Abstract
Increasing evidence suggests that tomato lycopene may be preventive against the formation and the development of lung cancer. Experimental studies demonstrated that lycopene may inhibit the growth of several cultured lung cancer cells and prevent lung tumorigenesis in animal models through various mechanisms, including a modulation of redox status, cell cycle arrest and/or apoptosis induction, a regulation of growth factor signaling, changes in cell growth-related enzymes, an enhancement of gap junction communication and a prevention of smoke-induced inflammation. In addition, lycopene also inhibited cell invasion, angiogenesis, and metastasis. Several lycopene metabolites have been identified, raising the question as to whether the preventive effects of lycopene on cancer risk is, at least in part, due to its metabolites. Despite these promising reports, it is difficult at the moment to directly relate available experimental data to human pathophysiology. More well controlled clinical intervention trials are needed to further clarify the exact role of lycopene in the prevention of lung cancer cell growth. Such studies should take into consideration subject selection, specific markers of analysis, the levels of carotenoids being tested, metabolism and isomerization of lycopene, interaction with other bioactive food components. This article reviews data on the cancer preventive activities of lycopene, possible mechanisms involved, and the relationship between lycopene consumption and human cancer risk.
Highlights
The human lung, due to the oxidative and ozone stress to which it is exposed, is vulnerable to oxidative damage
Bhuvaneswari et al [98] associated the chemopreventive effect of lycopene on the incidence of DMBA-induced hamster buccal pouch tumors with a simultaneous rise in the level of reduced glutathione, enzymes of the glutathione redox cycle, and glutathione S-transferase (GST) in the buccal pouch mucosa. (DMBA is a 9,10-dimethylbenz- anthracene, a potent tumor-initiating compound.) These results suggest that the lycopene-induced increase in the levels of GSH and the phase II enzyme GST inactivates carcinogens by forming conjugates, products that are less toxic and readily excreted
In vitro experiments showed that apo-10‘- lycopenoic acid inhibits lung cancer cell growth and activates retinoic acid receptor signaling [118], the corresponding effects were not observed in the lungs of the mice after 16 weeks of treatment
Summary
The human lung, due to the oxidative and ozone stress to which it is exposed, is vulnerable to oxidative damage. The lung operates under a higher oxygen pressure environment than other internal organs This can result in the conversion of high concentrations of antioxidants into pro-oxidants. Evidence from observational epidemiological studies rapidly accumulated and tended to support an inverse association of lung cancer incidence with -carotene intake and with serum concentrations of -carotene. Epidemiological studies show that populations consuming a tomato-rich diet, containing high levels of lycopene, exhibit lower risk of certain types of cancers, including lung cancer [23]. Carotenoids like lycopene are unstable and highly reactive towards oxygen and free radicals [25] This reactivity of lycopene is the basis for its anti-oxidant activity in biological systems that might contribute to its efficacy as a chemoprevention agent. This review summarizes the most current knowledge with respect to lycopene role in the prevention of lung cancer
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
