Green tea and skin cancer: photoimmunology, angiogenesis and DNA repair

被引:148
作者
Katiyar, Suchitra
Elmets, Craig A.
Katiyar, Santosh K. [1 ]
机构
[1] Univ Alabama Birmingham, Dept Dermatol, Birmingham, AL 35294 USA
[2] Birmingham VA Med Ctr, Birmingham, AL 35294 USA
基金
美国国家卫生研究院;
关键词
green tea polyphenols; photocarcinogenesis; DNA repair; cyclobutane pyrimidine dimer; immunosuppression; contact hypersensitivity; angiogenesis; IL-10; IL-12;
D O I
10.1016/j.jnutbio.2006.08.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Human skin is constantly exposed to numerous noxious physical, chemical and environmental agents. Some of these agents directly or indirectly adversely affect the skin. Cutaneous overexposure to environmental solar ultraviolet (UV) radiation (290-400 nm) has a variety of adverse effects on human health, including the development of melanoma and nonmelanoma skin cancers. Therefore, there is a need to develop measures or strategies, and nutritional components are increasingly being explored for this purpose. The polyphenols present in green tea (Camellia sinensis) have been shown to have numerous health benefits, including protection from UV carcinogenesis. (-)-Epigallocatechin-3-gallate (EGCG) is the major and most photoprotective polyphenolic component of green tea. In this review article, we have discussed the most recent investigations and mechanistic studies that define and support the photoprotective efficacy of green tea polyphenols (GTPs) against UV carcinogenesis. The oral administration of GTPs in drinking water or the topical application of EGCG prevents UVB-induced skin tumor development in mice, and this prevention is mediated through: (a) the induction of immunoregulatory cytokine interleukin (IL) 12; (b) IL-12-dependent DNA repair following nucleotide excision repair mechanism; (c) the inhibition of UVinduced immunosuppression through IL-12-dependent DNA repair; (d) the inhibition of angiogenic factors; and (e) the stimulation of cytotoxic T cells in a tumor microenvironment. New mechanistic information strongly supports and explains the chemopreventive activity of GTPs against photocarcinogenesis. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:287 / 296
页数:10
相关论文
共 69 条
[1]   IDENTIFICATION OF THE MOLECULAR TARGET FOR THE SUPPRESSION OF CONTACT HYPERSENSITIVITY BY ULTRAVIOLET-RADIATION [J].
APPLEGATE, LA ;
LEY, RD ;
ALCALAY, J ;
KRIPKE, ML .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 170 (04) :1117-1131
[2]   Chemoprevention of photocarcinogenesis by selected dietary botanicals [J].
Baliga, MS ;
Katiyar, SK .
PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES, 2006, 5 (02) :243-253
[3]  
CHAPMAN RS, 1995, PHOTOCHEM PHOTOBIOL, V61, P223
[4]   UV EXPOSURE REDUCES IMMUNIZATION RATES AND PROMOTES TOLERANCE TO EPICUTANEOUS ANTIGENS IN HUMANS - RELATIONSHIP TO DOSE, CD1A-DR+ EPIDERMAL MACROPHAGE INDUCTION, AND LANGERHANS CELL DEPLETION [J].
COOPER, KD ;
OBERHELMAN, L ;
HAMILTON, TA ;
BAADSGAARD, O ;
TERHUNE, M ;
LEVEE, G ;
ANDERSON, T ;
KOREN, H .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (18) :8497-8501
[5]   Ultraviolet radiation and tumor immunity [J].
de Gruijl, FR .
METHODS, 2002, 28 (01) :122-129
[6]   ESTIMATE OF THE WAVELENGTH DEPENDENCY OF ULTRAVIOLET CARCINOGENESIS IN HUMANS AND ITS RELEVANCE TO THE RISK ASSESSMENT OF A STRATOSPHERIC OZONE DEPLETION [J].
DEGRUIJL, FR ;
VANDERLEUN, JC .
HEALTH PHYSICS, 1994, 67 (04) :319-325
[7]  
DEGRUIJL FR, 1993, CANCER RES, V53, P53
[8]   Retinoid chemoprevention in the high-risk patient [J].
DiGiovanna, JJ .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1998, 39 (02) :S82-S85
[9]  
FIORENTINO DF, 1991, J IMMUNOL, V147, P3815
[10]  
FIORENTINO DF, 1991, J IMMUNOL, V146, P3444