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Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Dietary Lycopene Downregulates Carotenoid 15,15'-Monooxygenase and PPAR- in Selected Rat Tissues^1–3,

Division of Nutritional Sciences, University of Illinois, Urbana, IL 61801

⁴ To whom correspondence should be addressed: E-mail: jwerdman{at}uiuc.edu.

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 (PPAR-)] 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- were differentially expressed among rat tissues. CMO1 and PPAR- 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- 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-, 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 ß-carotene, retinoid, and/or lipid metabolism.

KEY WORDS: • lycopene • ß-carotene 15,15'- monooxygenase • ß-carotene 9',10'-monooxygenase • rats • prostate

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