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Medicinal Plants Classification Biosynthesis and ... - Index of

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24<br />

Rosa Martha Perez Gutierrez, Adriana Maria Neira Gonzalez et al.<br />

carotene content in national br<strong>and</strong> multivitamins. Four studies contributing 109,394 subjects<br />

were available for analysis. The average daily beta-carotene dosage in these trials ranged<br />

from 20 to 30 mg daily. High-dose β-carotene supplementation appears to increase the risk <strong>of</strong><br />

lung cancer among current smokers. Although beta-carotene was prevalent in multivitamins,<br />

high-dose β-carotene was observed among multivitamin formulas sold to promote visual<br />

health (Tanvetyanon <strong>and</strong> Bepler, 2008).<br />

Gastrointestinal Cancer<br />

The incidence <strong>of</strong> esophageal adenocarcinoma has been increasing rapidly among many<br />

countries. Antioxidant intake is a potentially modifiable protective factor, although the results<br />

from individual studies are inconclusive. In an study, were evaluated the associations<br />

between vitamin C, vitamin E, or β-carotene/vitamin A <strong>and</strong> the risk <strong>of</strong> esophageal<br />

adenocarcinoma or the adjacent gastric cardia (gastroesophageal junction) adenocarcinoma.<br />

Studies (1 cohort, 9 case-control; 1,057 esophageal <strong>and</strong> 644 cardia cases). Higher intakes <strong>of</strong><br />

vitamin C, β-carotene/vitamin A, <strong>and</strong> vitamin E were inversely associated with the risk <strong>of</strong><br />

esophageal adenocarcinoma. β-Carotene intake was also inversely associated with the risk <strong>of</strong><br />

cardia adenocarcinoma. Pooled results from observational studies suggest that antioxidant<br />

intake may be protective against esophageal adenocarcinoma; the data do not support a<br />

consistent association between antioxidant intake <strong>and</strong> the risk <strong>of</strong> cardiac carcinoma. These<br />

findings suggest possible etiological differences between these two adjacent malignancies<br />

(Kubo <strong>and</strong> Corley, 2007).<br />

Oxidative stress may cause gastrointestinal cancers. Epidemiologic studies <strong>of</strong> vitamin A,<br />

retinol (preformed vitamin A), <strong>and</strong> provitamin A carotenoids in relation to the risk <strong>of</strong> gastric<br />

cancer have documented inconsistent results. The evidence on whether antioxidant<br />

supplements are effective in preventing gastrointestinal cancers is contradictory. Results<br />

supported not find evidence that the studied antioxidant supplements prevent gastrointestinal<br />

cancers. On the contrary, they seem to increase overall mortality (Bjelakovic et al., 2008).<br />

Mechanisms <strong>of</strong> -Carotene in Cancer<br />

Although several mechanisms have been proposed to explain the putative role <strong>of</strong> βcarotene<br />

in cancer, no studies have investigated a possible influence <strong>of</strong> β-carotene on<br />

caveolin-1 (cav-1) pathway, an important intracellular signalling deregulated in cancer.<br />

Here, different human colon <strong>and</strong> prostate cancer cell lines, expressing (HCT-116, PC-3<br />

cells) or not (Caco-2, LNCaP cells) cav-1, were treated with varying concentrations <strong>of</strong><br />

β-carotene (0.5-30 muM) for different periods <strong>of</strong> time (3-72 h) <strong>and</strong> the effects on cell<br />

growth were investigated. The results <strong>of</strong> this study show that: a) β-carotene acted as a<br />

growth-inhibitory agent in cav-1-positive cells, but not in cav-1-negative cells; b) in<br />

cav-1-positive cells, the carotenoid down-regulated in a dose- <strong>and</strong> time-dependent<br />

manner the expression <strong>of</strong> cav-1 protein <strong>and</strong> mRNA levels <strong>and</strong> inhibited AKT<br />

phosphorylation which, in turn, stimulated apoptosis by increasing the expression <strong>of</strong> β-

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