Medicinal Plants Classification Biosynthesis and ... - Index of

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Rosa Martha Perez Gutierrez, Adriana Maria Neira Gonzalez et al.
Although initial studies suggested that persons with lower levels of serum retinol have
higher future rates of lung cancer, this idea was not confirmed in subsequent investigations.
Prediagnostic levels of β-carotene in blood, however, have been inversely related with risk of
lung cancer. Even if ultimately shown to be causal, the relation between diet and lung cancer
is modest compared with the deleterious effect of cigarette smoking.
In a supplementation study, high β-carotene intake was associated with a decrease in
DNA adduct levels in nonsmokers but with an increase in such adducts in smokers (Welch et
al., 1999 ). Suggested mechanisms for this effect are complex and debated (Lotan, 1999). In
in vitro models, β-carotene may serve as an antioxidant or as a prooxidant, depending on the
redox potential of the biologic environment in which it acts, as reviewed previously ( Palozza
et al., 2003). Although β-carotene exerts a growth inhibitory and proapoptotic effect on
malignant colonic cell lines (Palozza et al., 2005) , it also enhances DNA oxidative damage
and modifies p53-related pathways of cell proliferation and apoptosis when cells are exposed
to tobacco smoke condensate (Palozza et al., 2004) .
Although β-carotene may act as a cocarcinogen, there is no evidence that smokers should
avoid consuming β-carotene rich foods such as fruit and vegetables, in which other
components, such as vitamins C and E, may counteract a potentially deleterious interaction of
β-carotene with smoking. In a study, former smokers were more likely to take supplements
than current or never smokers, as reported elsewhere. This behavior, which may have been
part of a healthier lifestyle for women who decided to stop smoking, may have unexpected
adverse effects when supplements include β-carotene. Not smoking and consuming relatively
high doses of β-carotene were associated with the lowest level of risk of tobacco-related
cancer, in agreement with ongoing public health advice (Paolini et al., 2003).
In conclusion, the interaction between tobacco and β-carotene, which was initially
described for lung cancer (Albanes et al., 1996), may extend to other tobacco-related cancers.
In our cohort, tobacco-related cancers represented 23.0% of all cancers observed during the
study period. This rate is slightly lower than the 30% reported in the literature (Stein and
Colditz, 2004) but consistent with the study population‘s relatively low exposure to tobacco.
This proportion emphasizes the public health importance of our results. Because the observed
interaction between β-carotene and smoking on tobacco-related cancer risk could strongly
influence a global effect of β-carotene on risk of neoplasms, future studies on the effect of
this nutrient should include stratification by smoking status. In general, studies should
systematically investigate potential interactions between nutrients and environmental or
genetic factors (Palli et al., 2004).
The generally accepted causes of lung cancer are inhalant: tobacco smoke; dusts or
fumes containing carcinogen, such as arsenic, asbestos, chloromethyl ether and chromates;
and gases such as radon (Peto et al., 1981). However, the fact that not all persons exposed to
even high concentrations of these airborne pollutants develop cancer suggests that there are
substances that can prevent or inhibit carcinogenesis. An appealing hypothesis involves the
following simplified chain of events. Many carcinogens create free oxidative radicals that
damage cells; damaged cells are prone to develop malignant changes; and antioxidants can
neutralize free radicals, thereby preventing cell damage and the subsequent development of
cancer (Block, 1992). This hypothesis would be strengthened if it could be consistently
demonstrated that persons who developed cancer had lower concentrations of antioxidant