Relationship Between Plasma Carotenoids and Prostate Cancer.pdf

نویسندگان

  • Maya Vadiveloo
  • Shine Chang
  • John W. Erdman
  • Steven K. Clinton
  • Sara S. Strom
  • Yuko Yamamura
  • Cherie M. Duphorne
  • Margaret R. Spitz
  • Christopher I. Amos
  • John H. Contois
  • Xiangjun Gu
  • Richard J. Babaian
  • Peter T. Scardino
  • Stephen D. Hursting
چکیده

Carotenoids, particularly lycopene, are thought to decrease prostate cancer risk, but the relationship between plasma carotenoid concentrations and risk in various populations has not been well characterized. Comparing 118 non-Hispanic Caucasian men mainly from southeast Texas with nonmetastatic prostate cancer with 52 healthy men from the same area, we conducted a case-control analysis evaluating associations between risk and plasma levels of total carotenoids, -cryptoxanthin, αand trans-β-carotene, lutein and zeaxanthin, total lycopenes, trans-lycopene, total cislycopenes, and cis-lycopene isoforms 1, 2, 3, and 5. Risk for men with high plasma levels of α-carotene, trans-β-carotene, β-cryptoxanthin, and lutein and zeaxanthin was less than half that for those with lower levels. In contrast, we observed no significant associations for total lycopenes, all-translycopene, and cis-lycopene isomer peaks 2, 3, and 5, although high levels of cis-lycopene isomer peak 1 were inversely associated with risk. Analysis of men with aggressive disease (Gleason scores of ≥7, n= 88) vs. less aggressive cases (Gleasonscoresof<7,n=30) failed toreveal significantassociations between carotenoid levels and the risk of diagnosis with aggressive disease. These findings suggest that, in these men,highercirculating levelsof β-cryptoxanthin,α-carotene, trans-β-carotene, and lutein and zeaxanthin may contribute to lower prostate cancer risk but not to disease progression. Introduction Despite much effort spent investigating the role of carotenoids in prostate carcinogenesis, whether and how carotenoids influence cancer risk are still somewhat ambiguous. In general, dietary studies have consistently suggested an inverse association between prostate cancer risk and consumption of carotenoids in tomato products (1). At the same time, studies using biological measures of tomato-based carotenoids have been less uniform in their findings (2–8). Such inconsistency may result in part from differences between studies. Closer investigation of carotenoids, including consideration of their biochemical structures, may help resolve some of these discrepancies, particularly for lycopene, one of the primary carotenoids in tomatoes. Measuring the quantities of carotenoids that are relevant to prostate carcinogenesis is complicated. For example, dietary assessment of lycopene intake may capture biological exposure inaccurately because lycopene concentrations in foods can vary by the period of cultivation and method of food processing (9,10). Dietary assessment methods also do not easily accommodate variations in carotenoid bioavailability; individual differences in digestion, metabolism, and even patterns of food intake can all influence lycopene absorption. Consuming lycopene-containing foods NUTRITION AND CANCER, 53(2), 127–134 Copyright © 2005, Lawrence Erlbaum Associates, Inc. S. Chang, S. S. Strom, Y. Yamamura, C. M. Duphorne, M. R. Spitz, C. I. Amos, J. H. Contois, X. Gu, and S. D. Hursting are affiliated with the Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030. J. H. Contois is currently affiliated with Liposcience Inc., Raleigh, NC 27616. S. D. Hursting is currently affiliated with the University of Texas-Austin and the M. D. Anderson Cancer Center, Austin, TX 78712. J. W. Erdman Jr. is affiliated with the Division of Nutritional Sciences, University of Illinois, Urbana, IL 61801. S. K. Clinton is affiliated with the Department of Internal Medicine, Division of Medical Oncology, The Ohio State University College of Medicine, Columbus, OH 43210. M. Vadiveloo was affiliated with the Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892 and is currently affiliated with the Frances Stern Nutrition Center, Tufts-New England Medical Center, Boston, MA 02111. R. J. Babaian is affiliated with the Department of Urology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030. P. T. Scardino is affiliated with Memorial Sloan-Kettering Cancer Center, New

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تاریخ انتشار 2016