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Carotenoid monooxygenase II knock‐out mice exhibit phenotypical differences and altered lycopene accumulation pattern compared to C57Bl6 mice
Author(s) -
Ford Nikki A.,
Lintig Johannes,
Wyss Adrian,
Erdman John W.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1105.9
Subject(s) - lycopene , carotenoid , medicine , endocrinology , wild type , in vivo , spleen , chemistry , seminal vesicle , biology , andrology , biochemistry , mutant , gene , microbiology and biotechnology , prostate , cancer
Carotenoid monooxygenase II (CMO‐II) cleaves lycopene excentrically in vitro . Little is known about CMO‐II in vivo and therefore we evaluated feed intake, weight change, and lycopene accumulation in 11 male and 8 female CMO‐II knock‐out (CMO‐II KO) mice. Twenty‐three to twenty‐seven week old CMO‐II KO mice consumed a 10% tomato powder diet for 60 days and were compared to 27 week old C57Bl6 wild‐type mice. Twenty‐four hours prior to sacrifice, some mice were orally intubated with 3μCi of 14 C‐lycopene in cottonseed oil. We verified successful loss of expression of CMO‐II by Real‐Time PCR. No differences in feed intake, weight, or health status were observed in CMO‐II KO mice compared to C57Bl6 wild‐type mice. Student's t‐test showed total lycopene concentration was higher in the adrenals (p=0.005) and uterus (p=0.02) of CMO‐II KO mice compared with wild‐type while no differences were found in the liver, seminal vesicles, or spleen. Organ weights were evaluated as a percentage of body weight. CMO‐II KO mice had significantly smaller livers (p=0.003), thymus (p=0.036), and seminal vesicles (p=0.034), but larger testes (p=0.0003). Preliminary evidence indicates CMO‐II KO mice have phenotypical differences from wild‐type mice and metabolize lycopene differently than wild‐type mice. (Funded in part by NIH grant PHS‐1‐RO1 CA125384.)