Enrichment of tomato paste with 6% tomato peel increases lycopene and beta-carotene bioavailability in men.

A high intake of tomato products is associated with a lower incidence of upper aerodigestive tract and prostate cancers. This beneficial effect might be explained by a higher intake of carotenoids such as lycopene and/or beta-carotene. Because tomato peels, usually eliminated during tomato processing, are a valuable source of these carotenoids, we designed a study to examine whether a tomato paste enriched in tomato peels (ETP, 6% peel) increases the absorption of these carotenoids compared to a classically made tomato paste (CTP). Carotenoid bioaccessibility was evaluated using an in vitro digestion model by measuring the amount of carotenoids transferred from the pastes to micelles. Carotenoid absorption by human intestinal cells (Caco-2) was evaluated after the addition of carotenoid-rich micelles (obtained from the in vitro digestion of the 2 pastes). Carotenoid bioavailability in humans was assessed by measuring chylomicron carotenoid responses in a postprandial experiment in which 8 healthy men consumed 2 meals containing either the ETP or the CTP. ETP contained 47.6 mg lycopene (58% more than CTP) and 1.75 mg beta-carotene (99% more than CTP) per 100 g of paste. In micelles, 30% more lycopene and 81% more beta-carotene were recovered after ETP than after CTP in vitro digestion. The amount of carotenoids absorbed by Caco-2 cells was 75% greater (P < or = 0.05) for lycopene and 41% greater (P < or = 0.05) for beta-carotene after the addition of micelles from ETP than from CTP. After ETP intake the chylomicron beta-carotene response was 74% greater than after CTP intake, and the lycopene response tended to be greater (34.1%, P = 0.093). Peel enrichment of tomato paste with tomato peel is an interesting option for increasing lycopene and beta-carotene intakes.

Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI).

The carotenoid lutein is thought to play a role in the human eye and to protect against age-related macular degeneration. Lutein transport in the human intestine has not been characterized. We examined lutein transport processes using Caco-2 TC-7 monolayers as a model for human intestinal epithelium. Purified lutein was mixed with phospholipids, lysophospholipids, cholesterol, mono-olein, oleic acid and taurocholate to obtain lutein-rich mixed micelles that mimicked those found under physiological conditions. The micelles were added to the apical side of Caco-2 TC-7 cell monolayers for 30 min or 3 h at 37 degrees C. Absorbed lutein, i.e. the sum of lutein recovered in the scraped cells and in the basolateral chamber, was quantified by HPLC. Transport rate was measured (i) as a function of time (from 15 to 60 min), (ii) as a function of micellar lutein concentration (from 1.5 to 15 microM), (iii) at 4 degrees C, (iv) in the basolateral to apical direction, (v) after trypsin pretreatment, (vi) in the presence of beta-carotene and/or lycopene, (vii) in the presence of increasing concentrations of antibody against SR-BI (scavenger receptor class B type 1) and (viii) in the presence of increasing concentrations of a chemical inhibitor of the selective transfer of lipids mediated by SR-BI, i.e. BLT1 (blocks lipid transport 1). The rate of transport of lutein as a function of time and as a function of concentration was saturable. It was significantly lower at 4 degrees C than at 37 degrees C (approx. 50%), in the basal to apical direction than in the opposite direction (approx. 85%), and after trypsin pretreatment (up to 45%). Co-incubation with beta-carotene, but not lycopene, decreased the lutein absorption rate (approx. 20%) significantly. Anti-SR-BI antibody and BLT1 significantly impaired the absorption rate (approx. 30% and 57% respectively). Overall, these results indicate that lutein absorption is, at least partly, protein-mediated and that some lutein is taken up through SR-BI.