Recommended dietary allowances (RDAs) for genomic stability

被引:57
作者
Fenech, M [1 ]
机构
[1] CSIRO, Adelaide, SA 5000, Australia
关键词
RDA; recommended dietary allowance; diet; vitamins; micronutrients; genomic stability; DNA damage; micronucleus; DNA methylation; DNA strand breaks; chromosome aberrations;
D O I
10.1016/S0027-5107(01)00168-3
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Diet as a key factor in determining genomic stability is more important than previously imagined because we now know it impacts on all relevant pathways, i.e. exposure to dietary carcinogens, activation/detoxification of carcinogens, DNA repair, DNA synthesis and apoptosis. Current recommended dietary allowances for vitamins and minerals are based largely on the prevention of diseases of deficiency such as scurvy in the case of Vitamin C. Because diseases of development, degenerative disease and ageing itself are partly caused by damage to DNA, it seems logical that we should focus better our attention on defining optimal requirements of key minerals and vitamins for preventing damage to both nuclear and mitochondrial DNA. To date our knowledge on optimal micronutrient levels for genomic stability is scanty and disorganised. Appropriately designed placebo, controlled trials are required to define recommended dietary allowances for genomic stability. Recently, it has been shown that above RDA intakes of folic acid and Vitamin B12 are required to reduce the micronucleus index in humans by 25%. In the future, clinical trials with a defined wider array of complementary DNA damage end-points would be necessary. That there is a need for an international collaborative group to establish RDAs for genomic stability is self-evident and this paper is a call for such a process to begin. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:51 / 54
页数:4
相关论文
共 20 条
[11]   Folate, vitamin B12, homocysteine status and DNA damage in young Australian adults [J].
Fenech, M ;
Aitken, C ;
Rinaldi, J .
CARCINOGENESIS, 1998, 19 (07) :1163-1171
[12]   Chromosomal damage rate, aging, and diet [J].
Fenech, M .
TOWARDS PROLONGATION OF THE HEALTHY LIFE SPAN: PRACTICAL APPROACHES TO INTERVENTION, 1998, 854 :23-36
[13]  
Holliday R, 1995, Understanding ageing
[14]   FRAGILE SITES IN CHROMOSOMES - POSSIBLE MODEL FOR THE STUDY OF SPONTANEOUS CHROMOSOME BREAKAGE [J].
JACKY, PB ;
BEEK, B ;
SUTHERLAND, GR .
SCIENCE, 1983, 220 (4592) :69-70
[15]   Moderate folate depletion increases plasma homocysteine and decreases lymphocyte DNA methylation in postmenopausal women [J].
Jacob, RA ;
Gretz, DM ;
Taylor, PC ;
James, SJ ;
Pogribny, IP ;
Miller, BJ ;
Henning, SM ;
Swendseid, ME .
JOURNAL OF NUTRITION, 1998, 128 (07) :1204-1212
[16]   Mapping the role of NAD metabolism in prevention and treatment of carcinogenesis [J].
Jacobson, EL ;
Shieh, WM ;
Huang, AC .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 1999, 193 (1-2) :69-74
[17]   Quality control by DNA repair [J].
Lindahl, T ;
Wood, RD .
SCIENCE, 1999, 286 (5446) :1897-1905
[18]   Chromosomal aberrations in PARP-/- mice:: Genome stabilization in immortalized cells by reintroduction of poly(ADP-ribose) polymerase cDNA [J].
Simbulan-Rosenthal, CM ;
Haddad, BR ;
Rosenthal, DS ;
Weaver, Z ;
Coleman, A ;
Luo, RB ;
Young, HM ;
Wang, ZQ ;
Ried, T ;
Smulson, ME .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (23) :13191-13196
[19]   Polymorphisms in the methylenetetrahydrofolate reductase gene are associated with susceptibility to acute leukemia in adults [J].
Skibola, CF ;
Smith, MT ;
Kane, E ;
Roman, E ;
Rollinson, S ;
Cartwright, RA ;
Morgan, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (22) :12810-12815
[20]   Micronuclei in lymphocytes and exfoliated buccal cells of postmenopausal women with dietary changes in folate [J].
Titenko-Holland, N ;
Jacob, RA ;
Shang, N ;
Balaraman, A ;
Smith, MT .
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 1998, 417 (2-3) :101-114