Tomatoes are the fourth most commonly consumed fresh vegetable and the most frequently consumed canned vegetable in the American diet. There is emerging epidemiology data supporting the connection between increased tomato consumption and reduced risk for both cardiovascular disease and prostate cancer. Here we will summarize the nutrient and the phytochemical content of tomatoes and tomato products, and how these bioactive components might act together to modulate disease development. Recent animal studies have investigated tomatoes, lycopene, and prostate cancer using the N-methyl-N-nitrosourea and Dunning rat models. These animal studies also suggest that diets containing tomatoes may decrease the risk or the progression of prostate cancer. Due to the frequency and the extent of tomato consumption, the supporting epidemiological and animal data, which connect increased intakes with decreased cancer and cardiovascular disease risk, tomato's role in the American diet is of undeniable importance as part of a healthy diet.

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The health benefits of lycopene as an anticarcinogenic compound have been widely studied but little is known about the metabolic products of lycopene produced in vivo. We investigated lycopene metabolites in the liver of F344 male rats that had been prefed a lycopene-containing diet (0.25 g lycopene/kg diet). After 30 d of feeding, they were given a single oral dose of 14C-labeled lycopene (421.8 kBq). The metabolic products of both nonradioactive and 14C-labeled lycopene in rat liver were extracted and separated using HPLC and analyzed by UV/VIS spectrometry, online radioactive detection, and off-line and in-line positive ion electrospray ionization MS. Among a number of metabolite products formed, we identified apo-8'-lycopenal (lambdamax = 473 nm and m/z = 417). The putative compound, apo-12'-lycopenal, was detected but no apo-10'-lycopenal was present. A number of other very polar, short-chain and/or short chromophore compounds with UV/VIS absorption <300 nm were present but were not characterized. These data show that lycopene is cleaved in vivo by rats at different positions to produce apo-12'-lycopenal, and other unidentified metabolites in addition to apo-8'-lycopenal. Apo-8'-lycopenal and the putative apo-12'-lycopenal are identified as lycopene metabolites in rat liver in vivo.

In vitro studies have suggested that lycopene is an efficient substrate for carotenoid 9'10'-monooxygenase II (CMO2) but an inhibitor of carotenoid 15,15'-monooxygenase I (CMO1). The objectives of this study were to clone the rat CMO2 gene, determine whether feeding lycopene for different lengths of time (3-37 d) altered the expression of genes related to carotenoid cleavage [CMO1, CMO2 and peroxisomal proliferator-activated receptor gamma (PPAR-gamma)] or increased the activity of selected phase I and phase II detoxification enzymes in rat tissues. The cloned rat CMO2 gene was 92 and 82% homologous to the mouse and human CMO2 nucleotide sequence, respectively. The relative abundance of CMO1, CMO2, and PPAR-gamma were differentially expressed among rat tissues. CMO1 and PPAR-gamma expression were decreased in the kidney and adrenal with lycopene intake (P < 0.05), whereas CMO2 expression was reduced only in the kidney. Lycopene did not alter hepatic phase I activity, but hepatic quinone reductase activity increased after 3 and 7 d of lycopene feeding (P < 0.05). Lycopene intake decreased a PPAR-gamma target gene, fatty acid binding protein 3 (FABP3), in the kidney and adrenal (P < 0.05). Thus, these data show that although the intake of 0.25 g lycopene/kg diet does not induce hepatic P450 detoxification enzymes, lycopene feeding alters CMO1, PPAR-gamma, and FABP3 mRNA expression in selected rat tissues with a moderate effect on kidney CMO2 expression. These data suggest that lycopene may play an important role in the modulation of beta-carotene, retinoid, and/or lipid metabolism.

Epidemiologic evidence suggests a possible role for lycopene-rich foods in the prevention of prostate cancer and cardiovascular disease. Despite active research in disease reduction, there is a paucity of information on the absorption, biodistribution and metabolism of lycopene. The aim of this study was to evaluate the biodistribution of 14C-lycopene (specific activity, 1.83 microCi/mg) and 14C-labeled products after an oral dose of 22 microCi of 14C-lycopene in male rats that had been prefed a lycopene-containing diet (0.25 g lycopene/ kg diet) for 30 d. The percentage of 14C excreted in feces and urine over the 168 h was 68%. Quantitatively, serum 14C levels were maintained between 3 and 24 h then decreased at 72 h (P < 0.05). At all time points the majority of tissue 14C was in the liver (approximately 72%), although total hepatic 14C decreased after 24 h. In a comparison of the extrahepatic tissue at 168 h, the 14C was greatest in adipose tissue followed by spleen and then adrenal; approximately 80% of the 14C in the liver was in the cis and all-trans configuration at all time points. At 3 h, the 14C in seminal vesicles was primarily in the all-trans plus 5-cis forms (70%), but by 168 h, 55% of 14C was present as 14C-polar products. Despite the presence of unlabeled lycopene in the prostate, the primary 14C form was in 14C-polar products (67-92%), even at 3 h. The percentage and amount of 14C-polar products in the dorsolateral prostate lobe increased from 3 to 24 h and then reached a plateau. The data suggest that lycopene may be metabolized differently among tissues in rats prefed lycopene.