67 research outputs found
Effects of dietary carotenoids on mouse lung genomic profiles and their modulatory effects on short-term cigarette smoke exposures
Male C57BL/6 mice were fed diets supplemented with either Ξ²-carotene (BC) or lycopene (LY) that were formulated for human consumption. Four weeks of dietary supplementations results in plasma and lung carotenoid (CAR) concentrations that approximated the levels detected in humans. Bioactivity of the CARs was determined by assaying their effects on the activity of the lung transcriptome (~8,500 mRNAs). Both CARs activated the cytochrome P450 1A1 gene but only BC induced the retinol dehydrogenase gene. The contrasting effects of the two CARs on the lung transcriptome were further uncovered in mice exposed to cigarette smoke (CS) for 3Β days; only LY activated ~50 genes detected in the lungs of CS-exposed mice. These genes encoded inflammatory-immune proteins. Our data suggest that mice offer a viable in vivo model for studying bioactivities of dietary CARs and their modulatory effects on lung genomic expression in both health and after exposure to CS toxicants
Bioavailability of the Polyphenols: Status and Controversies
The current interest in polyphenols has been driven primarily by epidemiological studies. However, to establish conclusive evidence for the effectiveness of dietary polyphenols in disease prevention, it is useful to better define the bioavailability of the polyphenols, so that their biological activity can be evaluated. The bioavailability appears to differ greatly among the various phenolic compounds, and the most abundant ones in our diet are not necessarily those that have the best bioavailability profile. In the present review, we focus on the factors influencing the bioavailability of the polyphenols. Moreover, a critical overview on the difficulties and the controversies of the studies on the bioavailability is discussed
Insight Into the Metabolism of Lycopene: Focus on Androgen -Dependent Tissues
129 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2005.This research has shown that lyc metabolites accumulate in the prostate, seminal vesicles and adrenal gland compared to the other analyzed tissues. Moreover, modulated carotenoid cleavage enzyme(s) expression in the adrenal, prostate and kidney suggested that the accumulated lyc metabolites in these tissues be involved in the observed transcriptional changes. In essence, lyc has previously been reported to improve antioxidant status but the presented data suggests that lyc could also modulate prostate cancer related genes.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD
Dietary Lycopene Downregulates Carotenoid 15,15β²-Monooxygenase and PPAR-Ξ³ in Selected Rat Tissues
Loss of Carotene-9β²,10β-Monooxygenase Expression Increases Serum and Tissue Lycopene Concentrations in Lycopene-Fed Mice123
Two enzymes have been identified for the oxidative metabolism of carotenoids in mammals. Carotene-15,15β-monooxygenase (CMO-I) primarily centrally cleaves Ξ²,Ξ²-carotene to form vitamin A. We hypothesize that carotene-9β²,10β-monooxygenase (CMO-II) plays a key role in metabolism of acyclic nonprovitamin A carotenoids such as lycopene. We investigated carotenoid bioaccumulation in young adult, male, wild-type (WT) mice or mice lacking CMO-II (CMO-II KO). Mice were fed an AIN-93G diet or identical diets supplemented with 10% tomato powder, 130 mg lycopene/kg diet (10% lycopene beadlets), or placebo beadlets for 4 or 30 d. Lycopene preferentially accumulated in CMO-II KO mouse tissues and serum compared with WT mouse tissues. Ξ²-Carotene preferentially accumulated in some CMO-II KO mouse tissues compared with WT mouse tissues. Relative tissue mRNA expression of CMO-I and CMO-II was differentially expressed in mouse tissues, and CMO-II, but not CMO-I, was expressed in mouse prostate. In conclusion, the loss of CMO-II expression leads to increased serum and tissue concentrations of lycopene in tomato-fed mice
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