 mg kg BW/day), for 26weeks. The results showed that the NNK exposure alone induced both preneoplastic lesions and lung tumors that are pathologically similar to humans. Although the LYC supplementation did not significantly inhibit the incidences of lung tumors, the LYC supplementation was associated with a low mortality rate compared to ferrets treated with NNK alone. Interestingly, the NNK treatment was associated with induction of liver cancer, which was ameliorated by LYC supplementation. Both hepatic and plasma LYC were detected by HPLC in the LYC supplemented groups. In summary, the development of both preneoplastic and neoplastic lesions in ferret lungs by injecting NNK alone provides an excellent model for studying lung carcinogenesis. Although the effects of LYC against lung tumors are inconclusive, the LYC supplementation was associated with both lower NNK induced mortality and hepatic damage in this model.